EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2355

EOS Med Chem is TOP 100 of China CRO & CMO company, mainly in custom synthesis.
2019 CHINA CPHI E2A62
2019 WORLD CPHI 101C45
FDA New, GMP Do
Clinical Phase II, III Intermediates
GMP Custom synthesis, Full Document

R&D Center: 8000 sq, More than 100 hoods
Pilot Plant: 20000sq, 40 reactors from 5-200L
Manufacturing Site: 800000sq, 40 reactors from 100-5000L
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Email: info@eosmedchem.com ; eosmedchem@gmail.com

Name: Tubulysin M, CAS: 936691-46-2, stock 21.1g, assay 98.6%, MWt: 727.95, Formula: C38H57N5O7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: Tubulysin M is a highly cytotoxic peptide isolated from the myxobacterial species Archangium geophyra and Angiococcus disciformis[1]. Tubulysin displays extremely potent cytotoxic activity in mammalian cells, including multidrug-resistant cell lines, with IC50 values in the lower nanomolar range[2]. Tubulysin M is a cytotoxic activity tubulysin which inhibits tubulin polymerization and leads to cell cycle arrest and apoptosis[3].

Name: Valemetostat (tosylate) DS-3201 (tosylate), CAS: 1809336-93-3, stock 26.3g, assay 98.3%, MWt: 660.22, Formula: C33H42ClN3O7S, Solubility: DMSO : 125 mg/mL (189.33 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: Valemetostat tosylate (DS-3201 tosylate) is a first-in-class EZH1/2 dual inhibitor, used in the research of relapsed/refractory peripheral T-cell lymphoma[1].
IC50 & Target: EZH1/2[1]

Name: Tecarfarin (sodium) ATI-5923 (sodium), CAS: 1004551-83-0, stock 12.8g, assay 98.6%, MWt: 482.31, Formula: C21H13F6NaO5, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Tecarfarin sodium (ATI-5923 sodium) is a novel orally active non-competitive vitamin K epoxide reductase (VKOR) antagonist, impairs the activation of the vitamin K-dependent clotting factors II, VII, IX and X[1].
Tecarfarin sodium has the antithrombotic activity[2].
IC50 & Target: VKOR[1]

Name: Thalidomide-O-amido-C3-NH2 (TFA) Cereblon Ligand-Linker Conjugates 16 (TFA);E3 Ligase Ligand-Linker Conjugates 52 (TFA), CAS: 2022182-58-5, stock 23.9g, assay 98.9%, MWt: 502.40, Formula: C20H21F3N4O8, Solubility: DMSO : 125 mg/mL (248.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: Thalidomide-O-amido-C3-NH2 TFA is a synthesized E3 ligase ligand-linker conjugate that incorporates the Thalidomide based cereblon ligand and a linker used in PROTAC technology.

Name: EN6, CAS: 1808714-73-9, stock 8.1g, assay 98.3%, MWt: 368.34, Formula: C19H14F2N4O2, Solubility: DMSO : 5 mg/mL (13.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Autophagy, Target: Proton Pump;Autophagy, Biological_Activity: EN6 is a small-molecule in vivo activator of autophagy that covalently targets cysteine 277 in the ATP6V1A subunit of the lysosomal the vacuolar H+ ATPase (v-ATPase). EN6-mediated ATP6V1A modification decouples the v-ATPase from the Rags, leading to inhibition of mTORC1 signaling, increased lysosomal acidification and activation of autophagy. EN6 clears TDP-43 aggregates, a causative agent in frontotemporal dementia, in a lysosome-dependent manner[1].

Name: Nomegestrol (acetate), CAS: 58652-20-3, stock 0.2g, assay 98.9%, MWt: 370.48, Formula: C23H30O4, Solubility: DMSO : 62.5 mg/mL (168.70 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Progesterone Receptor, Biological_Activity: Nomegestrol acetate is a potent, highly selective progestogen, which is characterized as a full agonist at the progesterone receptor, with no or minimal binding to other steroid receptors, including the androgen and glucocorticoid receptors[1].
IC50 & Target: Progesterone receptor[1]

Name: Nilotinib AMN107, CAS: 641571-10-0, stock 37.6g, assay 98.3%, MWt: 529.52, Formula: C28H22F3N7O, Solubility: DMSO : 6 mg/mL (11.33 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Autophagy, Target: Bcr-Abl;Autophagy, Biological_Activity: Nilotinib is a second generation tyrosine kinase inhibitor (TKI), is significantly more potent against BCR-ABL than Imatinib, and is active against many Imatinib-resistant BCR-ABL mutants.
IC50 & Target: Bcr-Abl[1]
In Vitro: The novel, selective Abl inhibitor, Nilotinib (AMN107), is designed to interact with the ATP-binding site of BCR-ABL with a higher affinity than Imatinib. In addition to being significantly more potent compared with Imatinib (IC50<30 nM), Nilotinib also maintains activity against most of the BCR-ABL point mutants that confer Imatinib resistance[1]. Nilotinib demonstrates significant antitumor efficacy against GIST xenograft lines and Imatinib-resistant GIST cell lines. The parent cell lines GK1C and GK3C show Imatinib sensitivity with IC50 of 4.59±0.97 µM and 11.15±1.48 µM, respectively. The Imatinib-resistant cell lines GK1C-IR and GK3C-IR show Imatinib resistance with IC50 values of 11.74±0.17 µM (P<0.001) and 41.37±1.07 µM (P<0.001), respectively[2].
In Vivo: The percentage of tumor growth inhibition (TGI) is 83.8% for Imatinib and 69.6% for Nilotinib in the GK1X xenograft line (n.s.). In the GK2X xenograft line, TGI is 83.0% for Imatinib and 85.3% for Nilotinib (n.s.). Additionally, the GK3X xenograft line TGI is 31.1% for Imatinib and 47.5% for Nilotinib (n.s.). These results suggest that, except for the GK1X xenograft line, Nilotinib shows equivalent or higher antitumor effects than Imatinib[2]. Nilotinib has a significant healing effect on the macroscopic and microscopic pathologic scores and ensures considerable mucosal healing in the indomethacin-induced enterocolitis rat model. While Nilotinib decreased the PDGFR α and β levels and apoptotic scores in the colon, it did not have a significant effect on the weight and TNF-α levels. Further experimental investigations could provide more definitive evidence for humans[3].

Name: MI-1061, CAS: 1410737-34-6, stock 22.7g, assay 98.1%, MWt: 582.45, Formula: C30H26Cl2FN3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease;Apoptosis, Target: Apoptosis;E1/E2/E3 Enzyme;MDM-2/p53, Biological_Activity: MI-1061 is a potent, orally bioavailable, and chemically stable MDM2 (MDM2-p53 interaction) inhibitor (IC50=4.4 nM; Ki=0.16 nM). MI-1061 potently activates p53, induces apoptosis, and has anti-tumor activity[1].
IC50 & Target: IC50: 4.4 nM (MDM2)[1] 
Ki: 0.16 nM (MDM2)
In Vitro: MI-1061 achieves IC50=100 and 250 nM in the SJSA-1 and HCT-116 p53+/+ cell lines, respectively, and has IC50>10000 nM in the p53 knockout cell line HCT-116 p53–/–cell line[1].
In Vivo: MI-1061 is capable of achieving tumor regression in the SJSA-1 xenograft tumor model in mice with oral administration[1].

Name: NQO1 activator 1, CAS: 1800405-30-4, stock 10.7g, assay 98.1%, MWt: 240.26, Formula: C14H12N2O2, Solubility: DMSO : 250 mg/mL (1040.54 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NQO1 activator 1 is an orally available NAD+ modulator. It reacts with NAD(P)H:quinone oxidoreductase 1 (NQO1) as a substrate, resulting in increases in intracellular NAD+ levels via NADH oxidation. Elevated NAD+ levels triggers the activation of SIRT1 and AMPK, and subsequently activates PGC-1α. NQO1 activator 1 improves energy metabolism and mitochondrial dysfunction in MELAS fibroblasts[1].
IC50 & Target: NQO1[1]

Name: SIS17, CAS: 2374313-54-7, stock 8.4g, assay 98.6%, MWt: 366.60, Formula: C21H38N2OS, Solubility: DMSO : 125 mg/mL (340.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: SIS17 is a mammalian histone deacetylase 11 (HDAC 11) inhibitor with an IC50 value of 0.83 μM, inhibits the demyristoylation HDAC11 substrate, serine hydroxymethyl transferase 2, without inhibiting other HDACs[1].
IC50 & Target: IC50: 0.83 μM (HDAC 11)[1]

Name: Methyl cellulose, CAS: 9004-67-5, stock 25.5g, assay 98.3%, MWt: 1000, Formula: N/A, Solubility: , Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Methylcellulose is a natural polymer which gels on heating. Methylcellulose is not toxic.

Name: DAMGO (TFA), CAS: 950492-85-0, stock 21.9g, assay 98.3%, MWt: 627.61, Formula: C28H36F3N5O8, Solubility: H2O : 125 mg/mL (199.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: DAMGO TFA is a μ-opioid receptor (μ-OPR ) selective agonist with a Kd of 3.46 nM for native μ-OPR[1].

Name: Pomalidomide-C2-NH2 (hydrochloride) Cereblon Ligand-Linker Conjugates 15 (hydrochloride), CAS: 2305369-00-8, stock 22.5g, assay 98.3%, MWt: 352.77, Formula: C15H17ClN4O4, Solubility: DMSO : 125 mg/mL (354.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: Pomalidomide-C2-NH2 hydrochloride is a synthesized E3 ligase ligand-linker conjugate that incorporates the Pomalidomide based cereblon ligand and a linker used in PROTAC technology.

Name: Dexamethasone palmitate DXP, CAS: 14899-36-6, stock 15.2g, assay 98.3%, MWt: 630.87, Formula: C38H59FO6, Solubility: DMSO : 250 mg/mL (396.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: Dexamethasone palmitate (DXP) is a prodrug of Dexamethasone, which is a glucocorticoid receptor agonist[1]. Dexamethasone palmitate (DXP) has a 47-fold lower affinity for the glucocorticoid receptor than Dexamethasone[2]. Anti-inflammatory agent.

Name: SKF-34288 (hydrochloride) 3-Mercaptopicolinic acid (hydrochloride), CAS: 320386-54-7, stock 20g, assay 98.5%, MWt: 191.64, Formula: C6H6ClNO2S, Solubility: H2O : 5 mg/mL (26.09 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SKF-34288 hydrochloride (3-Mercaptopicolinic acid) is a phosphoenolpyruvate carboxykinase (PEPCK) inhibitor.
SKF-34288 hydrochloride is a potent hypoglycemic agent via inhibition of glucose synthesis through the specific inhibition of PEPCK in the gluconeogenesis pathway[1]. SKF-34288 hydrochloride inhibits Asn metabolism and results in an increase in amino acids and amides[2].
IC50 & Target: IC50: PEPCK[1]

Name: CP-409092 (hydrochloride), CAS: 225240-86-8, stock 34.8g, assay 98.3%, MWt: 333.81, Formula: C17H20ClN3O2, Solubility: DMSO : 41.67 mg/mL (124.83 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: CP-409092 hydrochloride is a partial agonist of GABAA receptor, with anti-anxiety activity[1].

Name: 5-Methoxy-DL-tryptophan, CAS: 28052-84-8, stock 37.9g, assay 98.3%, MWt: 234.25, Formula: C12H14N2O3, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Inosine 5'-monophosphate (disodium) salt (hydrate), CAS: 352195-40-5, stock 38g, assay 98.6%, MWt: 1000, Formula: N/A, Solubility: H2O : 125 mg/mL (Need ultrasonic); H2O : 250 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: SPP, CAS: 341498-08-6, stock 33.4g, assay 98.7%, MWt: 340.42, Formula: C14H16N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SPP is a cleavable disulfide linker, can be used to form cytotoxic compound- linker conjugate[1].

Name: Phosphonoacetic acid, CAS: 4408-78-0, stock 35.6g, assay 99%, MWt: 140.03, Formula: C2H5O5P, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: PROTAC Bcl2 degrader-1, CAS: 2378801-85-3, stock 10.7g, assay 98.7%, MWt: 941.84, Formula: C45H45BrN6O10S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;PROTAC, Target: Bcl-2 Family;PROTAC, Biological_Activity: PROTAC Bcl2 degrader-1 (Compound C5) is a PROTAC, which potently and selectively induces the degradation of Bcl-2 (IC50, 4.94 μM; DC50, 3.0 μM) and Mcl-1 (IC50, 11.81 μM) by introducing the E3 ligase cereblon (CRBN)-binding ligand pomalidomide to Mcl-1/Bcl-2 dual inhibitor Nap-1[1].
IC50 & Target: IC50: 4.94 μM (Bcl-2), 11.81 μM (Mcl-1)[1] 
DC50: 3.0 μM (Bcl-2)[1]

Name: PROTAC Mcl1 degrader-1, CAS: 2163793-38-0, stock 13.5g, assay 98.7%, MWt: 909.84, Formula: C45H45BrN6O8S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;PROTAC, Target: Bcl-2 Family;PROTAC, Biological_Activity: PROTAC Mcl1 degrader-1 (compound C3), a proteolysis targeting chimera (PROTAC), is a potently and selectively Mcl-1 inhibitor with an IC50 of 0.78 μM. PROTAC Mcl1 degrader-1 induces the ubiquitination and proteasomal degradation of Mcl-1 by introducing the E3 ligase cereblon (CRBN)-binding ligand pomalidomide to Mcl-1 inhibitor S1-6 with μM-range affinity[1].

Name: SBI-553, CAS: 1849603-72-0, stock 19.9g, assay 98%, MWt: 450.55, Formula: C26H31FN4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neurotensin Receptor;Neurotensin Receptor, Biological_Activity: SBI-553 is a potent and brain penetrant NTR1 allosteric modulator, with an EC50 of 0.34 μM[1].
IC50 & Target: EC50: 0.34 μM (NTR1)[1].

Name: BMS-986020 (sodium), CAS: 1380650-53-2, stock 14.1g, assay 98.1%, MWt: 504.51, Formula: C29H25N2NaO5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (297.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: BMS-986020 sodium is a high-affinity lysophosphatidic acid receptor 1 (LPA1) antagonist[1].
BMS-986020 sodium inhibits bile acid and phospholipid transporters with IC50s of 4.8 µM, 6.2 µM, and 7.5 µM for BSEP, MRP4, and MDR3, respectively[2]. BMS-986020 sodium is used for the treatment of idiopathic pulmonary fibrosis (IPF)[3].
IC50 & Target: IC50: 4.8 µM (BSEP); 6.2 µM (MRP4); 7.5 µM (MDR3)[2]

Name: Arotinolol, CAS: 68377-92-4, stock 7.4g, assay 98.7%, MWt: 371.54, Formula: C15H21N3O2S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Arotinolol is a nonselective α/β-adrenergic receptor blocker and a vasodilating β-blocker. Arotinolol is an antihypertensive agent for the treatment of a variety of cardiovascular pathologies as well as non-cardiovascular diseases[1].
IC50 & Target: IC50: α/β-adrenergic receptor
In Vivo: Arotinolol (oral gavage; 200 mg/kg; 8 weeks) can significantly decrease central arterial pressure (CAP) and pulse wave velocity (PWV), in addition, it reduces aortic collagen depositions and finally improves arterial stiffness in SHR mouse[1].

Name: PROTAC ERRα ligand 2, CAS: 2306388-57-6, stock 38.4g, assay 98.1%, MWt: 445.31, Formula: C20H13F6NO4, Solubility: DMSO : 62.5 mg/mL (140.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: PROTAC ERRα ligand 2 is an estrogen-related receptor α (ERRα) inverse agonist with an IC50 of 5.67 nM. PROTAC ERRα ligand 2 (IC50=5.67 nM) displays a ~11-fold improved potency than XCT790 (IC50=61.3 nM)[1].

Name: LDN-192960 (hydrochloride), CAS: 2309172-48-1, stock 29g, assay 98.5%, MWt: 401.35, Formula: C18H22Cl2N2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage, Target: DYRK;Haspin Kinase, Biological_Activity: LDN-192960 hydrochloride is an inhibitor of Haspin and Dual-specificity Tyrosine-regulated Kinase 2 (DYRK2) with IC50s of 10 nM and 48 nM, respectively[1].
IC50 & Target: IC50: 10 nM (Haspin); 48 nM (DYRK2)[1]
In Vitro: LDN-192960 hydrochloride (10 μM) is selective and inhibits ten of the other kinases by ≥90%, with only five being potently inhibited (IC50<1 μM), including CLK1 (IC50=0.21 μM), DYRK1A (IC50= 0.10 μM), DYRK2 (IC50=2 nM), DYRK3 (IC50=19 nM) and PIM1 (IC50=0.72 μM)[1].

Name: MC-VC-PABC-Aur0101, CAS: 1438849-92-3, stock 17.3g, assay 98.8%, MWt: 1341.66, Formula: C68H100N12O14S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: Drug-Linker Conjugates for ADC, Biological_Activity: MC-VC-PABC-Aur0101 is a drug-linker conjugate for ADC with potent antitumor activity by using Aur0101 (an auristatin microtubule inhibitor), linked via the ADC linker MC-VC-PABC.

Name: LHVS, CAS: 170111-28-1, stock 29.3g, assay 98.9%, MWt: 527.68, Formula: C28H37N3O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: Cathepsin;Parasite, Biological_Activity: LHVS is a potent, non-selective cysteine protease inhibitor[1]. LHVS effectively blocks T. gondii microneme protein secretion (IC50=10 μM), gliding motility, and cell invasion[2].
IC50 & Target: Cysteine protease[1]

Name: Poly(4-vinylphenol), CAS: 24979-70-2, stock 14.1g, assay 98.5%, MWt: 1000, Formula: (C8H8O)x, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Tipepidine (hydrochloride), CAS: 1449686-84-3, stock 8.7g, assay 98.3%, MWt: 311.89, Formula: C15H18ClNS2, Solubility: DMSO : 41.67 mg/mL (133.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Tipepidine hydrochloride reversibly inhibits dopamine (DA) D2 receptor-mediated GIRK currents (IDA(GIRK)) with an IC50 of 7.0 μM. Tipepidine hydrochloride subsequently activates VTA dopamine neuron[1]. Tipepidine hydrochloride, a non-narcotic antitussive, exerts an antidepressant-like effect[2].
IC50 & Target: IC50: 7.0 μM (dopamine D2 receptor)[1]
In Vivo: Tipepidine (i.p.; 10-40 mg/kg; 0.5-23 hours) significantly decreases the immobility time in the forced swimming test in ACTH-treated rats. Tipepidine (i.p.; 40 mg/kg) increases the extracellular dopamine level of the nucleus accumbens (NAc) in ACTH-treated rats[2].

Name: N-Dodecyl-β-D-maltoside Lauryl Maltoside, CAS: 69227-93-6, stock 19.7g, assay 98%, MWt: 510.62, Formula: C24H46O11, Solubility: H2O : 125 mg/mL (244.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Dodecyl-β-D-maltoside (Lauryl Maltoside) is a derivatives of pyrene (Py), and it is a alkyl maltopyranoside detergent, especially in transporters and respiratory complexes. N-Dodecyl-β-D-maltoside has also been employed in applications such as in the purification and stabilization of RNA polymerase and detection of protein-lipid interactions[1].

Name: m-Tyramine (hydrobromide), CAS: 38449-59-1, stock 22.5g, assay 98.3%, MWt: 218.09, Formula: C8H12BrNO, Solubility: DMSO : 125 mg/mL (573.16 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: m-Tyramine hydrobromide is an endogenous trace amine neuromodulator. m-Tyramine hydrobromide has effects on the adrenergic and dopaminergic receptor[1, 2].

Name: Sulfaclozine (sodium) Sulfachloropyrazine (sodium), CAS: 23307-72-4, stock 32g, assay 98.9%, MWt: 306.70, Formula: C10H8ClN4NaO2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Bacterial;Parasite, Biological_Activity: Sulfaclozine sodium (Sulfachloropyrazine sodium) is an efficacious sulphonamide derivative with antibacterial and anticoccidial effects. Sulfaclozine sodium is commonly used for the treatment of various poultry diseases (particularly, collibacteriosis, fowl cholera and coccidiosis)[1].
IC50 & Target: Bacterial; Parasite[1]
In Vitro: The elimination of Sulfaclozine in the three systems: UV/TiO2, UV/K2S2O8, and UV/TiO2/K2S2O8. Sulfaclozine is weakly adsorbed on the surface of TiO2 at pH 7 (< 5%) but efficiently eliminated with the following three systems: UV/TiO2, UV/K2S2O8, and UV/TiO2/K2S2O8 in ultra pure water. Moreover, 12 of Sulfaclozine by-products are identified and reaction pathways show that, in addition of •OH and SO4•− radicals, the conduction-band electrons are responsible for the formation of some main by-products either directly or by the formation of superoxide radicals[2].
In Vivo: Sulfaclozine (60 mg/kg; intravenous injection or oral administration; male broiler chickens) can be used primarily for the treatment of parasitic and microbial infections of the digestive tract rather than for the treatment of systemic infections[1].

Name: 10β,17β-dihydroxyestra-1,4-dien-3-one DHED, CAS: 549-02-0, stock 38.4g, assay 98.5%, MWt: 288.38, Formula: C18H24O3, Solubility: DMSO : 250 mg/mL (866.91 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: 10β,17β-dihydroxyestra-1,4-dien-3-one (DHED) is a brain-targeting bioprecursor prodrug of the main human estrogen, 17β-estradiol, alleviates hot flushes in rat models of thermoregulatory dysfunction of the brain[1].
In Vivo: 10β,17β-dihydroxyestra-1,4-dien-3-one (DHED), is an inactive bioprecursor prodrug of 17β-estradiol converting to 17β-estradiol only in the brain. DHED as an E2-bioprecursor may be a viable approach for delivering E2 selectively into the brain for the potential treatment of hot flushes[1].

Name: Tivozanib AV-951;KRN951, CAS: 475108-18-0, stock 35.4g, assay 98.4%, MWt: 454.86, Formula: C22H19ClN4O5, Solubility: DMSO : 25 mg/mL (54.96 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK, Target: VEGFR, Biological_Activity: Tivozanib (AV-951; KRN951) is a highly potent and selective VEGFR 1/2/3 inhibitor with IC50s of 0.21, 0.16, and 0.24 nM in cell assay, respectively.
IC50 & Target: IC50: 0.21 nM (VEGFR 1), 0.16 nM (VEGFR 2), 0.24 nM (VEGFR 3)[1]
In Vitro: Tivozanib potently inhibits VEGF-induced VEGFR2 phosphorylation in endothelial cells (IC50=0.16 nM). It also inhibits ligand-induced phosphorylation of PDGFRβ and c-Kit (IC50=1.72 and 1.63 nM, respectively). Tivozanib blocks VEGF-dependent, but not VEGF-independent, activation of mitogenactivated protein kinases and proliferation of endothelial cells. It inhibits VEGF-mediated migration of human umbilical vein endothelial cells[1].
In Vivo: Following p.o. administration to athymic rats, Tivozanib decreases the microvessel density within tumor xenografts and attenuates VEGFR-2 phosphorylation levels in tumor endothelium. It also displays antitumor activity against a wide variety of human tumor xenografts, including lung, breast, colon, ovarian, pancreas, and prostate cancer[1].

Name: Clavulanate (lithium), CAS: 61177-44-4, stock 38.4g, assay 98%, MWt: 205.09, Formula: C8H8LiNO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Clavulanate lithium is a potent β-lactamase inhibitor and acts as an antibiotic[1][2].
IC50 & Target: β-lactamase[1]
In Vitro: Clavulanate lithium has weak antibacterial activity against most organisms when administered alone, but given in combination with beta-lactam antibiotics prevents antibiotic inactivation by microbial lactamase[1]. 
Clavulanate lithium (0.25, 0.5 mg/L) causes a relatively slow inhibition of growth, and a higher concentration (1 mg/L) is only marginally more effective than 0.5 mg/L [2].

Name: GSK205, CAS: 1263068-83-2, stock 10g, assay 98.4%, MWt: 481.45, Formula: C24H25BrN4S, Solubility: DMSO : 250 mg/mL (519.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: GSK205 is a potent, selective TRPV4 antagonist with an IC50 of 4.19 μM for inhibiting TRPV4-mediated Ca2+ influx[1][2].
IC50 & Target: IC50: 4.19 μM (TRPV4)[2]
In Vitro: GSK205 (100 μM) potently antagonizes TRPV4 in 3T3-F442A adipocytes, as it effectively blocks the calcium influx caused by TRPV4 agonist[1]. 
GSK205 (5 μM; 4 days; T3-F442A adipocytes) treatment results in increases expression of thermogenic genes (Mcp1, Mip1α, Mcp3, Rantes and Vcam, et al.) and is also accompanied by a decrease in the proinflammatory gene program. This shift resembles the gene expression changes seen in TRPV4-deficient adipocytes[1].
In Vivo: GSK205 (10 mg/kg; intraperitoneal injection; twice daily; for 7 days; for 4 weeks; male C57BL/6J mice) treatment shows significantly increases expression of thermogenic genes such as Ucp1, Pgc1a, Cidea and Cox8b. GSK205 treatment causes a reduced expression of the proinflammatory chemokines, macrophage marker and Tnfa in the EPI fat. GSK205 treatment significantly improves glucose tolerance in diet-induced obese (DIO) mice. There are no apparent sign of sickness or weight loss[1]. 
GSK205 has a relatively short half-life of 2 hours in the plasma and adipose tissues[1].

Name: DCPLA-ME DCPLA methyl ester, CAS: 56687-67-3, stock 17.4g, assay 98.5%, MWt: 322.53, Formula: C21H38O2, Solubility: DMSO : 15.62 mg/mL (48.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: DCPLA-ME, the methyl ester form of DCPLA, is a potent PKCε activator for use in the treatment of neurodegenerative diseases[1].
IC50 & Target: PKCε[1]

Name: HSL-IN-3, CAS: 346656-34-6, stock 24.3g, assay 98.2%, MWt: 262.11, Formula: C14H19BO4, Solubility: DMSO : 250 mg/mL (953.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: HSL-IN-3 (example 42), a boronic acid ester derivative, is an inhibitor of hormone-sensitive lipase (HSL)[1].
IC50 & Target: HSL[1].

Name: Etelcalcetide (hydrochloride) AMG 416 (hydrochloride); KAI-4169 (hydrochloride), CAS: 1334237-71-6, stock 34.8g, assay 98.9%, MWt: 1353.33, Formula: C38H73N21O10S2.17/2HCl, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CaSR, Biological_Activity: Etelcalcetide hydrochloride (AMG 416 hydrochloride) is a synthetic peptide as an activator of the calcium sensing receptor (CaSR). Etelcalcetide hydrochloride is effective in lowering parathyroid hormone (PTH) concentrations in patients receiving dialysis with secondary hyperparathyroidism receiving hemodialysis[1].

Name: Raphin1 (acetate), CAS: 2242616-04-0, stock 33.9g, assay 98.1%, MWt: 291.13, Formula: C10H12Cl2N4O2, Solubility: DMSO : 41.67 mg/mL (143.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Raphin1 acetate is an orally bioavailable, selective inhibitor of the regulatory phosphatase PPP1R15B (R15B). Raphin1 acetate binds strongly to the R15B-PP1c holophosphatase (Kd=33 nM), and shows ~30-fold selective in binding R15B-PP1c over R15A-PP1c. Raphin1 acetate crosses the blood-brain barrier, and reduces organismal and molecular deficits in a mouse model of a protein misfolding disease[1].
IC50 & Target: Kd: 33 nM (R15B-PP1c holophosphatase)[1]
In Vitro: Raphin1 acetate causes a rapid and transient accumulation of its phosphorylated substrate, resulting in a transient attenuation of protein synthesis[1]. 
Raphin1 acetate inhibits the recombinant R15B-PP1c holoenzyme, but not the closely related R15A-PP1c, by interfering with substrate recruitment[1].
In Vivo: Raphin1 acetate improves weight of HD82Q mice treated from 4 to ∼10 weeks of age with 2 mg/kg of Raphin1 once a day by oral gavage. Raphin1 acetate also decreases SDS-insoluble huntingtin assemblies and nuclear inclusions in the cortex of HD82Q mice[1].

Name: Vanin-1-IN-1, CAS: 2173134-00-2, stock 28.3g, assay 98.6%, MWt: 354.41, Formula: C18H22N6O2, Solubility: DMSO : 125 mg/mL (352.70 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vanin-1-IN-1 is an inhibitor of vanin-1 enzyme which is a cell surface associated, giycosyiphosphatidyS inositol (GPi) anchored protein and plays an important role in metabolism and inflammation[1].
IC50 & Target: vanin-1 enzyme[1]

Name: 3-Formyl rifamycin, CAS: 13292-22-3, stock 20.1g, assay 98.5%, MWt: 725.78, Formula: C38H47NO13, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (86.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Formyl rifamycin is an intermediate of Rifampicin.

Name: TD-0212 (TFA), CAS: 1073549-11-7, stock 31.6g, assay 98.7%, MWt: 641.67, Formula: C30H35F4N3O6S, Solubility: DMSO : 125 mg/mL (194.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;GPCR/G Protein, Target: Neprilysin;Angiotensin Receptor, Biological_Activity: TD-0212 TFA is an orally active dual pharmacology angiotensin II type 1 receptor (AT1) antagonist and neprilysin (NEP) inhibitor, with a pKi of 8.9 for AT1 and a pIC50 of 9.2 for NEP[1].
IC50 & Target: pKi: 8.9 (AT1) .
pIC50: 9.2 (NEP)[1].
In Vitro: TD-0212 provides the enhanced activity of dual AT1/NEP inhibition with a potentially lower risk of angioedema relative to dual ACE/NEP inhibition[1].
In Vivo: TD-0212 produces blood pressure reductions similar to omapatrilat and combinations of AT1 receptor antagonists and NEP inhibitors in models of renin-dependent and -independent hypertension[1].

Name: Odapipam NNC 756, CAS: 131796-63-9, stock 17.1g, assay 98.7%, MWt: 329.82, Formula: C19H20ClNO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Odapipam (NNC 756) is a selective, high affinity and benzazepine dopamine D1 receptor antagonist with a Kd of 0.18 nM. Odapipam is also a superior positron emission tomography (PET) radiotracer[1][2].
IC50 & Target: Dopamine D1 receptor[1]
In Vivo: The metabolism of Odapipam has been studied with phenobarbital-induced rat liver microsomes. During the incubation of Odapipam, five different metabolites are formed. The electron-ionization (EI+) mass spectra of the metabolites indicated the formation of N-desmethyl-Odapipam, 1-hydroxy-Odapipam, the two isomers of 3′-hydroxy-Odapipam and a metabolite which is dehydrogenated in the dihydrobenzofuran moiety[3].

Name: FAK ligand-Linker Conjugate 1, CAS: 2307461-45-4, stock 22.2g, assay 98.6%, MWt: 583.58, Formula: C25H28F3N5O6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Target Protein Ligand-Linker Conjugate, Biological_Activity: FAK ligand-Linker Conjugate 1 incorporates a ligand for FAK, and a PROTAC linker, which recruit E3 ligases (such as VHL, CRBN, MDM2, and IAP). FAK ligand-Linker Conjugate 1 can be extensively used for PROTAC-mediated protein degradation[1].

Name: TFMB-(R)-2-HG, CAS: 1445700-01-5, stock 6.7g, assay 98.6%, MWt: 288.22, Formula: C13H11F3O4, Solubility: DMSO : ≥ 250 mg/mL (867.39 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TFMB-(R)-2-HG, a cell membrane-permeable version of (R)-2-HG, is a carcinogenic factor in Acute myeloid leukemia (AML).
TFMB-(R)-2-HG impairs SCF ER-Hoxb8 cells differentiation in response to estrogen withdrawal[1].
IC50 & Target: Carcinogenic factor[1]

Name: WYE-687 (dihydrochloride), CAS: 1702364-87-1, stock 30.9g, assay 99%, MWt: 601.53, Formula: C28H34Cl2N8O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR, Target: PI3K;mTOR, Biological_Activity: WYE-687 dihydrochloride is an ATP-competitive mTOR inhibitor with an IC50 of 7 nM[1]. WYE-687 dihydrochloride concurrently inhibits activation of mTORC1 and mTORC2[2]. WYE-687 also inhibits PI3Kα and PI3Kγ with IC50s of 81 nM and 3.11 μM, respectively[1].

Name: Clomethiazole, CAS: 533-45-9, stock 7.1g, assay 98.2%, MWt: 161.65, Formula: C6H8ClNS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Neuronal Signaling;Membrane Transporter/Ion Channel, Target: Cytochrome P450;GABA Receptor;GABA Receptor, Biological_Activity: Chlormethiazole is an potent and orally active GABAA agonist[1]. Chlormethiazole inhibits cytochrome P450 isoforms: CYP2A6 and CYP2E1 in human liver microsomes. Chlormethiazole is an anticonvulsant agent and has the potential for treating convulsive status epilepticus[2].
In Vitro: Clomethiazole (1 mM), in the absence of GABA, to α1/β1/γ2 or α1/β2/γ2 subunit-containing cells produced large whole-cell currents[1].
Clomethiazole activate GABAA currents in α1/β1/γ2- and α1/β2/γ2-containing cells, with EC50 values of 0.3 and 1.5 mM, respectively[1].
Clomethiazole (30 μM) at low concentration also potentiates the action of GABA in both cell types, equivalent to a 3-fold increase in potency and up to 1.8-fold increase in maximal current[1].
Clomethiazole inhibits cytochrome P450 isoforms, CYP2A6 and CYP2E1 with IC50 values of 24 µM and 42 µM, respectively, in human liver microsomes, meanwhile all other isoforms exhibiting values > 300 µM[2].

Name: (R)-Trolox, CAS: 53101-49-8, stock 29.1g, assay 99%, MWt: 250.29, Formula: C14H18O4, Solubility: DMSO : 250 mg/mL (998.84 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Tyrosinase, Biological_Activity: (R)-Trolox is a water soluble vitamin E analogue and a competitive tyrosinase inhibitor with a Ki value of 0.83 mM and a ID50 value of 1.88 mM[1]. The (R)-Trolox has stronger tyrosinase affinity than the (S) enantiomer (Ki value of 0.61 mM)[1].
In Vitro: As compared to the control containing no inhibitor, DMSO suppresses the tyrosinase activity at tested levels, 100 and 200 µL in a total volume of 3.0 mL. The inhibition of DMSO on the mushroom tyrosinase is dosedependent. Additions of DMSO at the two levels in the tyrosinase digests containing (R)-Trolox ((R)-HTCCA) results in further inhibitions of the tyrosinase activity. The influence of the DMSO on the inhibitory effects of (R)-Trolox against the tyrosinase is also dose-dependent[1].

Name: (R)-FT671, CAS: 1959551-27-9, stock 23.7g, assay 98.6%, MWt: 533.48, Formula: C24H23F4N7O3, Solubility: DMSO : 150 mg/mL (281.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (R)-FT671 is the R-isomer of FT671. FT671 is a potent, non-covalent and selective USP7 inhibitor with an IC50 of 52 nM and binds to the USP7 catalytic domain with a Kd of 65 nM[1].

Name: Remibrutinib, CAS: 1787294-07-8, stock 15.9g, assay 98.4%, MWt: 507.53, Formula: C27H27F2N5O3, Solubility: DMSO : 125 mg/mL (246.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: Remibrutinib, is a potent and orally active bruton tyrosine kinase (BTK) inhibitor with an IC50 value of 1 nM. Remibrutinib inhibits BTK activity with an IC50 value of 0.023 μM in blood[1]. Remibrutinib has the potential for Chronic urticaria (CU) treatment[2].
IC50 & Target: IC50: 1 nM (BTK)[1]
In Vitro: In a biochemical enzyme assay,Remibrutinib (example 6) inhibits Btk enzymatic activity with an IC50 value of 1 nM[1].
In vitro B cell activation assay, Remibrutinib inhibits Btk enzymatic activity in blood with an IC50 value of 0.023 μM, the whole blood is collected from the abdominal aorta of anaesthetized adult male Lewis rats[1].

Name: Phosphoenolpyruvic acid (tricyclohexylammonium salt), CAS: 35556-70-8, stock 22.4g, assay 98.4%, MWt: 465.56, Formula: C21H44N3O6P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Phosphoenolpyruvic acid tricyclohexylammonium salt is a glycolysis metabolite with a high-energy phosphate group, penetrates the cell membrane and exhibits cytoprotective and anti-oxidative activity[1].

Name: SNT-207858 (free base), CAS: 1104662-66-9, stock 10g, assay 98.8%, MWt: 616.62, Formula: C32H43Cl2N5O3, Solubility: DMSO : 125 mg/mL (202.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: SNT207858 free base is a selective, blood brain barrier penetrating, potent and orally active melanocortin-4 (MC-4) receptor antagonist. SNT207858 free base has an IC50 of 22 nM (binding) and 11 nM (function) on the MC-4 receptor[1].
IC50 & Target: MC-4 receptor[1]
In Vitro: SNT207858 binds to the MC-4 receptor with an affinity of 22 nM and shows a 170-fold selectivity vs. MC-3 and a 40-fold selectivity vs. MC-5[1].
In Vivo: SNT207858 (30 mg/kg; oral administration; once daily; 15 days) significantly reduces the tumor induced weight loss in mice[1].

Name: Nintedanib BIBF 1120, CAS: 656247-17-5, stock 18g, assay 98.6%, MWt: 539.62, Formula: C31H33N5O4, Solubility: DMSO : 20 mg/mL (37.06 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;FGFR, Biological_Activity: Nintedanib (BIBF 1120) is a potent triple angiokinase inhibitor for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β with IC50s of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM, respectively.
IC50 & Target: IC50: 34 nM (VEGFR1), 13 nM (VEGFR2), 13 nM (VEGFR3), 69 nM (FGFR1), 37 nM (FGFR1), 108 nM (FGFR1), 59 nM (PDGFRα), 65 nM (PDGFRβ)
In Vitro: Nintedanib (BIBF 1120) binds to the ATP-binding site in the cleft between the amino and carboxy terminal lobes of the kinase domain. Nintedanib (BIBF 1120) inhibits proliferation of PDGF-BB stimulated BRPs with EC50 of 79 nM in cell assays. Nintedanib (BIBF 1120) (100 nM) blocks activation of MAPK after stimulation with 5% serum plus PDGF-BB. Nintedanib (BIBF 1120) prevents PDGF-BB stimulated proliferation with an EC50 of 69 nM in cultures of human vascular smooth muscle cells (HUASMC)[1].
In Vivo: Nintedanib (BIBF 1120) (25-100 mg/kg daily p.o.) is highly active in all tumor models, including human tumor xenografts growing in nude mice and a syngeneic rat tumor model. This is evident in the magnetic resonance imaging of tumor perfusion after 3 days, reducing vessel density and vessel integrity after 5 days, and profound growth inhibition[1]. Nintedanib (BIBF 1120) is orally available and displays encouraging efficacy in in vivo tumor models while being well tolerated[2].

Name: Cyclo(his-pro) (TFA) Cyclo(histidyl-proline) (TFA);Histidylproline diketopiperazine (TFA), CAS: 936749-56-3, stock 19.6g, assay 98.3%, MWt: 348.28, Formula: C13H15F3N4O4, Solubility: H2O : 125 mg/mL (358.91 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB;Metabolic Enzyme/Protease, Target: NF-κB;Endogenous Metabolite, Biological_Activity: Cyclo(his-pro) TFA (Cyclo(histidyl-proline) TFA) is an orally active cyclic dipeptide structurally related to tyreotropin-releasing hormone[1]. Cyclo(his-pro) TFA could inhibit NF-κB nuclear accumulation. Cyclo(his-pro) TFA can cross the brain-blood-barrier and affect diverse inflammatory and stress responses[2].
In Vitro: Cyclo(his-pro) TFA (Cyclo(histidyl-proline) TFA; 50 μM; 1-48 hours) increases the nuclear level of Nrf2 and inhibits NF-κB nuclear translocation. Cyclo(His-Pro) alone has no effect on nuclear translocation of these transcription factors[2]. 
Cyclo(his-pro) TFA (50 μM; prior to PQ exposure for 48 hours) abolishes protein nitration that followed paraquat (PQ) exposure and lessenes its functional consequences, as shown by decrease in cell apoptosis, detected by caspase 3 activity and by cytochrome c release[2]. 
Cyclo(his-pro) TFA inhibits NF-κB nuclear accumulation induced by paraquat in rat pheochromocytoma PC12 cells via the Nrf2/heme oxygenase-1 pathway[2]. 
In Vivo: Cyclo(his-pro) TFA (Cyclo(histidyl-proline) TFA; 1.8 mg/ear; topical application on the right ear; 30 min prior to TPA) reduces TPA-induced ear oedema confirming that it can exert anti-inflammatory effect[2]. 
Cyclo(his-pro) TFA exerts in vivo anti-inflammatory effects in the central nervous system by down-regulating hepatic and cerebral TNFα expression thereby counteracting LPS-induced gliosis. Moreover, by up-regulating Bip, Cyclo(his-pro) increases the ER stress sensitivity andtriggers the unfolded protein response to alleviate the ER stress[3].

Name: Stearyldiethanolamine, CAS: 10213-78-2, stock 1g, assay 98.3%, MWt: 357.61, Formula: C22H47NO2, Solubility: DMSO : 41.67 mg/mL (116.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Stearyldiethanolamine is one of the compounds used in development for antibacterial freshness-keeping film or antibacterial nonwoven fabric[1].

Name: AGX51, CAS: 330834-54-3, stock 25.9g, assay 98.7%, MWt: 431.52, Formula: C27H29NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AGX51 is a first-in-class pan-Id (inhibitors of DNA-binding/differentiation proteins) antagonist and degrader. AGX51 inhibits the Id1-E47 interaction, leading to ubiquitin-mediated degradation of Ids, cell growth arrest, and reduces viability. AGX51 inhibits pathologic ocular neovascularization[1].

Name: ASLAN003, CAS: 1035688-66-4, stock 5.3g, assay 98.3%, MWt: 356.32, Formula: C19H14F2N2O3, Solubility: DMSO : 130 mg/mL (364.84 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: ASLAN003 is an orally active and potent inhibitor of DHODH (Human Dihydroorotate Dehydrogenase) which has the potential to be a first-in-class candidate in AML (Acute Myelogenous Leukemia). ASLAN003 has antitumor activity[1].
IC50 & Target: DHODH[1]

Name: VU0364770 (hydrochloride), CAS: 1414842-70-8, stock 3.3g, assay 98.1%, MWt: 269.13, Formula: C12H10Cl2N2O, Solubility: DMSO : 100 mg/mL (371.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: VU0364770 hydrochloride is a selective and potent positive allosteric modulator (PAM) of mGlu4. VU0346770 hydrochloride exhibits EC50s of 290 nM and 1.1 μM at rat mGlu4 and human mGlu4 receptor, respectively. VU0364770 hydrochloride exhibits antagonist activity at mGlu5 with a potency of 17.9 μM and PAM activity at mGlu6 with a potency of 6.8 μM. VU0364770 hydrochloride also possesses activity at MAO with Ki values of 8.5 and 0.72 μM for human MAO-A and human MAO-B, respectively[1].

Name: (S,R,S)-AHPC-propargyl VH032-propargyl;VHL ligand 7, CAS: 2098799-78-9, stock 30.5g, assay 98.6%, MWt: 526.65, Formula: C27H34N4O5S, Solubility: DMSO : 100 mg/mL (189.88 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for E3 Ligase, Biological_Activity: (S,R,S)-AHPC-propargyl (VH032-propargyl) is a VHL ligand which is used in “click reaction” for PROTACs[1].

Name: Thalidomide-propargyl, CAS: 2098487-39-7, stock 16g, assay 98.9%, MWt: 312.28, Formula: C16H12N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for E3 Ligase, Biological_Activity: Thalidomide-propargyl is the Thalidomide-based Cereblon ligand used in the recruitment of CRBN protein. Thalidomide-propargyl can be connected to the ligand for protein by a linker to form the IMiD containing PROTACs[1].

Name: Thalidomide-O-PEG2-propargyl E3 ligase Ligand-Linker Conjugates 32, CAS: 2098487-52-4, stock 3.3g, assay 98.5%, MWt: 400.38, Formula: C20H20N2O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: Thalidomide-O-PEG2-propargyl (E3 ligase Ligand-Linker Conjugates 32) is a synthesized E3 ligase ligand-linker conjugate that incorporates the Thalidomide based cereblon ligand and 2-unit PEG linker used in PROTAC technology[1].

Name: Telomerase-IN-2, CAS: 1610878-54-0, stock 36.4g, assay 98.1%, MWt: 633.69, Formula: C34H39N3O9, Solubility: DMSO : 250 mg/mL (394.51 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Telomerase, Biological_Activity: Telomerase-IN-2 is a telomerase inhibitor, and inhibits telomerase activity by decreasing expression of dyskerin, with an IC50 of 0.89 µM. Anti-cancer activity[1].
IC50 & Target: IC50: 0.89 µM (Telomerase)[1]

Name: CDK4/6-IN-4, CAS: 2138499-06-4, stock 36.1g, assay 98.4%, MWt: 522.59, Formula: C27H32F2N8O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CDK4/6-IN-4, the active metabolite of Abemaciclib, is a selective CDK4/6 inhibitor for the treatment of cancer[1].

Name: H-Arg-Lys-OH, CAS: 40968-46-5, stock 38.7g, assay 98.7%, MWt: 302.37, Formula: C12H26N6O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: H-Arg-Lys-OH is a dipeptide formed from L-arginyl and L-lysine residues.

Name: Phe-Lys(Trt)-PAB, CAS: 1116085-99-4, stock 8.4g, assay 98.3%, MWt: 640.81, Formula: C41H44N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Phe-Lys(Trt)-PAB is a cathepsin cleavable ADC linker used for the antibody-drug conjugates (ADCs)[1].

Name: Fmoc-Phe-Lys(Trt)-PAB-PNP, CAS: 1116086-09-9, stock 3.3g, assay 98.3%, MWt: 1028.15, Formula: C63H57N5O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Fmoc-Phe-Lys(Trt)-PAB-PNP is a cleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs)[1].

Name: Aloc-D-Ala-Phe-Lys(Aloc)-PAB-PNP, CAS: 253863-34-2, stock 22.3g, assay 98.3%, MWt: 802.83, Formula: C40H46N6O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Aloc-D-Ala-Phe-Lys(Aloc)-PAB-PNP is a cleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: Cbz-Phe-(Alloc)Lys-PAB-PNP, CAS: 159857-90-6, stock 30.1g, assay 98.4%, MWt: 781.81, Formula: C41H43N5O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Cbz-Phe-(Alloc)Lys-PAB-PNP is an cleavable linker for antibody-drug conjugates (ADC) design.

Name: SPP-DM1, CAS: 452072-20-7, stock 11.9g, assay 98.9%, MWt: 967.54, Formula: C44H59ClN4O14S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: Drug-Linker Conjugates for ADC, Biological_Activity: SPP-DM1 is a drug-linker conjugate for ADC with potent antitumor activity by using DM1 (a potent microtubule-disrupting agent), linked via the ADC linker SPP[1].

Name: Duocarmycin Analog, CAS: 372954-15-9, stock 7.3g, assay 98.9%, MWt: 611.09, Formula: C34H31ClN4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: DNA Alkylator/Crosslinker;ADC Cytotoxin, Biological_Activity: Duocarmycin Analog is an analog of Duocarmycin, and used as an DNA alkylator and ADC cytotoxin[1].

Name: Seco-Duocarmycin SA, CAS: 144667-38-9, stock 36.4g, assay 98.1%, MWt: 513.93, Formula: C25H24ClN3O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: DNA Alkylator/Crosslinker;ADC Cytotoxin, Biological_Activity: Seco-Duocarmycin SA is a highly potent DNA alkylator, and is used as an ADC cytotoxin[1].

Name: DM3-SMe, CAS: 796073-70-6, stock 5.6g, assay 98.4%, MWt: 812.43, Formula: C38H54ClN3O10S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Antibody-drug Conjugate/ADC Related, Target: Microtubule/Tubulin;Microtubule/Tubulin;ADC Cytotoxin, Biological_Activity: DM3-SMe is a maytansine derivative and a tubulin inhibitor, and is a cytotoxic moiety of antibody-drug conjugates (ADCs), which can be linked to antibody through disulfide bond or stable thioether bond. DM3-SMe shows highly cytotoxic activity in vitro with an IC50 of 0.0011 nM[1][2].

Name: DM4-SMe, CAS: 796073-68-2, stock 33.9g, assay 98.7%, MWt: 826.46, Formula: C39H56ClN3O10S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Antibody-drug Conjugate/ADC Related, Target: Microtubule/Tubulin;Microtubule/Tubulin;ADC Cytotoxin, Biological_Activity: DM4-SMe is a metabolite of antibody-maytansin conjugates (AMCs) and a tubulin inhibitor, and also a cytotoxic moiety of antibody-drug conjugates (ADCs), which can be linked to antibody through disulfide bond or stable thioether bond. DM4-SMe inhibits KB cells with an IC50 of 0.026 nM[1][2].

Name: VH032-PEG3-acetylene, CAS: 2098799-80-3, stock 10.4g, assay 98%, MWt: 614.75, Formula: C31H42N4O7S, Solubility: DMSO : 50 mg/mL (81.33 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: VH032-PEG3-acetylene is a synthesized E3 ligase ligand-linker conjugate that incorporates the VH032 based VHL ligand and a linker used in PROTAC technology[1].

Name: DM4-SPDP, CAS: 2245698-48-8, stock 33.8g, assay 98.9%, MWt: 981.57, Formula: C45H61ClN4O14S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Antibody-drug Conjugate/ADC Related, Target: Microtubule/Tubulin;Microtubule/Tubulin;Drug-Linker Conjugates for ADC, Biological_Activity: DM4-SPDP is a drug-linker conjugate composed of a potent antitubulin agent DM4 and a linker SMCC to make antibody drug conjugate[1]. SPDP is a short-chain crosslinker for amine-to-sulfhydryl conjugation via NHS-ester and pyridyldithiol reactive groups that form cleavable (reducible) disulfide bonds with cysteine sulfhydryls[2][3].

Name: Vat-Cit-PAB-Monomethyl Dolastatin 10, CAS: 1415329-13-3, stock 3.1g, assay 98.5%, MWt: 1176.51, Formula: C60H93N11O11S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Antibody-drug Conjugate/ADC Related, Target: Microtubule/Tubulin;Microtubule/Tubulin;Drug-Linker Conjugates for ADC, Biological_Activity: Vat-Cit-PAB-Monomethyl Dolastatin 10 is a drug-linker conjugate for ADC with potent antitumor activity by using Monomethyl Dolastatin 10 (a potent tubulin inhibitor), linked via the ADC linker Vat-Cit-PAB.

Name: Seco-Duocarmycin TM, CAS: 236102-87-7, stock 7.2g, assay 98.6%, MWt: 448.47, Formula: C25H24N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: DNA Alkylator/Crosslinker;ADC Cytotoxin, Biological_Activity: Seco-Duocarmycin TM is a DNA alkylator agent belonging to Duocarmycins family that inhibits DNA synthesis. Seco-Duocarmycin TM is a cytotoxic agent, used as the cytotoxic component in antibody-drug conjugates (ADC)[1]</suo>.

Name: DM4-SMCC, CAS: 1228105-52-9, stock 28g, assay 98.8%, MWt: 1114.69, Formula: C54H72ClN5O16S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: Drug-Linker Conjugates for ADC, Biological_Activity: DM4-SMCC is a drug-linker conjugate for ADC with antitumor activity by using DM4 (an antitubulin agent), linked via the non-cleavable SMCC linker[1].

Name: PEG4-SPDP, CAS: 1305053-43-3, stock 13.7g, assay 98.9%, MWt: 488.57, Formula: C20H28N2O8S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PEG4-SPDP is a cleavable ADC linker used for the antibody-drug conjugates (ADCs).

Name: Mal-PEG2-VCP-NB, CAS: 2395887-69-9, stock 31.8g, assay 98.4%, MWt: 783.78, Formula: C36H45N7O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Mal-PEG2-VCP-NB is a nonclaevable ADC linker containing a Maleimide group, 2-unit PEG and a VCP NB.

Name: CCK-B Receptor Antagonist 2, CAS: 155412-88-7, stock 3.7g, assay 98.4%, MWt: 484.55, Formula: C27H28N6O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: CCK-B Receptor Antagonist 2, compound 15b, is a potent and orally active Gastrin/CCK-B antagonist with an IC50 value of 0.43 nM. CCK-B Receptor Antagonist 2 also inhibits gastrin/CCK-A activity with an IC50 of 1.82 μM[1].
IC50 & Target: IC50: 0.43 nM (Gastrin/CCK-B); 1.82 μM (Gastrin/CCK-A)[1]
In Vivo: CCK-B Receptor Antagonist 2 (0.1 μmol/kg; intravenous injection) has an inhibition effect on pentagastrin-induced gastric acid secretion in anethsetized rats with an ED50 of 8.3 nmol/kg[1].

Name: Bis-PEG1-NHS ester, CAS: 65869-64-9, stock 19.8g, assay 98.9%, MWt: 356.28, Formula: C14H16N2O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Bis-PEG1-NHS ester is a nonclaevable 1-unit PEG linker for antibody-drug-conjugation (ADC).

Name: Adavosertib AZD1775;MK-1775, CAS: 955365-80-7, stock 25.8g, assay 99%, MWt: 500.60, Formula: C27H32N8O2, Solubility: DMSO : 125 mg/mL (249.70 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: Wee1, Biological_Activity: Adavosertib (AZD-1775; MK-1775) is a potent Wee1 inhibitor with an IC50 of 5.2 nM.
IC50 & Target: IC50: 5.2 nM (Wee1)
In Vitro: Adavosertib (MK-1775) enhances the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells. Adavosertib (MK-1775) inhibits CDC2 Y15 phosphorylation in cells, abrogates DNA damaged checkpoints induced by 5-FU treatment, and causes premature entry of mitosis determined by induction of Histone H3 phosphorylation[1]. Adavosertib (MK-1775) abrogates the radiation-induced G2 block in p53-defective cells but not in p53 wild-type lines[2]. The combination of NSC 613327 with Adavosertib (MK-1775) produces robust anti-tumor activity and remarkably enhances tumor regression response (4.01 fold) compared to NSC 613327 treatment in p53-deficient tumors[3].
In Vivo: In vivo, Adavosertib (MK-1775) potentiates the anti-tumor efficacy of 5-FU at tolerable doses[1]. Adavosertib (MK-1775) (60 mg/kg twice daily, p.o.) enhances H1299 xenograft tumor response to fractionated radiotherapy[2]. Adavosertib (MK-1775) (30 mg/kg. p.o.) regresses tumor growth in PANC198, PANC215 and PANC185 as compared to GEM treated mice[3].

Name: NHPI-PEG4-C2-Pfp ester, CAS: 2101206-46-4, stock 25.1g, assay 98.7%, MWt: 577.45, Formula: C25H24F5NO9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: NHPI-PEG4-C2-Pfp ester is used as a linker for antibody-drug conjugates (ADC).

Name: PDP-Pfp, CAS: 160580-70-1, stock 13.7g, assay 98%, MWt: 381.34, Formula: C14H8F5NO2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PDP-Pfp is a reducible ADC linker used for the agents that target for the extracellular loop 1 (ECL1) of TM4SF1 (transmembrane 4 L6 family member 1)[1].

Name: PDEC-NB, CAS: 874302-76-8, stock 26.6g, assay 98.2%, MWt: 352.39, Formula: C14H12N2O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PDEC-NB is a disulfide cleavable linker used for the antibody-drug conjugate (ADC)[1].

Name: Fmoc-Ala-Ala-Asn-PABC-PNP, CAS: 1834516-06-1, stock 23.3g, assay 98.7%, MWt: 766.75, Formula: C39H38N6O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Fmoc-Ala-Ala-Asn-PABC-PNP is a peptide cleavable ADC linker[1].

Name: Phe-Lys(Fmoc)-PAB, CAS: 2149584-03-0, stock 36.4g, assay 98.6%, MWt: 620.74, Formula: C37H40N4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Phe-Lys(Fmoc)-PAB is a cathepsin cleavable ADC linker used for the antibody-drug conjugates (ADCs)[1].

Name: Mal-C2-NHS ester, CAS: 103750-03-4, stock 22.7g, assay 98.1%, MWt: 294.26, Formula: C13H14N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Mal-C2-NHS ester is a noncleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs)[1].

Name: trans-Sulfo-SMCC, CAS: 1286837-77-1, stock 35g, assay 98.3%, MWt: 414.39, Formula: C16H18N2O9S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: trans-Sulfo-SMCC is a non-cleavable and membrane permeable ADC crosslinker.

Name: Mal-PEG2-NHS ester, CAS: 1433997-01-3, stock 11.1g, assay 98.8%, MWt: 354.31, Formula: C15H18N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Mal-PEG2-NHS ester is a nonclaevable ADC linker containing a Maleimide group, 2-unit PEG and an NHS ester.

Name: SNPB, CAS: 663598-85-4, stock 21.2g, assay 98.7%, MWt: 371.39, Formula: C13H13N3O6S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SNPB is a cleavable linker that is used for making antibody-drug conjugate (ADC).

Name: Mal-amido-PEG1-C2-NHS ester, CAS: 1260092-50-9, stock 31.6g, assay 98.7%, MWt: 381.34, Formula: C16H19N3O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Mal-amido-PEG1-C2-NHS ester is a nonclaevable ADC linker containing a maleimide group and an NHS ester. The NHS ester can be used to label the primary amines (-NH2) of proteins, amine-modified oligonucleotides, and other amine-containing molecules[1][2]

Name: Mal-amido-PEG5-C2-NHS ester, CAS: 1315355-92-0, stock 1.2g, assay 98.9%, MWt: 557.55, Formula: C24H35N3O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Mal-amido-PEG10-C2-NHS ester is a nonclaevable ADC linker containing a maleimide group and an NHS ester. The NHS ester can be used to label the primary amines (-NH2) of proteins, amine-modified oligonucleotides, and other amine-containing molecules[1][2]

Name: Mal-amido-PEG10-C2-NHS ester, CAS: 1137109-22-8, stock 27.6g, assay 98.6%, MWt: 777.81, Formula: C34H55N3O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Mal-amido-PEG10-C2-NHS ester is a nonclaevable ADC linker containing a maleimide group and an NHS ester. The NHS ester can be used to label the primary amines (-NH2) of proteins, amine-modified oligonucleotides, and other amine-containing molecules[1][2].

Name: PDB-Pfp, CAS: 2088570-81-2, stock 4.8g, assay 98.7%, MWt: 395.37, Formula: C15H10F5NO2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PDB-Pfp is a reducible ADC linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: NHPI-PEG4-C2-NHS ester, CAS: 1415328-95-8, stock 21.9g, assay 98.7%, MWt: 508.48, Formula: C23H28N2O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: NHPI-PEG4-C2-NHS ester, example 40 (WO2014185985A1), is used as a linker for antibody-drug conjugates (ADC)[1].
In Vivo: NHPI-PEG4-C2-NHS ester，例40 (WO2014185985.A1)，可用作抗体偶联药物 (ADC) 的连接桥。

Name: NHPI-PEG3-C2-Pfp ester, CAS: 2101206-87-3, stock 37.2g, assay 98.9%, MWt: 533.40, Formula: C23H20F5NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: NHPI-PEG3-C2-Pfp ester is a nonclaevable 3-unit PEG linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: NHPI-PEG3-C2-NHS ester, CAS: 2101206-14-6, stock 36.3g, assay 98%, MWt: 464.42, Formula: C21H24N2O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: NHPI-PEG3-C2-NHS ester is a nonclaevable 3-unit PEG linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: NHPI-PEG2-C2-Pfp ester, CAS: 2101206-47-5, stock 34.6g, assay 98.7%, MWt: 489.35, Formula: C21H16F5NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: NHPI-PEG2-C2-Pfp ester is a nonclaevable 2-unit PEG linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: NHPI-PEG2-C2-NHS ester, CAS: 2101206-31-7, stock 30.9g, assay 98.4%, MWt: 420.37, Formula: C19H20N2O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: NHPI-PEG2-C2-NHS ester is a nonclaevable 2-unit PEG linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: MC-PEG2-C2-NHS ester, CAS: 1263044-56-9, stock 4.3g, assay 98.8%, MWt: 467.47, Formula: C21H29N3O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: MC-PEG2-C2-NHS ester is a nonclaevable 2-unit PEG linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: Propargyl-C1-NHS ester, CAS: 132178-37-1, stock 21.3g, assay 98.9%, MWt: 195.17, Formula: C9H9NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Propargyl-C1-NHS ester is a nonclaevable linker for antibody-drug-conjugation (ADC).

Name: Ald-Ph-amido-C2-nitrate, CAS: 141534-26-1, stock 23.4g, assay 98.1%, MWt: 238.20, Formula: C10H10N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-C2-nitrate (Example XXIVb) is a thiazolidine derivative, used as a noncleavable ADC linker[1].

Name: SPDMV, CAS: 890409-85-5, stock 38.5g, assay 98.6%, MWt: 354.44, Formula: C15H18N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SPDMV is a glutathione cleavable ADC linker used for the antibody-drug conjugate (ADCs)[1].

Name: Propargyl-C2-NHS ester, CAS: 906564-59-8, stock 39.6g, assay 98.1%, MWt: 209.20, Formula: C10H11NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Propargyl-C2-NHS ester is a nonclaevable linker for antibody-drug-conjugation (ADC).

Name: Ald-Ph-amido-PEG4-C2-acid, CAS: 1309460-27-2, stock 0.8g, assay 98.5%, MWt: 397.42, Formula: C19H27NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG4-C2-acid is a noncleavable linker used for the antibody-drug conjugate (ADC).

Name: Ald-Ph-amido-PEG3-C-COOH, CAS: 1007215-91-9, stock 16.6g, assay 98.7%, MWt: 339.34, Formula: C16H21NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG3-C-COOH is a noncleavable linker used for the antibody-drug conjugate (ADC).

Name: Ald-Ph-amido-PEG2, CAS: 1061569-06-9, stock 29.4g, assay 98.2%, MWt: 237.25, Formula: C12H15NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG2 is a noncleavable ADC linker for antibody-drug conjugate[1].

Name: Ald-Ph-amido-PEG3-C1-Boc, CAS: 1007215-94-2, stock 25.8g, assay 98.2%, MWt: 395.45, Formula: C20H29NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG3-C1-Boc is an ADC linker, which belongs to a polyethylene glycol (PEG) linker.

Name: SPDMB, CAS: 2101206-29-3, stock 14.4g, assay 98.7%, MWt: 340.42, Formula: C14H16N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SPDMB is a glutathione cleavable ADC linker used for the antibody-drug conjugate (ADCs)[1].

Name: Propargyl-O-C1-amido-PEG2-C2-NHS ester, CAS: 2101206-30-6, stock 2g, assay 98.5%, MWt: 370.35, Formula: C16H22N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Propargyl-O-C1-amido-PEG2-C2-NHS ester is a nonclaevable 2-unit PEG linker for antibody-drug-conjugation (ADC).

Name: SPDB-sulfo, CAS: 1628113-16-5, stock 37.9g, assay 98.8%, MWt: 406.45, Formula: C13H14N2O7S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SPDB-sulfo is a glutathione cleavable ADC linker used for the antibody-drug conjugate (ADCs) [1].

Name: Propargyl-O-C1-amido-PEG4-C2-NHS ester, CAS: 2101206-92-0, stock 25.3g, assay 98.3%, MWt: 458.46, Formula: C20H30N2O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Propargyl-O-C1-amido-PEG4-C2-NHS ester is a nonclaevable 4-unit PEG linker for antibody-drug-conjugation (ADC).

Name: SPDV, CAS: 317331-86-5, stock 4.4g, assay 98%, MWt: 340.42, Formula: C14H16N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SPDV is a cleavable ADC linker used for diagnosis and treatment of cancer or B cell proliferative diseas.

Name: Ald-Ph-amido-PEG3-C2-Pfp ester, CAS: 2101206-21-5, stock 24.7g, assay 98.9%, MWt: 519.42, Formula: C23H22F5NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG3-C2-Pfp ester is an noncleavable ADC linker, which belongs to a polyethylene glycol (PEG) linker.

Name: PDdB-Pfp, CAS: 2101206-44-2, stock 32.5g, assay 98.4%, MWt: 423.42, Formula: C17H14F5NO2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PDdB-Pfp is a reducible ADC linker used for the agents that target for the extracellular loop 1 (ECL1) of TM4SF1 (transmembrane 4 L6 family member 1)[1].

Name: SPDMV-sulfo, CAS: 2101206-86-2, stock 8g, assay 98.4%, MWt: 434.51, Formula: C15H18N2O7S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SPDMV-sulfo is a glutathione cleavable ADC linker used for the antibody-drug conjugate (ADCs)[1].

Name: Cyclooctyne-O-NHS ester, CAS: 1425803-45-7, stock 25.4g, assay 98.7%, MWt: 279.29, Formula: C14H17NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Cytotoxin, Biological_Activity: Cyclooctyne-O-NHS ester is a derivative of Cyclooctyne, causes severe damage of HEK293 cells, and is used as an ADC cytotoxin[1].

Name: Cyclooctyne-O-PFP ester, CAS: 886209-60-5, stock 30.8g, assay 98.6%, MWt: 348.26, Formula: C16H13F5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Cytotoxin, Biological_Activity: Cyclooctyne-O-PFP ester is a used as an ADC cytotoxin, which connects antibody and linker[1].

Name: Ald-Ph-amido-PEG2-C2-Pfp ester, CAS: 2101206-60-2, stock 22.2g, assay 99%, MWt: 475.36, Formula: C21H18F5NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG2-C2-Pfp ester is a nonclaevable 2-unit PEG linker for antibody-drug-conjugation (ADC).

Name: Ald-Ph-amido-PEG2-C2-NHS ester, CAS: 1807521-07-8, stock 21.2g, assay 98.8%, MWt: 406.39, Formula: C19H22N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG2-C2-NHS ester is a nonclaevable 2-unit PEG linker for antibody-drug-conjugation (ADC).

Name: Ald-Ph-amido-PEG1-C2-Pfp ester, CAS: 2101206-67-9, stock 31.9g, assay 98.9%, MWt: 431.31, Formula: C19H14F5NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG1-C2-Pfp ester is a nonclaevable 1-unit PEG linker for antibody-drug-conjugation (ADC).

Name: SPDH, CAS: 1824718-79-7, stock 10.8g, assay 98.2%, MWt: 354.44, Formula: C15H18N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: SPDH is a cleavable ADC linker used for diagnosis and treatment of cancer or B cell proliferative diseas.

Name: PDdEC-NB, CAS: 1956318-90-3, stock 20.7g, assay 98.8%, MWt: 380.44, Formula: C16H16N2O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PDdEC-NB is a disulfide cleavable linker used for the antibody-drug conjugate (ADC).

Name: N3-C2-NHS ester, CAS: 850180-76-6, stock 36.5g, assay 98.5%, MWt: 212.16, Formula: C7H8N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: N3-C2-NHS ester is a noncleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: N3-C3-NHS ester, CAS: 943858-70-6, stock 24.6g, assay 98.3%, MWt: 226.19, Formula: C8H10N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: N3-C3-NHS ester is a noncleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: N3-C4-NHS ester, CAS: 478801-48-8, stock 13.8g, assay 98.4%, MWt: 240.22, Formula: C9H12N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: N3-C4-NHS ester is a noncleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: N3-C5-NHS ester, CAS: 866363-70-4, stock 10g, assay 98.6%, MWt: 254.24, Formula: C10H14N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: N3-C5-NHS ester is a noncleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: N3-Ph-NHS ester, CAS: 53053-08-0, stock 19.2g, assay 98.5%, MWt: 260.21, Formula: C11H8N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: N3-Ph-NHS ester is a noncleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: Ald-Ph-amido-PEG1-C2-NHS ester, CAS: 2101206-80-6, stock 8.5g, assay 98.2%, MWt: 362.33, Formula: C17H18N2O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Ald-Ph-amido-PEG1-C2-NHS ester is a nonclaevable 1-unit PEG linker for antibody-drug-conjugation (ADC).

Name: N3-PEG4-C2-Pfp ester, CAS: 1353012-00-6, stock 6g, assay 98.7%, MWt: 457.35, Formula: C17H20F5N3O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: N3-PEG4-C2-Pfp ester is a nonclaevable 4-unit PEG linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: N3-PEG3-C2-NHS ester, CAS: 1245718-89-1, stock 8.1g, assay 98.1%, MWt: 344.32, Formula: C13H20N4O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: N3-PEG3-C2-NHS ester is a nonclaevable 3-unit PEG linker used in the synthesis of antibody-drug conjugates (ADCs).

Name: PPC-NB, CAS: 1887040-81-4, stock 18.4g, assay 98.5%, MWt: 366.41, Formula: C15H14N2O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PPC-NB is a glutathione cleavable linker used for the antibody-drug conjugate (ADC)[1].

Name: Sulfo-SPP, CAS: 452072-27-4, stock 35g, assay 98.1%, MWt: 420.48, Formula: C14H16N2O7S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Sulfo-SPP is a heterobifunctional, thiol-cleavable and membrane impermeable crosslinker.

Name: NO2-SPP-sulfo-Me, CAS: 890409-87-7, stock 32.4g, assay 98.7%, MWt: 463.51, Formula: C15H17N3O8S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: NO2-SPP-sulfo-Me is a cleavable linker that is used for making antibody-drug conjugate (ADC)[1].

Name: DMAC-PDB, CAS: 663599-04-0, stock 10.7g, assay 98.3%, MWt: 300.40, Formula: C12H16N2O3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: DMAC-PDB is a cleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs)[1].

Name: PDP-C1-Ph-Val-Cit, CAS: 1610769-13-5, stock 30.9g, assay 99%, MWt: 591.75, Formula: C26H37N7O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: PDP-C1-Ph-Val-Cit is a cleavable ADC linker used for antibody-drug conjugates (ADCs).

Name: DC0-NH2, CAS: 615538-51-7, stock 18.8g, assay 98.3%, MWt: 550.01, Formula: C31H24ClN5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Cytotoxin, Biological_Activity: DC0-NH2 is an effector moiety for ADC and a simplified analog of DC1 with better stability. DC0-NH2 is about 1000-fold more cytotoxic than commonly used anticancer drugs (ex. Doxorubicin). DC0-NH2 can bind to the minor groove of DNA, followed by alkylation of adenine residues by its propabenzindole (CBI) component[1].
In Vitro: DC0-NH2 (0-3 nM; 72 hours) is highly potent against Ramos, Namalwa, and HL60/s cells with IC50 values in the 1 pM to 10 pM range, and has 100 pM range when tested on COLO 205 cells[1].

Name: MAC glucuronide linker-2, CAS: 229977-57-5, stock 38.2g, assay 98.1%, MWt: 455.41, Formula: C20H25NO11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: MAC glucuronide linker-2 is a cleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs)[1].

Name: A2aR/A2bR antagonist-1, CAS: 2239273-34-6, stock 24.9g, assay 98.7%, MWt: 426.47, Formula: C23H22N8O, Solubility: DMSO : 250 mg/mL (586.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: A2aR/A2bR antagonist-1 is an orally bioavailable, selective dual adenosine receptor (A2aR/A2bR) antagonist with immunomodulatory activity[1].
IC50 & Target: A2aR/A2bR[1]

Name: MRTX849, CAS: 2326521-71-3, stock 12.8g, assay 98.8%, MWt: 604.12, Formula: C32H35ClFN7O2, Solubility: DMSO : 200 mg/mL (331.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: MRTX849 is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. MRTX849 covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction[1][2].
IC50 & Target: KRAS G12C[1]
In Vitro: MRTX849 (0.1-10000 nM; 3-day/2D conditions; 12-day/3D conditions) potently inhibits cell growth in the vast majority of KRAS G12C-mutant cell lines with IC50s ranging between 10 and 973 nM in the 2D format and between 0.2 and 1042 nM in the 3D format[1]. 
MRTX849 (0.24-1000 nM; 24 hours) inhibits KRAS-dependent signaling targets including ERK1/2 phosphorylation (Thr202/Tyr204 ERK1; pERK), S6 phosphorylation (RSK-dependent Ser235/236; pS6) and expression of the ERK-regulated DUSP6[1].
In Vivo: MRTX849 (1-100 mg/kg; i.g.; daily until day 16) demonstrates dose-dependent anti-tumor efficacy over a well-tolerated dose range, and the maximally efficacious dose of MRTX849 is between 30-100 mg/kg/day[1].

Name: Minerval 2-Hydroxyoleic acid;2-OHOA, CAS: 56472-29-8, stock 12.5g, assay 98.9%, MWt: 298.46, Formula: C18H34O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Minerval (2-Hydroxyoleic acid) is a synthetic oleic acid (OA) derivative that binds to the plasma membrane and alters lipid organization. Minerval has anti-tumor effect[1].
In Vitro: Minerval (25-75 μM; 72 hours) impairs Jurkat cell growth in a time- and concentration-dependent manner, with an IC50 of ~40 μM[1]. 
Minerval (25-50 μM; 72 hours) also induces a marked and concentration-dependent increase in the proteolytic cleavage of PARP, a molecular marker of apoptosis[1]. 
In Vivo: Minerval markedly and significantly inhibits tumour growth in nude mice infected with Jurkat cells[1].

Name: Enpp-1-IN-1, CAS: 2289728-58-9, stock 38.4g, assay 98.2%, MWt: 343.40, Formula: C17H17N3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Enpp-1-IN-1 is a Ectonucleotide pyrophosphatase-phosphodiesterase 1 (enpp-1) inhibitor extracted from patent WO2019046778, Example 55[1].
IC50 & Target: enpp-1[1]

Name: S516, CAS: 1016543-77-3, stock 4.5g, assay 98.5%, MWt: 437.47, Formula: C21H19N5O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: S516 (Compound 22) is an active metabolite of CKD-516 and a potent tubulin polymerization inhibitor with an IC50 of 4.29 μM. S516 has marked antitumor activity[1].
IC50 & Target: IC50: 4.29 μM (tubulin polymerization)[1]
In Vitro: S516 has potent cytotoxicity with IC50s of 4.8 nM, 42.8 nM and 24.9 nM for HL-60, HCT116 and HCT15 cells, respectively[1]. 
S516 (Compound 22; 30 nM; 16 hours; HL60 cells) treatmemt causes significant arrest of cells at the G2/M phase, resulting in apoptosis with concomitant loss of G0/G1 phase[1].
In Vivo: S516 (Compound 22; 5-10 mg/kg; intraperitoneal injection; mice) treatment has promising antitumor activity (inhibition ratio (IR)> 63%) in human LX-1 lung cancer and CX-1 colon cancer mouse xenografts[1].

Name: GNF4877, CAS: 2041073-22-5, stock 6.8g, assay 98.4%, MWt: 494.52, Formula: C25H27FN6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Stem Cell/Wnt;PI3K/Akt/mTOR, Target: DYRK;GSK-3;GSK-3, Biological_Activity: GNF4877 is a potent DYRK1A and GSK3β inhibitor with IC50s of 6 nM and 16 nM, respectively, which leads to blockade of nuclear factor of activated T-cells (NFATc) nuclear export and increased β-cell proliferation (EC50 of 0.66 μM for mouse β (R7T1) cells)[1].
In Vitro: High glucose concentrations and glucokinase activators (GKAs) increase Ca2+ signalling in β-cells, and increase intracellular Ca2+ leads to activation of calcineurin and nuclear translocation of NFATc proteins. Indeed, concentrations of GNF4877 ((0.1 μM, 0.3 μM) well below the EC50 for β-cell proliferation are able to induce proliferation in the presence of high glucose or pharmacological activators of glucokinase. Finally, increasing intracellular Ca2+ with glibenclamide (a sulfonylurea receptor 1 inhibitor) or Bay K8644 (an L-type Ca2+ channel activator) show additive activity with GNF4877[1].
In Vivo: GNF4877 (50 mg/kg; oral gavage; twice a day; for 15 days; double transgenic RIP-DTA male mice) treatment induces β-cell proliferation, increases β-cell mass and insulin content, and improves glycaemic control[1].

Name: Dextran sulfate sodium salt (MW 16000-24000), CAS: 9011-18-1, stock 16.3g, assay 98%, MWt: 16000-24000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Anti-infection, Target: Apoptosis;HIV, Biological_Activity: Dextran sulfate sodium salt (MW 16000-24000) is a is a polymer of anhydroglucose with the molecular weight range of 16000-24000. Dextran sulfate sodium salt inhibits the replication of the human immunodeficiency virus by preventing the adsorption of the virus into host cells[1].

Name: Alisertib MLN 8237, CAS: 1028486-01-2, stock 13g, assay 98.4%, MWt: 518.92, Formula: C27H20ClFN4O4, Solubility: DMSO : 9.33 mg/mL (17.98 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Apoptosis;Cell Cycle/DNA Damage;Epigenetics;Autophagy, Target: Apoptosis;Aurora Kinase;Aurora Kinase;Autophagy, Biological_Activity: Alisertib (MLN 8237) is an orally active and selective Aurora A kinase inhibitor (IC50=1.2 nM), which binds to Aurora A kinase resulting in mitotic spindle abnormalities, mitotic accumulation. Alisertib (MLN 8237) induces apoptosis and autophagy through targeting the AKT/mTOR/AMPK/p38 pathway in leukemic cells. Antitumor activity[1][2][3].
IC50 & Target: IC50: 1.2 nM (Aurora A), 396.5 nM (Aurora B)[3]
In Vitro: Alisertib (MLN 8237) leads the MM cells to mitotic spindle abnormalities, mitotic accumulation, as well as inhibition of cell proliferation through apoptosis and senescence. Alisertib up-regulates p53 and tumor suppressor genes p21 and p27[1]. 
The decreased activity of Alisertib (MLN 8237) for the T217D/W277E Aurora A/TPX2 complex may reflect the increased affinity for ATP induced by cofactor binding to Aurora A[4]. 
Alisertib (MLN 8237) inhibits cell proliferation with IC50s ranging from 15 to 469 nM in different tumer cell lines[5].
In Vivo: Alisertib (MLN 8237) (30 mg/kg, p.o.) significantly reduces tumor burden and increases overall survival in xenograft-murine model of human-MM[1]. 
Alisertib (MLN 8237) (20, 30 mg/kg, p.o.) causes tumor growth inhibition in solid tumor xenograft models and regressions in in vivo models of lymphoma, and reduces FLT uptake in HCT-116 xenograft tumors[5].

Name: DS18561882, CAS: 2227149-22-4, stock 18.2g, assay 98.5%, MWt: 608.63, Formula: C28H31F3N4O6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DS18561882 is a highly potent, isozyme-selective methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) inhibitor with an IC50 value of 0.0063 μM. DS18561882 also has inhibitory effect on MTHFD1 (IC50=0.57 μM). DS18561882 exhibits a good oral pharmacokinetic profile[1].
IC50 & Target: IC50: 0.0063 μM (MTHFD2); 0.57 μM (MTHFD1)[1]
In Vitro: DS18561882 (0-150 nM) gives the lowest GI50 value (140 nM) against the MDA-MB-231 cell line[1].
In Vivo: DS18561882 (oral administration; 30, 100 or 300 mg/kg; twice daily) inhibits tumor growth inhibition with a dose-dependent manner, the tumor is completely inhibited (TGI: 67%) at the dose of 300 mg/kg in mice[1].
DS18561882 (oral administration; 10, 30, 100, or 300 mg/kg) has a good oral pharmacokinetic profile, including ACU (64.6, 264, 726 μg.h/ml ); Cmax (11.4, 56.5, 90.1 μg/ml); t1/2 (2.21, 2.16, 2.32 hours) for 30 mg/kg; 100mg/kg; 200 mg/kg, respectively[1].
DS18561882 is suspended in a 0.5% (w/v) methyl cellulose 400 solution in this article[1].

Name: Fmoc-Gly-Gly-Phe-OtBu, CAS: 236426-37-2, stock 38.8g, assay 98.7%, MWt: 557.64, Formula: C32H35N3O6, Solubility: DMSO : 200 mg/mL (358.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Fmoc-Gly-Gly-Phe-OtBu is a cleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs)[1].

Name: MC-Gly-Gly-Phe, CAS: 1599440-15-9, stock 3.4g, assay 98%, MWt: 472.49, Formula: C23H28N4O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: MC-Gly-Gly-Phe is a cleavable linker used for antibody-drug conjugates (ADC).

Name: PROTAC K-Ras Degrader-1, CAS: 2378258-52-5, stock 0.7g, assay 98.5%, MWt: 999.12, Formula: C53H62N10O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;PROTAC, Target: Ras;PROTAC, Biological_Activity: PROTAC K-Ras Degrader-1 (Compound 518) is potent K-Ras degrader based PROTAC, exhibits ≥70% degradation efficacy in SW1573 cells[1].
IC50 & Target: PROTAC, K-Ras[1]

Name: (1α,1'S,4β)-Lanabecestat (1α,1'S,4β)-AZD3293;(1α,1'S,4β)-LY3314814, CAS: 1384082-96-5, stock 38.7g, assay 98.3%, MWt: 412.53, Formula: C26H28N4O, Solubility: DMSO : 250 mg/mL (606.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Beta-secretase, Biological_Activity: (1α,1'S,4β)-Lanabecestat ((1α,1'S,4β)-AZD3293) is a Beta site APP Cleaving Enzymel (BACE1) inhibitor extracted from patent WO2012087237A1, compound 20a, has IC50s of 2.2 nM (TR-FRET assay) and 0.28 nM (sAPPp release assay), respectively[1].

Name: cis-9,10-Epoxystearic acid cis-9,10-Epoxyoctadecanoic acid, CAS: 24560-98-3, stock 14.6g, assay 98.2%, MWt: 298.46, Formula: C18H34O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: cis-9,10-Epoxystearic acid (cis-9,10-Epoxyoctadecanoic acid) is an endogenous constituent in human blood and urine. cis-9,10-Epoxystearic acid (cis-9,10-Epoxyoctadecanoic acid) can be produced from oleic acid by enzymic and non-enzymic epoxidation[1].

Name: PK11007, CAS: 874146-69-7, stock 36.2g, assay 98.5%, MWt: 427.86, Formula: C15H11ClFN5O3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: MDM-2/p53;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: PK11007 is a mild thiol alkylator with anticancer activity. PK11007 stabilizes p53 via selective alkylation of two surface-exposed cysteines without compromising its DNA binding activity. PK11007 induces mutant p53 cancer cell death by increasing reactive oxygen species (ROS) levels[1][2].
In Vitro: PK11007 (0-120 µM; 24 hours; four p53 wild-type cell lines and fours p53 mutant cell lines) treatment results in a large viability reduction in mutant p53 cell lines MKN1 (V143A), HUH-7 (Y220C), NUGC-3 (Y220C), and SW480 (R273H/P309S) at concentrations ranging from 15 to 30 µM. PK11007 induces mainly caspase-independent cell death[1]. 
PK11007 (0-60 µM; 3 hours or 6 hours; NUGC-4, NUGC-3, MKN1, HUH-6, and HUH-7 cancer cells) treatment up-regulates protein levels of the p53 target genes p21, MDM2, and PUMA in a mostly concentration-dependent manner in NUGC-3 (p53-Y220C), HUH-7 (p53-Y220C) and MKN1 (p53-V143A) cells, suggesting partial restoration of transcriptional activity to destabilized p53 mutants. PK11007 also increases p53 activity in HUH-6 and NUGC-4 cells, as indicated by the increase of MDM2, PUMA, and p21 protein levels[1]. 
PK11007 (15-20 µM; 4.5 hours or 6 hours; MKN1, HUH-7, NUGC-3, HUH-6 cells) treatment increases transcription of p53 target genes in three mutant p53 cell lines after 6-h treatment. PUMA and p21 mRNA levels are up-regulated by a factor of 2 upon treatment of NUGC-3, MKN, and HUH-7 cells, as well as NOXA for the latter two. MDM2 levels are halved in MKN1 and NUGC-3 cells[1]. 
PK11007 viability reduction is potentiated by glutathione depletion. To test whether PK11007 also increases ROS levels, NUGC-3, NUGC-4, HUH-6, HUH-7, and MKN1 cells with PK11007 are incubated for 2 h. There are elevated ROS levels in all cell lines after 2 h. In the mutant p53 cells MKN1, HUH-7, and NUGC-3, however, the ROS increase is higher at 60 µM PK11007 than in NUGC-4 and HUH-6 cells, suggesting that the higher PK11007 sensitivity of the mutant p53 cell lines is mediated by a stronger ROS induction. Basal and PK11007-induced ROS levels in MKN1 cells are at least twofold higher than in other cell lines[1]. 
PK11007 inhibits cell proliferation, induces apoptosis and alters genes involved in cell death are all consistent with the ability of PK11007 to reactivate mutant p53[2].

Name: AS2863619 (free base), CAS: 2241300-50-3, stock 34g, assay 98.6%, MWt: 332.32, Formula: C16H12N8O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;JAK/STAT Signaling;Stem Cell/Wnt, Target: CDK;STAT;STAT, Biological_Activity: AS2863619 free base enables conversion of antigen-specific effector/memory T cells into Foxp3+ regulatory T (Treg) cells for the treatment of various immunological diseases. AS2863619 free base is a potent, orally active cyclin-dependent kinase 8 (CDK8) and CDK19 inhibitor with IC50s of 0.61 nM and 4.28 nM, respectively. STAT5 activation enhanced by AS2863619 free base inhibition of CDK8/19, which consequently activates the Foxp3 gene[1].
In Vitro: AS2863619 (1 μM; 22 hours; mouse CD4+ T cells) treatment suppresses serine phosphorylation of the PSP motif of STAT5b to ~40% while enhancing tyrosine phosphorylation in the C-terminal domain to ~160% of control-treated samples[1].
In Vivo: AS2863619 (30 mg/kg; oral administration; daily; for 2 weeks; mice) treatment after sensitization with 2,4-dinitrofluorobenzene (DNFB) dampens the degree of the secondary response, with milder infiltration of inflammatory cells into the skin and decreases ratios of interferon-γ+ (IFN-γ+) cells in a skin contact hypersensitivity model, when compared with vehicle-treated control mice. Treg depletion before the elicitation of the secondary response abolishes AS2863619-induced suppression. KLRG1+ Foxp3+ T cells are specifically increased in DNFB sensitized AS2863619-treated mice[1].

Name: AS2863619, CAS: 2241300-51-4, stock 35.2g, assay 98.9%, MWt: 405.24, Formula: C16H14Cl2N8O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;JAK/STAT Signaling;Stem Cell/Wnt, Target: CDK;STAT;STAT, Biological_Activity: AS2863619 enables conversion of antigen-specific effector/memory T cells into Foxp3+ regulatory T (Treg) cells for the treatment of various immunological diseases. AS2863619 is a potent, orally active cyclin-dependent kinase 8 (CDK8) and CDK19 inhibitor with IC50s of 0.61 nM and 4.28 nM, respectively. STAT5 activation enhanced by AS2863619 inhibition of CDK8/19, which consequently activates the Foxp3 gene[1].
In Vitro: AS2863619 (1 μM; 22 hours; mouse CD4+ T cells) treatment suppresses serine phosphorylation of the PSP motif of STAT5b to ~40% while enhancing tyrosine phosphorylation in the C-terminal domain to ~160% of control-treated samples[1].
In Vivo: AS2863619 (30 mg/kg; oral administration; daily; for 2 weeks; mice) treatment after sensitization with 2,4-dinitrofluorobenzene (DNFB) dampens the degree of the secondary response, with milder infiltration of inflammatory cells into the skin and decreases ratios of interferon-γ+ (IFN-γ+) cells in a skin contact hypersensitivity model, when compared with vehicle-treated control mice. Treg depletion before the elicitation of the secondary response abolishes AS2863619-induced suppression. KLRG1+ Foxp3+ T cells are specifically increased in DNFB sensitized AS2863619-treated mice[1].

Name: AT-007, CAS: 2170729-29-8, stock 20.2g, assay 98.5%, MWt: 425.40, Formula: C17H10F3N3O3S2, Solubility: DMSO : 35.71 mg/mL (83.94 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aldose Reductase, Biological_Activity: AT-007 is an orally active central nervous system (CNS) penetrant Aldose Reductase inhibitor for treatment of Galactosemia with an IC50 value of 100 pM. AT-007 reduces toxic galactitol levels and prevents disease complications in GALT deficiency rats[1][2].
IC50 & Target: IC50: 100 pM (Aldose Reductase)[2]
In Vivo: AT-007 significantly reduces galactitol levels in GALT null rats in all traget tissues ( liver, brain and plasma), and does not increase galactose or Gal-1P levels[2].

Name: MYCi361 NUCC-0196361, CAS: 2289690-31-7, stock 31.3g, assay 98.3%, MWt: 594.86, Formula: C26H16ClF9N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: c-Myc, Biological_Activity: MYCi361 (NUCC-0196361) is a MYC inhibitor with the Kd of 3.2 μM for binding to MYC. MYCi361 (NUCC-0196361) suppresses tumor growth and enhances anti-PD1 immunotherapy[1].
In Vitro: MYCi361 inhibits the viability of MYC-dependent cancer cells including prostate cancer (MycCaP, LNCaP, and PC3), leukemia (MV4-11), lymphoma (HL-60 and P493-6), and neuroblastoma (SK-N-B2) with low-micromolar IC50 values[1].
In Vivo: MYCi361 inhibits MYC-dependent tumor growth in vivo. MYCi361 treatment (100 mg/kg/day for 2 days; then 70 mg/kg/day for 9 days) induces tumor regression in FVB or NSG male mice[1]. 
MYCi361 has moderate terminal elimination half-life of 44 and 20 h for intraperitoneal (i.p.) or oral (p.o.) dosing in mice, respectively[1]. 
MYCi361 suppresses tumor growth in mice, increases tumor immune cell infiltration, upregulates PD-L1 on tumors, and sensitizes tumors to anti-PD1 immunotherapy. However, MYCi361 demonstrates a narrow therapeutic index. An improved analog, MYCi975 shows better tolerability[1].

Name: MYCi975 NUCC-0200975, CAS: 2289691-01-4, stock 8.5g, assay 98.9%, MWt: 561.30, Formula: C25H16Cl2F6N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: c-Myc, Biological_Activity: MYCi975 (NUCC-0200975) is an orally active MYC inhibitor, which disrupts MYC/MAX interaction, promotes MYC T58 phosphorylation and MYC degradation, and impairs MYC driven gene expression. MYCi975 (NUCC-0200975) exhibits potent anti-tumor efficacy with good tolerability, increases tumor immune cell infiltration, and sensitizes tumors to anti-PD1 immunotherapy[1].
IC50 & Target: MYC[1]
In Vitro: MYCi975 (3 days) inhibits P493-6, MV411, and SK-N-B2 cells viability in an MYC-dependent manner with IC50s of 3.7, 3.9, 6.4 μM, respectively[1].
In Vivo: MYCi975 exhibits excellent pharmacokinetic profiles following p.o., i.p., or i.v. administration. The half-lives observed are 7 and 12 hours when dosed at 100 and 250 mg/kg p.o., respectively. The Cmax values attained are 41,533 ng/mL (74 μM) and 54,000 ng/mL (96 μM), respectively[1]. 
MYCi975 significantly inhibits tumor growth and increases survival in the MycCaP allograft model with animals tolerating a 100 mg/kg/day i.p. dosing for 14 days[1].

Name: AT9283, CAS: 896466-04-9, stock 7.5g, assay 98.5%, MWt: 381.43, Formula: C19H23N7O2, Solubility: DMSO : ≥ 100 mg/mL (262.17 mM), Clinical_Informat: Phase 2, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;Cell Cycle/DNA Damage;Epigenetics;Autophagy, Target: Apoptosis;Bcr-Abl;FLT3;JAK;JAK;JAK;Aurora Kinase;Aurora Kinase;Autophagy, Biological_Activity: AT9283 is a multi-targeted kinase inhibitor with potent activity against Aurora A/B, JAK2/3, Abl (T315I) and Flt3 (IC50s ranging from 1 to 30 nM). AT9283 inhibits growth and survival of multiple solid tumors in vitro and in vivo[1][2].
IC50 & Target: IC50: 1.2 nM (JAK2), 1.1 nM (JAK3), 3 nM (Aurora A), 3 nM (Aurora B)[1]
In Vitro: AT9283 leads to a clear polyploid phenotype by inhibiting the activity of Aurora B kinase in HCT116 cells with IC50 of 30 nM. Furthermore, AT9283 also produces the potent inhibition on HCT116 colony formation[1]. 
AT9283 induces apoptosis in a dose and time dependent manner and inhibits cell proliferation with an IC50 < 1 μM in B-NHL cell lines[2]. 
AT9283 inhibits growth, induces dose dependent cytotoxicity, and inhibits STAT3 signaling pathway in MM cell lines. T9283 inhibits phospho Histone H3 and phospho Aurora A at Thr 288. AT9283 increases G2/M phase and induces apoptosis of MM cells in a time-dependent manner[3].
In Vivo: In HCT116 human colon carcinoma xenograft bearing mice, AT9283 treatment (15 mg/kg and 20 mg/kg) for 16 days results in a significant tumor growth inhibition of 67% and 76%, respectively. In addition, AT9283 also exhibits a significantly longer half-life in tumors (2.5 hours) compared with plasma (0.5 hour) and modest oral bioavailability in mice[1]. 
AT9283 (15 mg/kg) and docetaxel (10 mg/kg) alone has modest anti-tumor activity. T9283 at 20 mg/kg and AT9283 (15 or 20 mg/kg) plus docetaxel (10 mg/kg) demonstrate a statistically significant tumor growth inhibition and enhance survival inmouse xenograft model of mantle cell lymphoma[2]. 
AT9283 (45 mg/kg, i.p.) inhibits tumor growth in mice. Two cycles of AT9283 45 mg/kg 14 hours after drug administration confirm decreased expression of phospho-Histone H3 and Aurora B in treated animals[3].

Name: Tetrahydrocortisol, CAS: 53-02-1, stock 5.3g, assay 98.3%, MWt: 366.49, Formula: C21H34O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Tetrahydrocortisol is cortisol metabolite. The urinary Tetrahydrocortisol/Tetrahydrocortisone ratio decreases with increasing 11β-hydroxysteroid dehydrogenase (11β-HSD) activity[1][2].

Name: MCL-1/BCL-2-IN-3, CAS: 2163793-55-1, stock 6.1g, assay 98.6%, MWt: 569.47, Formula: C27H25BrN2O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: MCL-1/BCL-2-IN-3 (Compound 2) is a potent and selective Mcl-1 and Bcl-2 dual inhibitor with IC50s of 5.95 and 4.78 μM, respectively[1].

Name: MCL-1/BCL-2-IN-2, CAS: 2163793-44-8, stock 35.6g, assay 98.6%, MWt: 427.31, Formula: C20H15BrN2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: MCL-1/BCL-2-IN-2 (Compound 6) is a potent and selective Mcl-1 and Bcl-2 dual inhibitor[1].

Name: GNF362, CAS: 1003019-41-7, stock 30.1g, assay 98.7%, MWt: 426.44, Formula: C22H21F3N6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: GNF362 is a selective, potent, and orally bioavailable inhibitor of inositol trisphosphate 3’ kinase B (Itpkb) with an IC50 of 9 nM. GNF362 also inhibits Itpka and Itpkc with IC50 values of 20 nM and 19 nM, respectively. Inositol trisphosphate 3’ kinase B (Itpkb) is a Ca2+-dependent kinase, which phosphorylates the 3’ position of Ins (1,4,5) P3 to generate inositol 1,3,4,5-tetrakisphosphate [Ins (1,3,4,5) P4][1].
In Vitro: GNF362 (0-10 mM) blocks Ins (1,3,4,5) P4 production, enhances antigen receptor-driven Ca2+ responses and lead to apoptosis of activated T cells in an Itpkb-dependent manner in lymphocytes[1].
GNF362 augments SOC responses following antigen receptor cross-linking, with an EC50 of 12 nM in primary B or T lymphocytes[1].
In Vivo: GNF362 (orally administration; 6 or 20 mg/kg; twice daily; 21 days) shows minimal block in antibody production but shows significant inhibition of joint swelling at 6 mg/kg, reduces inflammatory cell infiltrate, joint damage, and proteoglycan loss at 20 mg/kg[1].

Name: Sincalide (ammonium) Cholecystokinin octapeptide (ammonium); CCK-8 (ammonium);SQ19844 (ammonium), CAS: 70706-98-8, stock 14.6g, assay 98.3%, MWt: 1160.30, Formula: C49H65N11O16S3, Solubility: H2O : 12.5 mg/mL (10.77 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Sincalide ammonium (Cholecystokinin octapeptide ammonium) is a rapid-acting amino acid polypeptide hormone analogue of cholecystokinin (CCK) for intravenous use in postevacuation cholecystography. Sincalide ammonium is an agent that promotes gallbladder contraction by injection and helps diagnose gallbladder and pancreas disorders. The hepatobiliary physiologic effect of Sincalide ammonium is to increase bile secretion, cause the gallbladder to contract and relax the sphincter of Oddi, resulting in bile drainage into the duodenum[1][2].

Name: Tos-PEG4-t-butyl ester Tos-PEG4-Boc, CAS: 217817-01-1, stock 19.3g, assay 98.6%, MWt: 432.53, Formula: C20H32O8S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: Tos-PEG4-t-butyl ester (Tos-PEG4-Boc) is a PROTAC linker, which refers to the PEG composition. Tos-PEG4-t-butyl ester (Tos-PEG4-Boc) can be used in the synthesis of a series of PROTACs, such as BI-3663 (HY-111546). BI-3663 is a highly selective PTK2/FAK PROTAC, with cereblon ligands to hijack E3 ligases for PTK2 degradation, and inhibits PTK2 with an IC50 of 18 nM[1].

Name: D-Methionine sulfoxide, CAS: 21056-56-4, stock 22.9g, assay 98%, MWt: 165.21, Formula: C5H11NO3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-methionine sulfoxide is the D-isomer of Methionine sulfoxide. Methionine sulfoxide is an oxidation product of methionine. Methionine is the limiting amino acid in milk or leguminous proteins , which is easily oxidized during the course of storage or processing[1].

Name: Lanraplenib (succinate) GS-9876 (succinate), CAS: 1800047-00-0, stock 21.2g, assay 98.2%, MWt: 620.64, Formula: C23H25N9O.3/2C4H6O4, Solubility: DMSO : 83.33 mg/mL (134.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Syk, Biological_Activity: Lanraplenib succinate (GS-9876 succinate) is a highly selective and orally active SYK inhibitor (IC50=9.5 nM) in development for the treatment of inflammatory diseases. Lanraplenib succinate (GS-9876 succinate) inhibits SYK activity in platelets via the glycoprotein VI (GPVI) receptor without prolonging bleeding time (BT) in monkeys or humans[1][2][3].
IC50 & Target: IC50: 9.5 nM (SYK)[1]
In Vitro: Lanraplenib succinate (GS-9876 succinate) inhibits anti-IgM stimulated phosphorylation of AKT, BLNK, BTK, ERK, MEK, and PKCδ in human B cells with EC50 values of 24-51 nM. Lanraplenib monosuccinate inhibits anti-IgM mediated CD69 and CD86 expression on B-cells (EC50=112±10 nM and 164±15 nM, respectively) and anti-IgM /anti-CD40 co-stimulated B cell proliferation (EC50=108±55 nM). In human macrophages, Lanraplenib succinate inhibits IC-stimulated TNFα and IL-1β release (EC50=121±77 nM and 9±17 nM, respectively)[1]. 
Lanraplenib succinate (GS-9876 succinate) inhibits glycoprotein VI (GPVI)-induced phosphorylation of linker for activation of T cells and phospholipase Cγ2, platelet activation and aggregation in human whole blood, and platelet binding to collagen under arterial flow[2].

Name: BTL-104, CAS: 753451-66-0, stock 3.4g, assay 98.1%, MWt: 766.95, Formula: C40H50N10O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BTL-104 is a monobiotinylated Phos-tag derivative for the detection of phosphopeptides and phosphoproteins[1].

Name: BTL-105, CAS: 945007-11-4, stock 32.3g, assay 98.6%, MWt: 880.11, Formula: C46H61N11O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BTL-105 is a monobiotinylated Phos-tag derivative for the detection of phosphopeptides and phosphoproteins[1].

Name: AG-490 Tyrphostin AG 490, CAS: 133550-30-8, stock 24.1g, assay 98.5%, MWt: 294.30, Formula: C17H14N2O3, Solubility: DMSO : ≥ 50 mg/mL (169.89 mM), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Autophagy;JAK/STAT Signaling;Stem Cell/Wnt, Target: EGFR;EGFR;Autophagy;STAT;STAT, Biological_Activity: AG-490 is an tyrosine kinase inhibitor, inhibits EGFR and Stat-3.
IC50 & Target: EGFR and Stat-3[1]
In Vitro: AG490 inhibits the activation of Stat-3 by selectively blocking JAK2. AG490 is used to selectively inhibit JAK/Stat-3 activation. At a dose of 10 μM, Stat-3 phosphorylation is decreased by >95% and cell viability is maintained. AG490 at a dose of 10 μM results in >95% decrease in pStat-3 in EGF-stimulated A431 cells with no effect on Stat-3 mass[1]. AG-490 is a potent inhibitor of the JAK3/STAT, JAK3/AP-1, and JAK3/MAPK pathways and their cellular consequences. AG-490 abolishes IL-2-inducible [3H]thymidine incorporation in a dose-dependent manner, displaying an IC50 of 25 μM. AG-490 potently inhibits IL-2-mediated proliferation in T cells, results distinct from previous studies that showed this agent induced apoptosis in ALL cells while exerting apparently no effects on the growth of mitogen-stimulated normal T cells[2].
In Vivo: AG490 significantly inhibits the development of type 1 diabetes (T1D) (p = 0.02, p = 0.005; at two different time points). Monotherapy of newly diagnosed diabetic NOD mice with AG490 (1 mg/mouse) markedly results in disease remission in treated animals (n=23) in comparision to the absolute inability (0%; 0/10, p=0.003, Log-rank test) of DMSO and sustained eugluycemia is maintained for several months following drug withdrawal[3]. AG490 (1-10 µg) significantly attenuates ʎ-carrageenan-induced thermal hyperalgesia in a dose-dependent manner. AG490 also reduces mechanical hyperalgesia[4].

Name: NTP42, CAS: 2055599-51-2, stock 16.7g, assay 98.1%, MWt: 515.53, Formula: C25H23F2N3O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: NTP42 is a thromboxane A2 (TXA2) receptor antagonist with an IC50 of 3.278 nM for antagonizing T prostanoid receptor (TP)- mediated [Ca2+] mobilization following stimulation of cells with the alternative TP agonist U46609[1]. NTP42 can be used for the treatment of pulmonary arterial hypertension (PAH)[2].
In Vivo: NTP42 (0.25 mg/kg BID) is potent in a monocrotaline (MCT)-induced PAH rat model (28-day drug treatment is initiated within 24 h post-MCT) in haemodynamic assessments. NTP42 reduces the MCT-induced PAH, including mean pulmonary arterial pressure (mPAP) and right systolic ventricular pressure (RSVP). Moreover, NTP42 is superior to Sildenafil and Selexipag in significantly reducing pulmonary vascular remodelling, inflammatory mast cell infiltration and fibrosis in MCT-treated animals[2].

Name: (Rac)-E1R, CAS: 787623-60-3, stock 35.3g, assay 98.1%, MWt: 232.28, Formula: C13H16N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Sigma Receptor;Sigma Receptor, Biological_Activity: (Rac)-E1R (Compound 2) is the racemate of E1R. (Rac)-E1R is a sigma-1 receptor positive allosteric modulator (Sig1R PAM) for the treatment of cognition/memory disorders[1].
In Vitro: Sigma-1 receptor plays an important role in neuronal plasticity, a process implicated in the pathophysiology of neuropsychiatric diseases, such as Alzheimer’s disease, major depressive disorders, and schizophrenia[1].

Name: (2R,3S)-E1R, CAS: 1424832-60-9, stock 35.5g, assay 98.9%, MWt: 232.28, Formula: C13H16N2O2, Solubility: DMSO : 250 mg/mL (1076.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Sigma Receptor;Sigma Receptor, Biological_Activity: (2R,3S)-E1R (Compound 2c) is an enantiomer of E1R. (2R,3S)-E1R is a sigma-1 receptor positive allosteric modulator (Sig1R PAM) for the treatment of cognition/memory disorders[1].
In Vitro: Sigma-1 receptor plays an important role in neuronal plasticity, a process implicated in the pathophysiology of neuropsychiatric diseases, such as Alzheimer’s disease, major depressive disorders, and schizophrenia[1].

Name: (2S,3S)-E1R, CAS: 1424832-57-4, stock 0.4g, assay 98.6%, MWt: 232.28, Formula: C13H16N2O2, Solubility: DMSO : 500 mg/mL (2152.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Sigma Receptor;Sigma Receptor, Biological_Activity: (2S,3S)-E1R (Compound 2d) is an enantiomer of E1R. (2S,3S)-E1R is a sigma-1 receptor positive allosteric modulator (Sig1R PAM) for the treatment of cognition/memory disorders[1].
In Vitro: Sigma-1 receptor plays an important role in neuronal plasticity, a process implicated in the pathophysiology of neuropsychiatric diseases, such as Alzheimer’s disease, major depressive disorders, and schizophrenia[1].

Name: (2R,3R)-E1R, CAS: 1400888-63-2, stock 19.8g, assay 98.7%, MWt: 232.28, Formula: C13H16N2O2, Solubility: DMSO : 50 mg/mL (215.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Sigma Receptor;Sigma Receptor, Biological_Activity: (2R,3R)-E1R (Compound 2b) is an enantiomer of E1R. (2R,3R)-E1R is a sigma-1 receptor positive allosteric modulator (Sig1R PAM) for the treatment of cognition/memory disorders[1].
In Vitro: Sigma-1 receptor plays an important role in neuronal plasticity, a process implicated in the pathophysiology of neuropsychiatric diseases, such as Alzheimer’s disease, major depressive disorders, and schizophrenia[1].

Name: Iobenguane (sulfate) MIBG (sulfate), CAS: 87862-25-7, stock 29.2g, assay 99%, MWt: 324.13, Formula: C8H10IN3.1/2H2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Iobenguane sulfate (MIBG sulfate) is an analogue of the neurotransmitter norepinephrine with antitumor activity. Radioiodinated Iobenguane sulfate is clinically used as a tumor-targeted radiopharmaceutical in the diagnosis and treatment of adrenergic tumors. Iobenguane sulfate is a high-affinity substrate for cholera toxin that interferes with cellular mono(ADP-ribosylation)[1][2].
In Vitro: Iobenguane sulfate (MIBG sulfate) (2-20 μg/ml; 72 hours) inhibits cell growth in a panel of human and mouse leukemia, fibrosarcoma, melanoma, and neuroblastoma cell lines[1]. 
Iobenguane sulfate (MIBG sulfate) is a potent affector of endogenous mono(ADP-ribosyl) transferases of turkey and human erythrocyte membranes, exerting its effect in the μM concentration range[2].
In Vivo: Iobenguane sulfate (MIBG hemisulfate) (20 mg/kg; i.p.; daily on days 3-6) shows antitumor activity[1]. 
The survival of male strain AF mice inoculates with N1E115 neuroblastoma and treats according to NIH protocols for new drug testing with 9 daily injections of Iobenguane sulfate (40 mg/kg), Marking prolongation of sugvival but no cures were observed[1]. 
Iobenguane sulfate testes for its toxicity on male strain AF (N1Ell5) mice with 5 daily injections. At 50 mg/kg body weight, all animals died after 1-4 doses and 4/16 animals died on a schedule of 44 mg/kg[1].

Name: Hydrastinine, CAS: 6592-85-4, stock 23.5g, assay 98.1%, MWt: 207.23, Formula: C11H13NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hydrastinine is a major alkaloid constituent in goldenseal (Hydrastis canadensis). Hydrastinine can be used as a haemostatic agent[1].

Name: Nebracetam (hydrochloride) WEB 1881 FU (hydrochloride), CAS: 1177279-49-0, stock 3.6g, assay 98.8%, MWt: 240.73, Formula: C12H17ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Nebracetam hydrochloride, a nootropic M1-muscarinic agonist, induces a rise of intracellular Ca2+ concentration. Nebracetam hydrochloride exhibits an EC50 of 1.59 mM for elevating [Ca2+]i[1].
In Vivo: Nebracetam (10 mg/kg, p.o.) involves not only cholinergic mechanisms but also involves lymbic and hippocampal noradrenergic mechanisms[2].

Name: AR-C102222 (hydrochloride), CAS: 1781934-50-6, stock 32.3g, assay 98.5%, MWt: 418.83, Formula: C19H17ClF2N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: AR-C102222 hydrochloride is a potent, competitive, orally active and highly selective inducible nitric oxide synthase (iNOS) inhibitor, with an IC50 of 37 nM[1]. AR-C102222 hydrochloride has antinociception and anti-inflammatory activities[2].
In Vivo: AR-C102222 (3, 10, 30, 100 mg/kg, P.O.) attenuates arachidonic acid-induced ear inflammation and possesses anti-inflammatory activity[2]. 
AR-C102222 shows good efficacy in a rat adjuvant-induced arthritis model[3].

Name: Zoniporide (hydrochloride hydrate) CP-597396 (hydrochloride hydrate), CAS: 863406-85-3, stock 17.9g, assay 98.6%, MWt: 374.82, Formula: C17H19ClN6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Zoniporide (CP-597396) hydrochloride hydrate is a potent and selective inhibitor of sodium-hydrogen exchanger type 1 (NHE-1). Zoniporide hydrochloride hydrate inhibits human NHE-1 (IC50=14 nM), and has >150-fold selectivity versus other NHE isoforms. Zoniporide hydrochloride hydrate potently inhibits ex vivo NHE-1-dependent swelling of human platelets (IC50=59 nM)[1][2].
IC50 & Target: IC50: 14 nM (NHE-1)[1]
In Vivo: Zoniporide hydrochloride hydrate (0.25-4 mg/kg; i.v.; every hour for 2 hours) elicits a dose-dependent reduction in infarct size (ED50=0.45 mg/kg/h) in open chest anesthetized rabbits[1]. 
Zoniporide exhibits moderate plasma protein binding, has a t1/2 of 1.5 hours in monkeys, and has one major active metabolite[1]. 
Zoniporide hydrochloride hydrate treatment shows the AUC0-∞ and t1/2 are 0.07 μg h/mL and 0.5 hours, respectively[2].

Name: rel-α-Vitamin E rel-(+)-α-Tocopherol; rel-D-α-Tocopherol, CAS: 2074-53-5, stock 11.7g, assay 98.2%, MWt: 430.71, Formula: C29H50O2, Solubility: H2O : 60 mg/mL (139.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: rel-α-Vitamin E (rel-(+)-α-Tocopherol) is a vitamin with antioxidant properties and also a mixture[1].
In Vitro: Vitamin E is a lipid-soluble, chain-breaking type of antioxidant present in human blood. Vitamin E works as a free radical scavenger and has the primary function of destroying peroxyl radicals. Thus, it protects long-chain polyunsaturated fatty acids (e.g., cell membranes or low-density lipoprotein cholesterol) from oxidation or destruction. Its association with vitamin C is of great pathophysiological importance, because inhibition of lipid peroxidation by α-tocopherol occurs through its conversion into an oxidized α-tocopheroxyl radical, which in turn is regenerated to α-tocopherol through reduction by redox-active reagents[1]. 
α-Tocopherol can inhibit the recruitment of lymphocytes and eosinophils[1].
In Vivo: In order to longitudinally relate vitamin E status, evaluated by means of α- and γ-tocopherol measured in erythrocytes membranes, to inflammatory state and oxidative stress by means of total antioxidant capacity of plasma and lipid peroxidation biomarkers, and to assess its association to hard long-term outcomes (e.g., overall and cause-specific graft and recipient loss), and to be able to likewise account for liver, lung, and heart transplant recipients[1].

Name: Lenvatinib E7080, CAS: 417716-92-8, stock 19.4g, assay 98.5%, MWt: 426.85, Formula: C21H19ClN4O4, Solubility: DMSO : 37.5 mg/mL (87.85 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;FGFR;c-Kit;RET, Biological_Activity: Lenvatinib (E7080) is an oral, multi-targeted tyrosine kinase inhibitor that inhibits VEGFR1-3, FGFR1-4, PDGFR, KIT, and RET, shows potent antitumor activities[1][2].
In Vitro: Lenvatinib (E7080) has IC50s of 4, 5.2, 22 nM for VEGFR2 (KDR), VEGFR3 (Flt-4), and VEGFR1 (Flt-1), respectively. Lenvatinib inhibits PDGFRα, PDGFRβ, FGFR1, and KIT with IC50s of 51, 39, 46, and 100 nM, respectively[3].
In Vivo: Lenvatinib (E7080) (100 mg/kg, p.o.) significantly inhibits local tumor growth at the m.f.p., and at the end of treatment, Lenvatinib mesylate also significantly inhibits metastasis to both regional lymph nodes and distant lung[3]. 
Lenvatinib (E7080) inhibits the growth of H146 tumor at 30 and 100 mg/kg (BID, QDx21) in a dose-dependent manner and causes tumor regression at 100 mg/kg in H146 xenograft model. IHC analysis with anti-CD31 antibody shows that lenvatinib at 100 mg/kg decreases microvessel density more than anti-VEGF antibody and STI571 treatment[4].

Name: J14, CAS: 1043854-13-2, stock 28.5g, assay 98.3%, MWt: 517.04, Formula: C28H25ClN4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: J14 is a reversible sulfiredoxin inhibitor with an IC50 of 8.1 μM. J14 induces oxidative stress (intracellular ROS accumulation) by inhibiting sulfiredoxin, leading to cytotoxicity and cancer cell death[1].
IC50 & Target: IC50: 8.1 μM (Sulfiredoxin); ROS[1]
In Vitro: J14 (0-100 μM; 0-96 hours; A549 cells) treatment inhibits the growth of A549 cells in a concentration- and a time- dependent manner, and its half inhibitory concentration for the growth of A549 cells was 15.7 μM[1]. 
J14 (20 μM; 48-72 hours; A549 cells) treatment causes not only the release of cytochrome c into the cytosol, but also the activation of caspase-3 and caspase-9. J14 induces oxidative damage to mitochondria, resulting in caspase-mediated apoptosis[1]. 
J14 treatment significantly increases the accumulation of sulfinic peroxiredoxins and intracellular ROS. Excess accumulation of intracellular ROS causes oxidative damage, leading to cell death. J14 significantly induces cell death in A549 cells in a time-dependent manner, resulting in approximately 40% cell death in 96 hours[1]. 
J14 induces oxidative mitochondrial damage and apoptosis[1].
In Vivo: J14 (50 mg/kg; intraperitoneal injection; daily; for 16 days; BALB/c nude female mice) treatment significantly reduces the average tumor volume. The masses and weights of the primary tumors excised from the J14-treated mice are significantly lower compared with those of the control mice[1].

Name: 2-Di-1-ASP, CAS: 2156-29-8, stock 39.1g, assay 98.3%, MWt: 366.24, Formula: C16H19IN2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2-Di-1-ASP (Compound 18a) is a mono-stryryl dye, and widely used as mitochondrial stain and groove-binding fluorescent probes for double-stranded DNA. 2-Di-1-ASP is selective for G-quadruplex (G4) and double-stranded DNA[1].
In Vitro: 2-Di-1-ASP (Compound 18a) displays significant fluorescence enhancements in the presence of G-quadruplex (G4) structures (up to 300-fold), and good selectivity with respect to double-stranded DNA. 2-Di-1-ASP shows fluorimetric selectivity for parallel G4-DNA forms (c-kit2, c-kit87up, c-myc)[1].

Name: SNAP 94847 (hydrochloride), CAS: 1781934-47-1, stock 11.2g, assay 98.7%, MWt: 515.03, Formula: C29H33ClF2N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: SNAP 94847 hydrochloride is a novel, high affinity selective melanin-concentrating hormonereceptor1 (MCHR1) antagonist with (Ki= 2.2 nM, Kd=530 pM), it displays >80-fold and >500-fold selectivity over MCHα1A and MCHD2 receptors respectively. SNAP 94847 hydrochloride binds with high affinity to the mouse and rat MCHR1 with minimal cross-reactivity to other GPCR, ion channels, enzymes, and transporters[1][3].
IC50 & Target: Ki: 2.2 nM (MCHR1); Kd: 530 pM (MCHR1)[3]
In Vivo: SNAP 94847 hydrochloride (oral gavage; 20 mg/kg; 14 days) shows an exaggerated locomotor response to acute quinpirole [treatment: F(2,19)=11.31, treatment × time: F(34,323) = 4.061], the effect of SNAP 94847 on quinpirole-evoked ambulations over the entire observation period is significant compared to the untreated animals[2].
SNAP 94847 hydrochloride (oral administration; 20 mg/kg; 21 days) in drink water, produces a significant increase in ambulation relative to untreated animals [treatment: F(3,28) = 8.971; treatment × time: F(51,476)=11.50]. shows a marked increase in locomotion is apparent after 40 min in the SNAP 94847-treated group,this effect is significant over 180 min[2].
SNAP 94847 hydrochloride (oral administration; 10 mg/kg), has a good bioavailability (59%), low plasma and blood clearances of 4.2 L/hr/kg and 3.3 L/hr/kg, respectively, and the half-life was shown to be 5.2 h in rats in a PK study[3].

Name: Autotaxin-IN-3, CAS: 2156655-68-2, stock 16.3g, assay 98%, MWt: 443.46, Formula: C22H21N9O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Autotaxin-IN-3 is a Autotaxin(ATX) inhibitor with an IC50 of 2.4 nM, compound 33, sourced from patent WO2018212534A1[1].
In Vitro: Autotaxin is an enzyme which is responsible for the increase in lysophosphatidic acid in ascites and plasma, and it is a secretory enzyme important for converting lysophosphatidylchloine (LPC) into lysophosphatidic acid (LPA) as a bioactive signaling molecule[1].

Name: Thiochrome, CAS: 92-35-3, stock 9.6g, assay 98.3%, MWt: 262.33, Formula: C12H14N4OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Thiochrome, a natural oxidation product and metabolite of thiamine, is a selective M4 muscarinic receptor of acetylcholine (ACh) affinity enhancer. Thiochrome has neutral cooperativity with ACh at M1 to M3 receptors[1][2].
In Vivo: Thiochrome can increase the intensity of the reproduction process of the representatives of one-cell organisms worms, crustaceans, insects and fishes[1].

Name: L-745870 (hydrochloride), CAS: 1173023-36-3, stock 37.3g, assay 98.1%, MWt: 363.28, Formula: C18H20Cl2N4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: L-745870 hydrochloride is a high-affinity, selective and orally active human dopamine D4 receptor antagonist with a Ki of 0.43 nM, and considerably weaker D2 (Ki of 960 nM) and D3 (Ki of 2300 nM) receptors affinity. L-745870 hydrochloride has excellent brain penetration[1][2][3].
IC50 & Target: Ki: 0.43 nM (Human dopamine D4 receptor), 960 nM (Human dopamine D2 receptor), 2300 nM (Human dopamine D3 receptor)[1][3]
In Vitro: In vitro pharmacological studies revealed that L-745870 is an antagonist at human D4 receptors, in that L-745870 is capable of antagonizing the ability of D4 receptors to inhibit agonist-induced stimulation of [35S]-GTPgS binding; blocking the inhibition of forskolin-stimulated adenylate cyclase activity in transfected human embryonic kidney (HEK293) and Chinese hamster ovary (CHO) cells; blocking dopamine-induced inhibition of Ca2+ currents in transfected GH4C1 pituitary cells; inhibiting D4 activation of cloned G protein-coupled inwardly rectifying K+ channels; and antagonizing dopamine-induced stimulation of extracellular acidification in transfected cells[1][2].
In Vivo: L-745870 has good pharmacokinetic properties (20-60% oral bioavailability and plasma t1/2 2.1-2.8 hours) in both rat and monkey, and excellent brain penetration with high brain to plasma ratios in rat[2]. 
Evaluation of L-745870 in surrogate marker assays demonstrates that this compound is freely available for biological activity in the brain and that at doses of 5 to 60 mg/kg p.o. L-745870 would occupy 50% D4 receptors in the brain. L-745870 has no effect on apomorphine-induced stereotypy in rats but does induce catalepsy in mice, albeit at a high dose of 100 mg/kg p.o. that is likely to occupy D2 receptors in vivo. High doses of L-745870 might also be expected to cause extrapyramidal symptoms in primates because the levels in the CNS at these doses would be sufficient to antagonize D2 receptors. Following oral administration to squirrel monkeys, L745870 (10 mg/kg p.o.) induces mild sedation and extrapyramidal motor symptoms, notably bradykinesia, became apparent at 30 mg/kg. Lower doses of L-745870 has no observable behavioural effects in monkeys[1][2].

Name: Glyceryl monocaprate Monocaprin, CAS: 26402-22-2, stock 14.4g, assay 98.9%, MWt: 246.34, Formula: C13H26O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: HSV;Bacterial, Biological_Activity: Glyceryl monocaprate (Monolaurin) is a 1-monoglyceride of capric acid against gram-positive bacterial infections[1]. Glyceryl monocaprate (Monolaurin) has inhibitory effect on Herpes Simplex Virus (HSV) and offers an effective treatment for herpes labialiss[2].
IC50 & Target: IC50: Gram-positive Bacterial; HSV[1][2]
In Vitro: Glyceryl monocaprate (Monolaurin) has an antimicrobial activity against gram-positive ATCC SA 29123[1].
In Vivo: Glyceryl monocaprate (Monolaurin) combines with low-dose doxycycline offers an effective treatment for herpes labialiss, significantly reducing time to healing and pain compared with the placebo and monocaprin alone[2].

Name: (Rac)-LM11A-31 (dihydrochloride), CAS: 1214672-15-7, stock 34.4g, assay 98.1%, MWt: 316.27, Formula: C12H27Cl2N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (Rac)-LM11A-31 dihydrochloride is an isomer of LM11A-31 dihydrochloride. LM11A-31 dihydrochloride, a p75NTR (neurotrophin receptor p75) Ligand, is a potent proNGF (nerve growth factor) antagonist[1].

Name: cis-Urocanic acid (Z)-Urocanic acid;cis-UCA, CAS: 7699-35-6, stock 33.2g, assay 98.5%, MWt: 138.12, Formula: C6H6N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: cis-Urocanic acid is a 5-HT2A receptor agonist. cis-Urocanic acid binds to 5-HT receptor with relatively high affinity (Kd=4.6 nM). cis-Urocanic acid is an immune modulator that induces immunosuppression by binding to the 5-HT2A receptor[1].
IC50 & Target: 5-HT2A receptor[1]
In Vitro: Treatment with 100 μg/mL cis-Urocanic acid (cis-UCA) completely suppresses IL-6 and IL-8 secretion, decreases caspase-3 activity, and improves cell viability against UV-B irradiation. No significant effects on IL-6 or IL-8 secretion, caspase-3 activity, or viability of the non-irradiated cells are observed with 100 μg/mL cis-Urocanic acid in both cell types. The 5000 μg/mL concentration is toxic[1].

Name: trans-2-Undecenoic acid (E)-2-Undecenoic acid;(E)-Undec-2-enoic acid, CAS: 15790-94-0, stock 1.1g, assay 98.2%, MWt: 184.28, Formula: C11H20O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: trans-2-Undecenoic acid ((E)-2-Undecenoic acid) is an α,β-unsaturated carboxylic acid and is characterized by acid dimers. The corresponding dimers are connected via intermolecular hydrogen bonds of the carboxylic groups C=O···H-O[1].
In Vitro: The crystal packing of trans-2-Undecenoic acid (E)-undec-2-enoic acid) is described by layers of acid dimers parallel to the (0 4 1) plane which are featured by layers of polar headgroups and hydrophobic hydrocarbon chains. The carboxylic group and the following three carbon atoms (C2, C3, C4) of the trans-2-Undecenoic acid (E)-undec-2-enoic acid) molecule lie in one plane, whereas the atoms of the hydrocarbon chain starting from C4 until C11 adopt a nearly fully staggered conformation[1].

Name: CGP 20712 A CGP 20712 (mesylate), CAS: 105737-62-0, stock 31.8g, assay 98.7%, MWt: 590.57, Formula: C24H29F3N4O8S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: CGP 20712 A (CGP 20712 mesylate) is a highly selective β1-adrenoceptor antagonist with an IC50 of 0.7 nM. CGP 20712 A exhibits ~10,000-fold selectivity over β2-adrenoceptors[1].
IC50 & Target: IC50: 0.7 nM (β1-adrenoceptor)[1]
In Vitro: In myocytes, the activation of adenylate cyclase causes by β2-adrenoceptors is not detected in the presence of 10 nM, 100 nM or 1000 nM CGP 20712 A (CGP 20712 mesylate), which selectively antagonized beta1-adrenoceptors[2].
In Vivo: Pretreatment of 8-day-old rats with 5 mg/kg CGP 20712 A do not change the plasma ACTH response to insulin injection[3].

Name: Prinomastat (hydrochloride) AG3340 (hydrochloride);KB-R9896 (hydrochloride), CAS: 1435779-45-5, stock 5.8g, assay 98.2%, MWt: 459.97, Formula: C18H22ClN3O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Prinomastat hydrochloride (AG3340 hydrochloride) is a broad spectrum, potent, orally active metalloproteinase (MMP) inhibitor with IC50s of 79, 6.3 and 5.0 nM for MMP-1, MMP-3 and MMP-9, respectively. Prinomastat hydrochloride inhibits MMP-2, MMP-3 and MMP-9 with Kis of 0.05 nM, 0.3 nM and 0.26 nM, respectively. Prinomastat hydrochloride can cross blood-brain barrier. Antitumor avtivity[1][2][3][4].
In Vitro: Prinomastat (AG3340; 0.1-1 µg/mL; 4 days; C57MG/Wnt1 cells) inhibits Wnt1-induced MMP-3 production. Reversal of Wnt1-induced EMT and β-catenin transcriptional activity by Prinomastat[1]. 
Co-culture of L/Wnt3a cells and CT7 cells increases the Topflash activity in CT7 cells, and co-culturing both L/Wnt3a cells and MMP-3 overexpressing C57MG cells with CT7 cells increases the Topflash luciferase activity in CT7 cells beyond the level observed with L/Wnt3a cells, and these effects are all suppressed by Prinomastat (AG3340)[1]. 
Inhibition of entry of C57MG/Wnt1 cells into S phase by Prinomastat corresponds to a decrease in expression of cyclin D1 and Erk1/2 phosphorylation. The effect of Prinomastat on Wnt1-induced migration is then examined using an in vitro wound assay. As anticipated, the migration of C57MG/Wnt1 cells is increased by 1.8-fold when compared with C57MG cells.The effect of Wnt1 on the cellular distribution of vimentin is reversed by Prinomastat in C57MG/Wnt1 cells[1].
In Vivo: In a human fibrosarcoma mouse model (HT1080), the mice are treated therapeutically for 14-16 days with 50 mg/kg/day ip daily starting day 3 to 6 after tumour inoculation. Prinomastat is well tolerated by the animals, and there are no signs of weight loss or other adverse effects. Prinomastat has good tumour growth inhibition, with a short T1/2 of 1.6 hours[1].

Name: Indium(III) isopropoxide, CAS: 38218-24-5, stock 15.5g, assay 98.3%, MWt: 97.36, Formula: C3H8O.1/3In, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Indium(III) Isopropoxide is an organo-metallic compound. Indium(III) Isopropoxide uesd as a hydrogen transfer catalyst for conversion of benzylic alcohols into aldehydes or ketones via Oppenauer oxidation. Indium(III) Isopropoxide also can be used as metal precursor[1][2].
In Vitro: Indium(III) isopropoxide as an Oppenaueroxidation catalyst, and the conversion of primary or secondary alcohols into the corresponding aldehydes or ketones was promoted at room temperature using pivalaldehyde as an oxidant[1].

Name: Flumexadol, CAS: 30914-89-7, stock 3.7g, assay 98.7%, MWt: 231.21, Formula: C11H12F3NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Flumexadol is an orally active non-narcotic analgesic. Flumexadol is a selective and affinity 5-HT2C receptor agonist with a Ki of 25 nM for the (+)-enantiomer of Flumexadol, and is 40-fold selective over the 5-HT2A receptor[1][2].
In Vivo: In rats and dogs dosed with 14C-Flumexadol (CERM1841), the 14C is excreted in the urine. The 14C eliminated in the faeces of dog is significantly higher than for rat. Conjugated metabolites, mostly glucuronides, accounted for the greater part of the urinary radioactivity in both species. Biotransformation products are predominantly acids in both species, follows by significant amounts of basic metabolites, with very little neutral substances. The major urinary metabolite in rats is 3-trifluoromethylbenzoic acid and 3-trifluoromethylhipuric acid. In the dog it is 3-trifluoromethylmandelic acid in addition to the benzoic acid and its conjugate. The basic products identified in the urine of both species are unchanged drug and 1-amino-2-hydroxy-2-(3-trifluoromethylphenyl)ethane, with the first predominating[3].

Name: (Rac)-WAY-161503, CAS: 75704-24-4, stock 26.6g, assay 98.8%, MWt: 272.13, Formula: C11H11Cl2N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: (Rac)-WAY-161503 is a potent, selective, highly affinity 5-HT2C receptor agonist with a Ki of 4 nM and an EC50 of 12 nM. (Rac)-WAY-161503 displays higher affinity for 5-HT2C than 5-HT2A and 5-HT2B receptors. (Rac)-WAY-161503 has anti-obesity and antidepressant effects[1][2].
In Vivo: (Rac)-WAY-161503 (3-30 mg/kg; intraperitoneal injection; male C57BL/6J mice) treatment dose-dependently decreases locomotor activity, an effect that is blocked by the 5-HT2C/2B antagonist SER-082. Additionally, the decreased locomotor activity produced by 10 mg/kg DOI is potentiated in the 5-HT2A KO mice[1].

Name: FK962, CAS: 283167-06-6, stock 5.7g, assay 98.7%, MWt: 264.30, Formula: C14H17FN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FK962 is an enhancer of somatostatin release, exerts cognitive-enhancing actions[1].
IC50 & Target: Somatostatin release[1]
In Vitro: FK962 (1 nM-1 μM) significantly enhances high K+-evoked somatostatin release from rat hippocampal slices. FK962 also significantly reduces somatostatin-induced inhibition of Ca2+ channels at 1-100 nM in single rat hippocampal neurons using whole-cell patch-clamp[1].
In Vivo: FK962 (0.1, 0.3 or 1.0 mg/kg; i.p.) and Donepezil (a single dose of 1 mg/kg) act synergistically to improve cognition in rats: as an add-on therapy for Alzheimer's disease[2].

Name: N-Acetylcarnosine N-Acetyl-L-carnosine, CAS: 56353-15-2, stock 0.8g, assay 98.1%, MWt: 268.27, Formula: C11H16N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Acetylcarnosine, a natural histidine-containing dipeptide, is a source of pharmacological principal L-carnosine. N-Acetylcarnosine is a potent ophthalmic drug in treatment of human cataracts[1].
In Vivo: Right eyes of the rabbits (male grey chinchilla rabbits aged 3-4 months weighing 2-3 k) are instilled with 80 μL of formulation A containing 1 % N-Acetylcarnosine. The N-Acetylcarnosine prodrug eye drops optimize the clinical effects for the treatment of ophthalmic disorders (such as prevention and reversal of cataracts in human and animal eyes)[1].

Name: Myristyl nicotinate Tetradecyl nicotinate, CAS: 273203-62-6, stock 1.8g, assay 98.1%, MWt: 319.48, Formula: C20H33NO2, Solubility: DMSO : 9.62 mg/mL (30.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Myristyl nicotinate (Tetradecyl nicotinate) is an ester prodrug and a lipophilic derivative of Nicotinic acid. Myristyl nicotinate is being developed for delivery of Nicotinic acid into the skin for prevention of actinic keratosis and its progression to skin cancer. Myristyl nicotinate shows to stimulate epidermal differentiation in photodamaged skin, increasing skin NAD content and strengthening the skin barrier[1][2].
In Vitro: Myristyl nicotinate (Tetradecyl nicotinate) is used for treatment and prevention of conditions that involve skin barrier impairment such as chronic photodamage and atopic dermatitis or for mitigating skin barrier impairment that results from therapy such as retinoids or steroids[2].

Name: Isomaltotriose, CAS: 3371-50-4, stock 27.4g, assay 98.6%, MWt: 504.44, Formula: C18H32O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isomaltotriose is a sugar from enzymic hydrolyzates of the dextran from Leuconostoc mesenteroides NRRL B-512[1].

Name: CKI-7, CAS: 120615-25-0, stock 32.6g, assay 98.3%, MWt: 285.75, Formula: C11H12ClN3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;MAPK/ERK Pathway;Stem Cell/Wnt;Cell Cycle/DNA Damage;Metabolic Enzyme/Protease, Target: CDK;Ribosomal S6 Kinase (RSK);Casein Kinase;Casein Kinase;SGK, Biological_Activity: CKI-7 is a potent and ATP-competitive casein kinase 1 (CK1) inhibitor with an IC50 of 6 μM and a Ki of 8.5 μM. CKI-7 is a selective Cdc7 kinase inhibitor. CKI-7 also inhibits SGK, ribosomal S6 kinase-1 (S6K1) and mitogen- and stress-activated protein kinase-1 (MSK1). CKI-7 has a much weaker effect on casein kinase II and other protein kinases[1][2][3][4].
In Vitro: CKI-7 (0.1-10 μM; 5 days; ES cells) treatment significantly increases the expression of the early neuroectodermal marker Sox1 and the number of cells positive for the neural markers nestin and βIII-tubulin, in a concentration-dependent manner[1]. 
CKI-7 (5 μM; 5 days; ES cells) treatment suppresses SFEB-induced β-catenin stabilization on day 5, indicating that CKI-7 inhibits Wnt signaling[1].
In Vivo: In vivo dose-dependent anti-tumor activity of CKI-7 is demonstrated in a SCID-Beige mouse systemic tumor model utilzing a recently isolated Philadelphia chromosome positive acute lymphoblastic leukemia cell line. Standard cell cycle synchronization studies established that exposure to CKI-7 results in cell cycle dependent caspase 3 activation and apoptotic cell death[2].

Name: CB-103, CAS: 218457-67-1, stock 5g, assay 98.8%, MWt: 242.32, Formula: C15H18N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Neuronal Signaling, Target: Notch;Notch, Biological_Activity: CB-103 is a notch signaling pathway inhibitor extracted from patent US9296682B2. CB-103 is developed for the treatment of cancers[1].

Name: ONC206, CAS: 1638178-87-6, stock 8.2g, assay 98.4%, MWt: 408.44, Formula: C23H22F2N4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: ONC206 is an analogue of TRAIL inducer ONC201[1]. ONC206 is a selective antagonist of the D2-like dopamine receptors (DRD2/3/4) at nanomolar concentrations. ONC206 has broad-spectrum anti-tumor activity[2].
IC50 & Target: DRD2/3/4[2]
In Vitro: ONC206 selectively antagonizes the D2-like (DRD2/3/4), but not the D1-like (DRD 1/5), subfamily of dopamine receptors[2]. 
ONC206 significantly inhibits tumor cell migration and invasion in vitro[1]. 
ONC206 (0.05 μM; Over 48 hours) inhibits migration of ONC201- and TRAIL-resistant HCT116 Bax−/− cells without inducing cell death or inhibiting cell proliferation[1]. 
ONC206 engages the ISR and TRAIL pathway leading to tumor growth arrest and cell death[1]. 
ONC206 does not induce cell cycle arrest in a colorectal cell line with acquired ONC201-resistance[1]. 
In Vivo: ONC206 (100 mg/kg;p.o.; every 10 days) causes significant tumor growth inhibition[2].

Name: Gallopamil (hydrochloride) Methoxyverapamil (hydrochloride), CAS: 16662-46-7, stock 17.7g, assay 98.3%, MWt: 521.09, Formula: C28H41ClN2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Gallopamil hydrochloride (Methoxyverapamil hydrochloride), a methoxy derivative of Verapamil, is a phenylalkylamine calcium antagonist[1]. Gallopamil hydrochloride inhibits acid secretion in a concentration-dependent manner with an IC50 of 10.9 μM[2]. Gallopamil hydrochloride is a potent antiarrhythmic and vasodilator agent[3].
In Vivo: Gallopamil hydrochloride (Methoxyverapamil hydrochloride; i.v.; 0.2 mg/kg; for 5 min) markedly reduces ventricular tachycardia (VT) and totally prevents fibrillation (VF). Gallopamil significantly reduces systolic and diastolic blood pressure measured 5 min after injection without markedly influencing heart rate[3].

Name: Cefcapene pivoxil (hydrochloride), CAS: 147816-23-7, stock 34.2g, assay 98.8%, MWt: 604.10, Formula: C23H30ClN5O8S2, Solubility: DMSO : 125 mg/mL (206.92 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Cefcapene pivoxil hydrochloride, an antibiotic, is an orally active and potent 3rd-generation cephalosporin with a wide spectrum of anti-bacterial activity[1].Cefcapene pivoxil hydrochloride has the potential for the palmoplantar pustulosis (PPP) treatment[2].
IC50 & Target: IC50: bacterial[1]
In Vivo: Cefcapene pivoxil hydrochloride (oral administration; 100mg/kg; 4 days) is effective against invasive BLNAR strains in mice lung, stimates peak antibiotic concentrations of 1 to 2 μg/ml in the blood of mice from 30 to 120 min after intragastric administration[3].

Name: TGX-221, CAS: 663619-89-4, stock 11.8g, assay 98.1%, MWt: 364.44, Formula: C21H24N4O2, Solubility: DMSO : 33.33 mg/mL (91.46 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: TGX-221 is a potent, selective, and cell membrane permeable inhibitor of the PI3K p110β catalytic subunit, used for cancer treatment.
IC50 & Target: IC50: 8.5 nM (p110β), 211 nM (p110δ)[5]
In Vitro: TGX-221, BL05 and BL05-HA show selective cytotoxicity to LNCaP cells, which may be due to the deficiency of PTEN in this cell line and the accumulation of PIP3 in the cells[1]. TGX-221 (1 μM) does not affect the expression and phosphorylation of AMPK in C2C12 myoblasts[2]. TGX221 (0.1, 1, 10 µM) induces IL-6 release from ASM cells[2]. TGX-221 does not affect neurotensin-stimulated Akt phosphorylation when used alone, but it further suppresses neurotensin-stimulated phosphorylation of Akt when combined with gefitinib. TGX-221 abolishes the neurotensin-stimulated phosphorylation of Akt in Panc-1 cells[3].
In Vivo: TGX-221 (TGX221, 2.5 mg/kg i.v.) abolishes cyclic flow reductions in a Folts-like carotid artery stenosis preparation of thrombosis, without changing bleeding time, heart rate, blood pressure or carotid vascular conductance[4].

Name: Tyroserleutide (hydrochloride), CAS: 852982-42-4, stock 17.7g, assay 98.6%, MWt: 417.88, Formula: C18H28ClN3O6, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tyroserleutide hydrochloride, isolated from the degradation products of porcine spleen[1], is a small molecular tripeptide which inhibits tumor growth both in vitro and in vivo[2].
IC50 & Target: Antitumor tripeptide[1][2]
In Vitro: Tyroserleutide (YSL) exhibits immuno-modulating effects, such as enhancing concanavalin (ConA) induced proliferation of mouse spleen lymphocytes, phagocytosis of mouse peritoneal macrophages, and the activity of natural killer (NK) cells[1]. 
Tyroserleutide (YSL), an immunologically therapeutic tripeptide, can promote hepatocarcinoma cell (H22) apoptosis through downregulating Bcl-2 and cyclin D1 expression[2]. 
Tyroserleutide is an ideal choice for inducing apoptosis of liver tumor cells[2]. 
Tyroserleutide inhibits tumor growth and does not cause severe toxicities in the major organs. Tyroserleutide can inhibit tumor cell migration[2]. 
In Vivo: Tyroserleutide (10-80 μg/kg; injection (i.p.) one time every day until mice are dead) displays obvious anti-tumor activity. Tyroserleutide significantly prolongs the survival time of the murine H22 implanted mice[1].

Name: MMP-9-IN-1, CAS: 502887-71-0, stock 1.9g, assay 98.3%, MWt: 369.39, Formula: C16H17F2N3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: MMP-9-IN-1 is a specific matrix metalloproteinase-9 (MMP-9) inhibitor, which
selectively target the hemopexin (PEX) domain of MMP-9, but not other MMPs[1].
In Vitro: MMP-9-IN-1 (compound 2; 100 μM; 14 hours) does not cause notable cytotoxicity[1]. 
MMP-9-IN-1 (compound 2; 10 μM) significantly inhibits cell proliferation of HT-1080 and MDA-MB-435 cells[1].
In Vivo: MMP-9-IN-1 (compound 2; 20 mg/kg; intraperitoneal and intratumoral injection alternately; 6 days/week; for 14 weeks) results in a profound delay in tumor growth in NCR-Nu mice bearing MDA-MB-435/GFP tumor[1]. 
MMP-9-IN-1 inhibits cancer cell metastasis in vivo[1].

Name: Hyperforin (dicyclohexylammonium salt) Hyperforin DCHA, CAS: 238074-03-8, stock 9.5g, assay 98.6%, MWt: 718.10, Formula: C47H75NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel;Neuronal Signaling;Neuronal Signaling, Target: Calcium Channel;TRP Channel;Calcium Channel;TRP Channel, Biological_Activity: Hyperforin dicyclohexylammonium salt (Hyperforin DCHA) is a transient receptor canonical 6 (TRPC6) channels activator. Hyperforin dicyclohexylammonium salt modulates Ca2+ levels by activating Ca2+-conducting non-selective canonical TRPC6 channels. Hyperforin dicyclohexylammonium salt shows antidepressant effect[1][2].
In Vitro: Hyperforin dicyclohexylammonium salt (Hyperforin DCHA) has a multi-directional mechanism of action. It blocks conductance of ligand-gated (GABA, NMDA, and AMPA receptors) and voltage-gated channels (Ca2+, K+, and Na+)[2].

Name: (Rac)-ABT-202 (dihydrochloride), CAS: 1258641-38-1, stock 23.1g, assay 98.1%, MWt: 236.14, Formula: C9H15Cl2N3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (Rac)-ABT-202 dihydrochloride is a racemate of ABT-202. ABT-202 is an agonistor of nicotinic acetylcholine receptors (nAChRs) and can be used as an analgesic[1].

Name: (Rac)-IDO1-IN-5, CAS: 2166616-74-4, stock 13.9g, assay 98.6%, MWt: 396.45, Formula: C23H25FN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (Rac)-IDO1-IN-5 is a racemate of IDO1-IN-5. IDO1-IN-5 is a potent, selective and brain penetrated inhibitor of Indoleamine 2,3-Dioxygenase 1 (IDO1) activity, binds to apo-IDO1 lacking heme rather than mature heme-bound IDO1[1].

Name: (S)-IDO1-IN-5, CAS: 2166616-76-6, stock 8.6g, assay 98.9%, MWt: 396.45, Formula: C23H25FN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (S)-IDO1-IN-5 is the S-isomer of IDO1-IN-5. IDO1-IN-5 is a potent, selective and brain penetrated inhibitor of Indoleamine 2,3-Dioxygenase 1 (IDO1) activity, binds to apo-IDO1 lacking heme rather than mature heme-bound IDO1[1].

Name: Soya fatty acids, CAS: 68308-53-2, stock 29.8g, assay 98.5%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Soya fatty acids is a class of polyunsaturated fatty acids extracted from soybean[1][2].

Name: 5-ALA benzyl ester (hydrochloride) Benzyl-ALA (hydrochloride), CAS: 163271-32-7, stock 13.3g, assay 99%, MWt: 257.71, Formula: C12H16ClNO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5-ALA benzyl ester hydrochloride (Benzyl-ALA hydrochloride) is a protoporphyrin precursor used as a photodetection agent. 5-ALA benzyl ester hydrochloride induces protoporphyrin IX (PPIX) accumulation in colon carcinoma cell lines[1][2].
In Vitro: 5-ALA benzyl ester hydrochloride (Benzyl-ALA hydrochloride) (0.6-0.12 mM; 3 h) induces protoporphyrin IX (PPIX) accumulation in colon carcinoma cell lines SW480[2].
In Vivo: Reducing the dose of 5-ALA benzyl ester hydrochloride (31 mg/kg; i.v. ; 1 hours) results in a dose-dependent reduction in tumour porphyrin levels[3].

Name: WZ-3146, CAS: 1214265-56-1, stock 37.6g, assay 98.6%, MWt: 464.95, Formula: C24H25ClN6O2, Solubility: DMSO : 150 mg/mL (322.62 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: WZ3146 is a mutant selective EGFR inhibitor with IC50s of
2, 2, 5, 14 and 66 nM for EGFRL858R, EGFRL858R/T790M, EGFRE746_A750, EGFRE746_A750/T790M and EGFR, respectively.

IC50 & Target: IC50: 2 nM (EGFRL858R), 2 nM (EGFRL858R/T790M), 5 nM (EGFRE746_A750), 14 nM (EGFRE746_A750/T790M), 66 nM (EGFR) [1]
In Vitro: WZ3146 is a novel EGFR inhibitor, suppresses the growth of EGFR T790M containing cell lines and inhibits EGFR phosphorylation[1].

Name: CYC-116, CAS: 693228-63-6, stock 39.8g, assay 98.6%, MWt: 368.46, Formula: C18H20N6OS, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: CYC-116 is a potent aurora A and aurora B inhibitor with Kis of 8 and 9 nM, respectively.
IC50 & Target: Ki: 8 nM (aurora 1), 9 nM (aurora 2)[1]
In Vitro: CYC-116 also inhibits VEGFR2, Src, Lck AND FLT3 with with Kis of 44, 82, 280, 44 nM, respectively. CYC-116 may have broad-spectrum antitumor activity. CYC-116 shows potent antiproliferative activity against cancer cell lines with with IC50s of 0.599, 0.59, 0.241, 0.34, 0.725, 1.375, 0.471, 0.034, 0.372, 0.681, 0.151, 1.626, 0.775, 0.308, 0.110, 0.09 for MCF7, HeLa, Colo205, HCT-116, HT29, K562, CCRF-CEM, MV4-11, HL60, NCI-H460, A2780, BxPC3, HuPT4, Mia-Paca-2, Saos-2, Messa cells. Treatment with 1.25 μM CYC-116 for 7 h results in complete inhibition of histone H3 phosphorylation in HeLa cell lysates[1].
In Vivo: Oral administration of CYC-116 at dose levels of 75 and 100 mg/kg q.d. causes tumor growth delays of 2.3 and 5.8 days, which translates into specific growth delays of 0.32 and 0.81, respectively. The mean relative tumor volumes of mice receiving CYC-116 at both dose levels are less than those of vehicle-treated mice for the duration of the study period. At 100 mg/kg po q.d., the reduction in growth is statistically significant on days 6 and 9[1].

Name: Thalidomide-NH-PEG2-C2-NH2 (TFA), CAS: 2097509-36-7, stock 39.8g, assay 98.5%, MWt: 518.44, Formula: C21H25F3N4O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: Thalidomide-O-amido-PEG3-C2-NH2 TFA is a synthesized E3 ligase ligand-linker conjugate that incorporates the Thalidomide based cereblon ligand and 2-unit PEG linker used in PROTAC technology[1].

Name: N-Desmethyltamoxifen (hydrochloride), CAS: 15917-65-4, stock 28.4g, assay 99%, MWt: 393.95, Formula: C25H28ClNO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others;TGF-beta/Smad;Epigenetics;Metabolic Enzyme/Protease, Target: Estrogen Receptor/ERR;PKC;PKC;Drug Metabolite, Biological_Activity: N-Desmethyltamoxifen hydrochloride is the major metabolite of tamoxifen in humans. N-Desmethyltamoxifen, a poor antiestrogen, is a ten-fold more potent protein kinase C (PKC) inhibitor than Tamoxifen. N-Desmethyltamoxifen hydrochloride is also a potent regulator of ceramide metabolism in human AML cells, limiting ceramide glycosylation, hydrolysis, and sphingosine phosphorylation[1][2][3].
In Vitro: N-desmethyltamoxifen hydrochloride (20-500 ng/ml; 48 hours) has a profound inhibitory effect upon all seven glioma lines (T98G, U87, U138, U373, ALW, AUK, CAS cells)[1]. 
N-desmethyltamoxifen hydrochloride (1.5-10 μM; 114 hours) inhibits growth of MCF 7 human mammary carcinoma cells[2]. 
N-desmethyltamoxifen hydrochloride, resulting from the CYP3A4/5-mediated catalysis of tamoxifen, is the major primary quantitative metabolite of tamoxifen[3].

Name: Beta-Sitosterol (purity>98%) β-Sitosterol (purity>98%);22,23-Dihydrostigmasterol (purity>98%), CAS: 83-46-5, stock 36.6g, assay 98.1%, MWt: 414.71, Formula: C29H50O, Solubility: Ethanol : 3.85 mg/mL (9.28 mM; Need ultrasonic); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Beta-Sitosterol (purity>98%) is a plant sterol. Beta-Sitosterol (purity>98%) interfere with multiple cell signaling pathways, including cell cycle, apoptosis, proliferation, survival, invasion, angiogenesis, metastasis and inflammation[1].
In Vitro: Beta-Sitosterol is one of the most abundant dietary phytosterols. Beta-Sitosterol shows anticancer properties against breast cancer, prostate cancer, colon cancer, lung cancer, stomach cancer, ovarian cancer, and leukemia[1].

Name: Vasicine (hydrochloride) Peganine (hydrochloride), CAS: 7174-27-8, stock 30.4g, assay 98.8%, MWt: 224.69, Formula: C11H13ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vasicine hydrochloride (peganine hydrochloride) is a quinazoline alkaloid isolated from Justicia adhatoda. Vasicine (peganine) possesses anti- tuberculosis activity[1].

Name: 10,12-Tricosadiynoic acid, CAS: 66990-30-5, stock 39g, assay 98.7%, MWt: 346.55, Formula: C23H38O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: 10,12-Tricosadiynoic acid is a highly specific, selective, high affinity and orally active acyl-CoA oxidase-1 (ACOX1) inhibitor. 10,12-Tricosadiynoic acid can treat high fat diet- or obesity-induced metabolic diseases by improving mitochondrial lipid and ROS metabolism[1].
IC50 & Target: Acyl-CoA oxidase-1 (ACOX1)[1].
In Vitro: 10,12-Tricosadiynoic acid-CoA rapidly inhibits ACOX1 activity in a time- and concentration-dependent manner. The activity of ACOX1 decreases by nearly 95% after 5 min of incubation with 10 eq of 10,12-Tricosadiynoic acid-CoA. ACOX1 activity is inhibited only if free 10,12-Tricosadiynoic Acid is activated as the CoA thioester, the substrate form. Inhibition of ACOX1 by 10,12-Tricosadiynoic acid-CoA is irreversible. And the kinetics parameters KI and kinact are calculated to be 680 nm and 3.18 min−1, respectively[1]. 
10,12-Tricosadiynoic acid is the precursor of 10,12-Tricosadiynoic acid-CoA and is transformed into 10,12-Tricosadiynoic acid-CoA by peroxisomal very long chain acyl-CoA synthetase (VLACS) after entering into cells, and it inhibits ACOX1 in vivo[1].
In Vivo: 10,12-Tricosadiynoic acid (100 μg/kg; oral gavage; daily; for 8 weeks; male Wistar rats) treatment increases hepatic mitochondrial fatty acid oxidation (FAO) via activation of the SIRT1-AMPK (adenosine 5′-monophosphate-activated protein kinase) pathway and proliferator activator receptor α and reduces hydrogen peroxide accumulation in high fat diet-fed rats, which significantly decreases hepatic lipid and ROS contents, reduces body weight gain, and decreases serum triglyceride and insulin levels[1].

Name: SNS-314 SNS-314 Mesylate, CAS: 1146618-41-8, stock 25.7g, assay 98.7%, MWt: 527.04, Formula: C19H19ClN6O4S3, Solubility: DMSO : 50 mg/mL (94.87 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: SNS-314 is a potent and selective aurora kinase inhibitor with IC50s of 9, 31, and 6 nM for aurora A, B and C, respectively.
IC50 & Target: IC50: 9 nM (Aurora A), 31 nM (Aurora B), 6 nM (Aurora C)[1]
In Vitro: SNS-314 blocks proliferation in a broad panel of tumor cell lines (HCT116, A2780, PC-3, HeLa, MDA-MB-231, H-1299, and HT29) with IC50 values ranging from 1.8 nM in A2780 ovarian cancer cells to 24 nM in HT29 colon cancer cells[2].
In Vivo: In the HCT116 human colon cancer xenograft model, administration of 50 and 100 mg/kg SNS-314 leads to dose-dependent inhibition of histone H3 phosphorylation for at least 10 h. SNS-314 shows significant tumor growth inhibition in a dose dependent manner under a variety of dosing schedules including weekly, bi-weekly, and 5 days on/9 days off[2].

Name: (S)-Trolox, CAS: 53174-06-4, stock 18g, assay 98.9%, MWt: 250.29, Formula: C14H18O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (S)-Trolox is a water-soluble analogue of vitamin E, in which the phytyl chain is replaced with a carboxyl group. (S)-Trolox is frequently used as a model compound for studies of structural features, as well as a standard for evaluation of antioxidant activity. (S)-Trolox has potent and specific neuroprotective and antioxidant effects[1][2].
In Vitro: The neuroprotective efficacy of antioxidant molecules against iodoacetate (IAA) neurotoxicity in rat cerebellar granule cell (CGC) cultures is investigated. In the absence of MK-801, (S)-Trolox displays marginal neuroprotective effects. In the presence of MK-801 (10 μM), the neuroprotective efficacy of (S)-Trolox is greatly enhanced, giving rise to a recovery in MTT-reductase activity equivalent to 80–100% of control cultures. (S)-Trolox displays EC50 value of 78 μM. The fluorescence increase in IAA-stimulated DCFH-DA-loaded cultures is inhibited in a dose-dependent manner by the antioxidants (S)-Trolox with an IC50 value of 97 μM. The antioxidant (S)-Trolox demonstrate apotent and specific neuroprotective action in an in vitro model of neurodegeneration induced by inhibition of the glycolytic enzyme GAPDH[1].

Name: (Z)-Leukadherin-1 ADH-503 (free base), CAS: 2055362-72-4, stock 28.5g, assay 98.2%, MWt: 421.49, Formula: C22H15NO4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Complement System, Biological_Activity: (Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumorassociated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and enhances dendritic cell responses[1].
IC50 & Target: CD11b[1]
In Vitro: (Z)-Leukadherin-1 (ADH-503 free base; 4 μM; 8 days) reduces the numbers of total tumor-infiltrating CD11b+ cells and subsets of CD11b+ monocytes, granulocytes, eosinophils, and macrophages[1].
In Vivo: (Z)-Leukadherin-1 (ADH-503 free base; oral gavage; 30, 60, or 120 mg/kg; twice a day for 60 days) delayes tumor progression, leading to a significantly decreased tumor burden in time-point analysis and improved overall survival[1]. 
(Z)-Leukadherin-1 (oral gavage; 30, 100 mg/kg; twice a day; on days 1 and 5) has the mean half-life of 4.68 and 3.95 hours, a maximum concentration of 1716 and 2594 ng/ml and AUC0-t in the plasma of 6950 and 13962 ng.h/ml at 30 and 100 mg/kg dosing, respectively[1].

Name: Fingolimod (hydrochloride) FTY720, CAS: 162359-56-0, stock 23.4g, assay 98.4%, MWt: 343.93, Formula: C19H34ClNO2, Solubility: DMSO : ≥ 100 mg/mL (290.76 mM); H2O : 50 mg/mL (145.38 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Cytoskeleton;Cell Cycle/DNA Damage, Target: LPL Receptor;PAK;PAK, Biological_Activity: Fingolimod hydrochloride is a sphingosine 1-phosphate (S1P) antagonist with an IC50 of 0.033 nM in K562 and NK cells. Fingolimod hydrochloride also is a pak1 activator.
IC50 & Target: IC50: 0.033 nM (S1P, in K562 and NK cells)[1]
In Vitro: The monocyte-derived immature dendritic cells (iDCs) are pretreated with various concentrations of S1P for various periods of time prior to their incubation with NK cells. Four hours incubation of autologous or allogeneic iDCs with 0.2-20 μM of S1P significantly protectes these cells from NK cell lysis. The IC50 values of S1P are calculated at 160 nM for autologous iDCs, and 34 nM for allogeneic iDCs. Next, the inhibitory effect of S1P is revered by various concentrations of Fingolimod hydrochloride (FTY720) or SEW2871, with an IC50 effect of 173 or 15 nM, respectively[1]. The immunomodulator Fingolimod hydrochloride (FTY720) is a structural analogue of S1P and acts in its phosphorylated isoform as an unselective agonist on S1P1 and S1P3-5 and a selective functional antagonist on S1P1. FTY720 enhances serum S1P levels by inhibiting S1P lyase activity[2]. The number of Iba1+ cells in ipsilateral CA3 is counted, and the corresponding graph shows a significantly lower number of Iba1+ cells in CA3 of the Kainic acid (KA)+FTY720 group than in CA3 of KA group[3].
In Vivo: Administration of the immunomodulator Fingolimod hydrochloride (0.1 mg/kg i.v.) increases serum S1P, improves impaired systolic contractility and activates the PI3K-pathway in the heart. Administration of Fingolimod hydrochloride (FTY720) causes a significant rise in serum S1P levels in both sham-operated animals and animals challenged with LPS/PepG (P<0.0001)[2]. FTY720 attenuates microgliosis, modulates the microglia inflammatory phenotype by reducing LPS-mediated activation of p38 MAPK signalling pathway. Thus, FTY720 shares both direct neuroprotective and anti-inflammatory properties that can contribute to overall neuroprotection. In particular, the potential of FTY720 to switch microglia phenotype from a detrimental to a protective one represents a therapeutic mechanism for attenuating acute and chronic CNS damage[3].

Name: Linifanib ABT-869;AL-39324, CAS: 796967-16-3, stock 33.6g, assay 98.3%, MWt: 375.40, Formula: C21H18FN5O, Solubility: DMSO : ≥ 72 mg/mL (191.80 mM), Clinical_Informat: Phase 3, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Apoptosis;VEGFR;FLT3;PDGFR;Autophagy;c-Fms;c-Kit, Biological_Activity: Linifanib (ABT-869) is a potent and orally active multi-target inhibitor of VEGFR and PDGFR family with IC50s of 4, 3, 66, and 4 nM for KDR, FLT1, PDGFRβ, and FLT3, respectively. Linifanib (ABT-869) shows prominent antitumor activity. Linifanib (ABT-869) has much less activity against unrelated RTKs, soluble tyrosine kinases, or serine/threonine kinases[1][2].
IC50 & Target: IC50: 4 nM (KDR), 4 nM (FLT1), 66 nM (PDGFRβ), 3 nM (CSF-1R), 4 nM (FLT3), 14 nM (Kit)[1]
In Vitro: Linifanib exhibits IC50 values that range from 4 nM (KDR) to 190 nM (FLT4) for members of the VEGF and PDGF receptor families. Linifanib is also active against TIE2 and, to a lesser extent, RET, but is much less active (IC50>10 μM) against other nonrelated tyrosine kinases, such as steroid receptor coactivator and epidermal growth factor receptor. Phosphorylation of KDR induced by VEGF is inhibited by Linifanib with an IC50 of 4 nM in 3T3 murine fibroblasts engineered to express human KDR. A similar potency for inhibition of receptor autophosphorylation is seen with Linifanib when HUAECs are used as the target cell. Linifanib inhibits VEGF-stimulated phosphorylation of KDR completely at 10 nM and by 70% at 3 nM (IC50=2 nM)[1].
In Vivo: Linifanib is effective orally in the mechanism-based murine models of VEGF-induced uterine edema (ED50=0.5 mg/kg) and corneal angiogenesis (>50% inhibition, 15 mg/kg). ABT-869 exhibits efficacy in human fibrosarcoma and breast, colon, and small cell lung carcinoma xenograft models (ED50=1.5-5 mg/kg, twice daily) and is also effective (>50% inhibition) in orthotopic breast and glioma models. Reduction in tumor size and tumor regression is observed in epidermoid carcinoma and leukemia xenograft models, respectively[1].

Name: Axitinib AG-013736, CAS: 319460-85-0, stock 25.9g, assay 98.4%, MWt: 386.47, Formula: C22H18N4OS, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 20.83 mg/mL (53.90 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR, Biological_Activity: Axitinib is a multi-targeted tyrosine kinase inhibitor with IC50s of 0.1, 0.2, 0.1-0.3, 1.6 nM for VEGFR1, VEGFR2, VEGFR3 and PDGFRβ, respectively.
IC50 & Target: IC50: 0.1 nM (VEGFR1), 0.2 nM (VEGFR2), 0.1-0.3 nM (VEGFR3), 1.6 nM (PDGFRβ)[1]
In Vitro: Axitinib (AG-013736) is a potent and selective inhibitor of VEGFR 1 to 3. In transfected or endogenous RTK-expressing cells, Axitinib potently blocks growth factor-stimulated phosphorylation of VEGFR-2 and VEGFR-3 with average IC50 values of 0.2 and 0.1 to 0.3 nM, respectively. Cellular activity against VEGFR-1 is 1.2 nM (measured in the presence of 2.3% bovine serum albumin), equivalent to an absolute IC50 of ~0.1 nM, based on protein binding of Axitinib. The potency against murine VEGFR-2 (Flk-1) in Flk-1-transfected NIH-3T3 cells is 0.18 nM, similar to that of its human homologue. Axitinib shows ~8- to 25-fold higher IC50 against the closely related type III and V family RTKs, including PDGFR-β (1.6 nM), KIT (1.7 nM), and PDGFR-α (5 nM); nanomolar concentrations of Axitinib blocks PDGF BB-mediated human glioma U87MG cell (PDGFR-β-positive) migration but not proliferation[2].
In Vivo: A single oral dose of Axitinib (100 mg/kg) markedly suppresses murine VEGFR-2 phosphorylation for up to 7 h compared with control tumors. Axitinib rapidly inhibits VEGF-induced vascular permeability in the skin of mice; the inhibition is dose-dependent and directly correlated with drug concentration in mice. Pharmacokinetic/pharmacodynamic analysis indicate an unbound EC50 of 0.46 nM. Similar inhibitory effects are also shown in the skin of MV522 tumor-bearing mice without exogenous VEGF-A stimulation. Axitinib inhibits the growth of human xenograft tumors in mice. Axitinib produces dose-dependent growth delay regardless of initial tumor size, model type, or implant site[2].

Name: BMS-536924, CAS: 468740-43-4, stock 12.1g, assay 98.8%, MWt: 479.96, Formula: C25H26ClN5O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (104.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: IGF-1R;Insulin Receptor, Biological_Activity: BMS-536924 is an ATP-competitive IGF-1R/IR inhibitor with IC50 of 100 nM/73 nM.
IC50 value: 100 nM (IGF-1R); 73 nM (IR) [1]
Target: IGF-1R; IR
in vitro: BMS-536924 also inhibits FAK and Lck with IC50 of 150 nM and 341 nM, respectively. BMS-536924 inhibits cellular proliferation and disrupts Akt and MAPK phosphorylation [1]. BMS-536924 inhibits IGF-I-stimulated IGF-1R signaling in MCF10A cells and blocks constitutive IGF-1R activity in CD8-IGF-1R-MCF10A. Preincubation of MCF10A cells with 1 μM BMS-536924 completely blocks the ability of IGF-I to stimulate IGF-1R phosphorylation. IGF-I stimulation results in increased phosphorylation of ERK1/2, GSK3β, and Akt. BMS-536924 inhibits this ligand-induced phosphorylation. Treatment of the CD8-IGF-1R-MCF10A cells with BMS-536924 results in a dose-dependent inhibition of phosphorylation with partial inhibition at 0.01 μM and 0.1 μM, but complete receptor inhibition at a concentration of 1 μM. Maximal inhibition of phosphorylated IGF-1R is observed as early as 10 minutes following incubation. BMS-536924 retains its ability to inhibit IGF-1R phosphorylation for up to 48 hours. Addition of BMS-536924 time-dependently inhibits Akt phosphorylation starting at 1 hour. By 48 hours, Akt activation is completely blocked [2].
in vivo: Oral administration of BMS-536924 at 100-300 mpk strongly inhibits IGR-1R Sal tumor model. Efficacy is also observed in the nonengineered Colo205 human colon carcinoma mode. Oral administration of 3 on a once a day schedule (100-300 mpk) or a twice a day schedule (50, 100 mpk) demonstrates antitumor activity in this tumor model. Oral glucose tolerance test (OGTT) shows 100 mpk (b.i.d.) causes a significant elevation in glucose levels after glucose challenge. The pharmacokinetic parameters of BMS-536924, administered orally in poly(ethylene glycol) 400 and water (80:20 v/v), are determined in mouse, rat, dog, and monkey. Good bioavailability is evident in all species. Significant nonlinear pharmacokinetics is observed in rodents at increasing p.o. dose [1]. Oral administration of 70 mg/kg BMS-536924 significantly inhibits tumor growth (TGBC-1TKB cells) inoculated in nude mice. BMS-536924 up regulates apoptosis in xenografts tumors. The treatment doesn't have adverse effects on the body weight of mice or the glucose levels at the time of death, suggesting tolerable toxicity [3].

Name: Bosutinib SKI-606, CAS: 380843-75-4, stock 13.7g, assay 98.6%, MWt: 530.45, Formula: C26H29Cl2N5O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 46 mg/mL (86.72 mM), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy, Target: Src;Bcr-Abl;Autophagy, Biological_Activity: Bosutinib is a dual Src/Abl inhibitor with IC50s of 1.2 nM and 1 nM, respectively.
IC50 & Target: IC50: 1.2 nM (Src), 1 nM (Abl)[1]
In Vitro: Bosutinib (100 nM; 24/48 hours) results in a reduction of S and G2-M phase cells and an increase of cells with a DNA content of less than 2N[3]. 
Bosutinib inhibits the proliferation of all three cell lines, with IC50s ranging from 5 nM in the KU812 line to 20 nM for the K562 and MEG-01 cell lines[3]. 
Bosutinib (10-500 nM; 4 hours) ablates tyrosine phosphorylation of STAT5 at 25 nM[3].
In Vivo: Bosutinib (50-150 mg; p.o.; once a day for 5 days) remaines tumor free at 150 mg/kg, whereas at the lower doses, some relapse occurs over a 40-day period in K562 Xenografts in Nude Mice[3].

Name: Cediranib AZD2171, CAS: 288383-20-0, stock 31.9g, assay 98.6%, MWt: 450.51, Formula: C25H27FN4O3, Solubility: DMSO : ≥ 49 mg/mL (108.77 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy, Target: VEGFR;PDGFR;Autophagy, Biological_Activity: Cediranib (AZD2171) is a highly potent, orally available VEGFR tyrosine kinase inhibitor with IC50s of <1, <3, 5, 5, 36, 2 nM for Flt1, KDR, Flt4, PDGFRα, PDGFRβ, c-Kit, respectively.
IC50 & Target: IC50: <1 nM (Flt1), <3 nM (KDR), 5 nM (Flt4), 5 nM (PDGFRα), 36 nM (PDGFRβ), 2 nM (c-Kit)[1]
In Vitro: In human umbilical vein endothelial cells, Cediranib inhibits VEGF-stimulated proliferation and KDR phosphorylation with IC50 values of 0.4 and 0.5 nM, respectively. In a fibroblast/endothelial cell coculture model of vessel sprouting, Cediranib also reduces vessel area, length, and branching at subnanomolar concentrations[1].
In Vivo: Once-daily oral administration of Cediranib ablates experimental (VEGF-induced) angiogenesis and inhibits endochondral ossification in bone or corpora luteal development in ovary; physiologic processes that are highly dependent upon neovascularization. The growth of established human tumor xenografts (colon, lung, prostate, breast, and ovary) in athymic mice is inhibited dose-dependently by Cediranib, with chronic administration of 1.5 mg per kg per day producing statistically significant inhibition in all models. A histologic analysis of Calu-6 lung tumors treated with Cediranib reveals a reduction in microvessel density within 52 hours that becomes progressively greater with the duration of treatment. These changes are indicative of vascular regression within tumors[1].

Name: Dovitinib TKI258;CHIR-258, CAS: 405169-16-6, stock 28.3g, assay 98.6%, MWt: 392.43, Formula: C21H21FN6O, Solubility: DMSO : 25 mg/mL (63.71 mM; Need ultrasonic and warming), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;FLT3;PDGFR;FGFR;c-Kit, Biological_Activity: Dovitinib (TKI258; CHIR-258) is a multi-targeted tyrosine kinase inhibitor with IC50s of 1, 2, 8/9, 10/13/8, 27/210 nM for FLT3, c-Kit, FGFR1/3, VEGFR1/2/3 and PDGFRα/β, respectively.
IC50 & Target: IC50: 1 nM (FLT3), 2 nM (c-Kit), 8 nM (FGFR1), 9 nM (FGFR3), 1 nM (VEGFR1), 13 nM (VEGFR2), 8 nM (VEGFR3), 27 nM (PDGFRα), 210 nM (PDGFRβ)[1]
In Vitro: Dovitinib potently inhibits the FGF-stimulated growth of WT and F384L-FGFR3-expressing B9 cells with IC50 values of 25 nM. B9-MINV cells are resistant to the inhibitory activity of Dovitinib at concentrations up to 1 μM. Dovitinib inhibits cell proliferation of KMS11 (FGFR3-Y373C), OPM2 (FGFR3-K650E), and KMS18 (FGFR3-G384D) cells with IC50 of values of 90 nM (KMS11 and OPM2) and 550 nM, respectively[1]. Dovitinib significantly reduces the basal phosphorylation levels of FGFR-1, FGFR substrate 2α (FRS2-α) and ERK1/2 but not Akt in both SK-HEP1 and 21-0208 cells[2]. Dovitinib enhances the BMP-2-induced alkaline phosphatase (ALP) induction, which is a representative marker of osteoblast differentiation. Dovitinib also stimulates the translocation of phosphorylated Smad1/5/8 into the nucleus and phosphorylation of mitogen-activated protein kinases, including ERK1/2 and p38[3]. Dovitinib strongly inhibits both the interaction of TNIK with ATP (Ki, 13 nM) and the activation of Wnt signaling effectors such as β-catenin and TCF4. Dovitinib also induces caspase-dependent apoptosis in IM-9 cells without significant cytotoxicity in PBMCs[4].
In Vivo: Dovitinib (10 mg/kg, 30 mg/kg, 60 mg/kg, p.o.) shows significant antitumor effect in the KMS11-bearing mice model, and the growth inhibition is 48%, 78.5%, and 94% in the 10 mg/kg, 30 mg/kg, and 60 mg/kg treatment arms, respectively, compared with the placebo-treated mice[1]. Dovitinib (50 and 75 mg/kg) results in 97% and 98% tumor growth inhibition, respectively, and the maximal efficacy is at 50 mg/kg[2].

Name: Canertinib CI-1033;PD-183805, CAS: 267243-28-7, stock 0g, assay 98%, MWt: 485.94, Formula: C24H25ClFN5O3, Solubility: Methanol : 2.22 mg/mL (4.57 mM; Need ultrasonic); DMSO : 4.9 mg/mL (10.08 mM; Need warming); Ethanol : 12.5 mg/mL (25.72 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Canertinib (CI-1033;PD-183805) is a potent and irreversible EGFR inhibitor; inhibits cellular EGFR and ErbB2 autophosphorylation with IC50s of 7.4 and 9 nM.
IC50 & Target: IC50: 7.4 nM (EGFR), 9 nM (ErbB2)[1]
In Vitro: Canertinib significantly inhibits growth of cultured melanoma cells, RaH3 and RaH5, in a dose-dependent manner. IC50 is approximately 0.8 μM and by 5μM both cell lines are completely growth-arrested within 72 h of treatment. Incubation of exponentially growing RaH3 and RaH5 with 1 μM canertinib accumulated the cells in the G1-phase of the cell cycle within 24 h of treatment without induction of apoptosis. 1 μM canertinib inhibits ErbB1-3 receptor phosphorylation with a concomitant decrease of Akt-, Erk1/2- and Stat3 activity in both cell lines[2].
In Vivo: Canertinib shows superior in vivo antitumor activity, giving growth delays in A431 xenografts exceeding 50 days following oral administration[1]. The growth of human malignant melanoma xenografts, RaH3 and RaH5, in nude mice is significantly inhibited by i.p. injections of 40 mg/kg/day canertinib (Fig. 4). The anti-proliferative effect on melanoma xenografts is visible already within 4 days of treatment and further increased throughout the treatment period as observed through the differences in tumor volumes, reaching statistical significance within 18 days of treatment[2].

Name: Deforolimus Ridaforolimus; MK-8669; AP23573, CAS: 572924-54-0, stock 12.2g, assay 98.7%, MWt: 990.21, Formula: C53H84NO14P, Solubility: DMSO : ≥ 44 mg/mL (44.44 mM), Clinical_Informat: Phase 3, Pathway: PI3K/Akt/mTOR;Autophagy, Target: mTOR;Autophagy, Biological_Activity: Deforolimus (AP23573; MK-8669) is a potent and selective mTOR inhibitor; inhibits ribosomal protein S6 phosphorylation with an IC50 of 0.2 nM in HT-1080 cells.
IC50 & Target: IC50: 0.5 nM (HT-1080 cells)[1]
In Vitro: Treatment of HT-1080 fibrosarcoma cells with deforolimus results in a dose-dependent inhibition of phosphorylation of both S6 and 4E-BP1, with IC50s of 0.2 and 5.6 nM, respectively, and EC50s of 0.2 and 1.0 nM, respectively. In HT-1080 cells, the EC50 for inhibition of cell proliferation (0.5 nM) is similar to the EC50s for inhibition of S6 and 4E-BP1 phosphorylation. Exposure to deforolimus reduces the proliferation of cell lines representing a variety of tumor types. Administration of deforolimus to tumor cells in vitro elicit dose-dependent inhibition of mTOR activity with concomitant effects on cell growth and division. Deforolimus exhibits a predominantly cytostatic mode of action, consistent with the findings for other mTOR inhibitors. Potent inhibitory effects on vascular endothelial growth factor secretion, endothelial cell growth, and glucose metabolism[1].
In Vivo: Deforolimus inhibits tumor growth in mice bearing PC-3 (prostate), HCT-116 (colon), MCF7 (breast), PANC-1 (pancreas), or A549 (lung) xenografts. Deforolimus inhibits tumor growth in a dose-dependent manner, with 0.3 mg/kg being the lowest dose that inhibits tumor growth significantly and 3 and 10 mg/kg doses achieving maximum inhibition[1].

Name: Erlotinib (Hydrochloride) CP-358774 (Hydrochloride);NSC 718781 (Hydrochloride);OSI-774 (Hydrochloride), CAS: 183319-69-9, stock 38g, assay 98%, MWt: 429.90, Formula: C22H24ClN3O4, Solubility: DMSO : 6.2 mg/mL (14.42 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Autophagy, Target: EGFR;EGFR;Autophagy, Biological_Activity: Erlotinib Hydrochloride (CP-358774 Hydrochloride) inhibits purified EGFR kinase with an IC50 of 2 nM.
IC50 & Target: IC50: 2 nM (EGFR)[1]
In Vitro: Erlotinib Hydrochloride (CP-358774 Hydrochloride) is also a potent inhibitor of the recombinant intracellular (kinase) domain of the EGFR, with an IC50 of 1 nM. The proliferation of DiFi cells is strongly inhibited by Erlotinib with an IC50 of 100 nM for an 8-day proliferation assay[1]. The combination of B-DIM and Erlotinib (2 μM) results in a significant inhibition of colony formation in BxPC-3 cells when compared with either agent alone. The combination of B-DIM and Erlotinib (2 μM) results in a significant induction of apoptosis only in BxPC-3 cells when compare with the apoptotic effect of either agent alone[2].
In Vivo: There is a 1.49-fold statistically significant difference between AUC0-inf after p.o. administration of Erlotinib (5 mg/kg) comparing Bcrp1/Mdr1a/1b-/- and WT mice (7,419±1,720 versus 4,957±1,735 ng*h/mL respectively, P=0.01)[3]. The administration of Erlotinib (10 mg/kg/day, or 20 mg/kg/day) to Bleomycin (BLM)-treated rats shows no exacerbation of lung injuries in indices such as macroscopic findings, lung weights, histopathological scores (lung lesion density and lung fibrosis score), and pulmonary hydroxyproline (HyP) level. The result suggests that Erlotinib does not have any exacerbating effects on lung injuries induced by BLM in rats[4].

Name: Gefitinib ZD1839, CAS: 184475-35-2, stock 20.5g, assay 98.1%, MWt: 446.90, Formula: C22H24ClFN4O3, Solubility: DMSO : ≥ 50 mg/mL (111.88 mM), Clinical_Informat: Launched, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Autophagy, Target: EGFR;EGFR;Autophagy, Biological_Activity: Gefitinib (ZD1839) is an EGFR tyrosine kinase inhibitor, with IC50 of 2-37 nM in NR6wtEGFR cells.
IC50 & Target: IC50: 37 nM (Tyr1173 site, in NR6wtEGFR cells), 37 nM (Tyr992 site, in NR6wtEGFR cells)[1]
In Vitro: Gefitinib (0.01-0.1 mM) results in increased phosphotyrosine load of the receptor, increased signalling to ERK and stimulation of proliferation and anchorage-independent growth, presumably by inducing EGFRvIII dimerisation in long-term exposure of EGFRvIII-expressing cells. On the other hand, gefitinib (1-2 mM) significantly decreases EGFRvIII phosphotyrosine load, EGFRvIII-mediated proliferation and anchorage-independent growth[1]. Gefitinib (ZD1839) inhibits the monolayer growth of these EGF-driven untransformed cells with IC50 of 20 nM[2]. Gefitinib leads to an inhibition of CALU-3 and GLC82 cell proliferation, with an IC50 of 2 μM[3].
In Vivo: Gefitinib (150 mg/kg, p.o.) in conbination with Metformin induces a significant reduction in tumor growth in nude mice bearing H1299 or CALU-3 GEF-R cells that are grown subcutaneously as tumor xenografts[3]. In irradiated rats, Gefitinib treatment augmentes lung inflammation, including inflammatory cell infiltration and pro-inflammatory cytokine expression, while Gefitinib treatment attenuates fibrotic lung remodeling due to the inhibition of lung fibroblast proliferation[4].

Name: Lenalidomide CC-5013, CAS: 191732-72-6, stock 4.3g, assay 98.8%, MWt: 259.26, Formula: C13H13N3O3, Solubility: DMSO : ≥ 35 mg/mL (135.00 mM), Clinical_Informat: Launched, Pathway: Apoptosis;PROTAC, Target: Apoptosis;Ligand for E3 Ligase, Biological_Activity: Lenalidomide (CC-5013) is a derivative of Thalidomide and an orally active immunomodulator. Lenalidomide (CC-5013) is a ligand of ubiquitin E3 ligase cereblon (CRBN), and it causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKZF3, by the CRBN-CRL4 ubiquitin ligase. Lenalidomide (CC-5013) specifically inhibits growth of mature B-cell lymphomas, including multiple myeloma, and induces IL-2 release from T cells[1][2].
In Vitro: Lenalidomide is potent in stimulating T cell proliferation and IFN-γ and IL-2 production. Lenalidomide has been shown to inhibit production of pro inflammatory cytokines TNF-α, IL-1, IL-6, IL-12 and elevate the production of anti-inflammatory cytokine IL-10 from human PBMCs. Lenalidomide downregulates the production of IL-6 directly and also by inhibiting multiple myeloma (MM) cells and bone marrow stromal cells (BMSC) interaction, which augments the apoptosis of myeloma cells[2]. Dose-dependent interaction with the CRBN-DDB1 complex is observed with Thalidomide, Lenalidomide and Pomalidomide, with IC50 values of ~30 μM, ~3 μM and ~3 μM, respectively, These reduced CRBN expression cells (U266-CRBN60 and U266-CRBN75) are less responsive than the parental cells to antiproliferative effects Lenalidomide across a dose-response range of 0.01 to 10 μM[3]. Lenalidomide, a thalidomide analog, functions as a molecular glue between the human E3 ubiquitin ligase cereblon and CKIα is shown to induce the ubiquitination and degradation of this kinase, thus presumably killing leukemic cells by p53 activation[5].
In Vivo: The toxicity of Lenalidomide doses up to 15, 22.5, and 45 mg/kg via IV, IP, and PO routes of administration. Limited by solubility in our PBS dosing vehicle, these maximum achievable Lenalidomide doses are well tolerated with the exception of one mouse death (of four total dosed) at the 15 mg/kg IV dose. Notably, no other toxicities are observed in the study at IV doses of 15 mg/kg (n=3) or 10 mg/kg (n=45) or at any other dose level through IV, IP, and PO routes[4].

Name: Pazopanib (Hydrochloride) GW786034 (Hydrochloride), CAS: 635702-64-6, stock 16.7g, assay 98.5%, MWt: 473.98, Formula: C21H24ClN7O2S, Solubility: DMSO : 10 mg/mL (21.10 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;Autophagy;c-Fms;FGFR;c-Kit, Biological_Activity: Pazopanib Hydrochloride (GW786034 Hydrochloride) is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFRβ, c-Kit, FGFR1, and c-Fms with an IC50 of 10, 30, 47, 84, 74, 140 and 146 nM, respectively.
IC50 & Target: IC50: 10 nM (VEGFR1), 30 nM (VEGFR2), 47 nM (VEGFR3), 74 nM (c-Kit), 84 nM (PDGFRβ), 140 nM (FGFR1), 146 nM (c-Fms)[1]
In Vitro: Pazopanib shows good potency against all the human VEGFR receptors with an IC50 of 10, 30, and 47 nM for VEGFR-1, -2, and -3, respectively. Significant activity is also seen against the closely related tyrosine receptor kinases PDGFRβ, c-Kit, FGF-R1, and c-fms with IC50s of 84, 74, 140, and 146 nM, respectively. In cellular assays, in addition to inhibiting the VEGF-induced proliferation of HUVECs, Pazopanib potently inhibits VEGF-induced phosphorylation of VEGFR-2 in HUVEC cells with an IC50 of ~8 nM. Pazopanib possesses good pharmacokinetics in rat, dog, and monkey with low clearances (1.4-1.7 mL/min/kg) and good oral bioavailabilities (72, 47, 65%) dosed at 10, 1, and 5 mg/kg, respectively. The cytochrome P450 profile is also improved with inhibition >10 μM against the isozymes tested, with the exception of 2C9 (7.9 μM)[1].
In Vivo: Treatment of mice with 100 mg/kg of Pazopanib twice daily for five days results in significant inhibition in the degree of vascularization. The antiangiogenic activity of Pazopanib is examined in mice bearing established human xenografts (200−250 mm3) using HT29 (colon carcinoma), A375P (melanoma), and HN5 (head and neck carcinoma) tumors following a standard three-week course of therapy. The HN5 and HT29 xenografts responded better at all doses compared to the A375P model, which is historically more resistant to VEGFR-2 inhibitors. As support that the observed inhibition of xenograft growth is working through an antiangiogenic rather than antitumor mechanism, no antiproliferative activity is observed below 10 μM for Pazopanib against these human tumor lines (HT29, HN5, A375P) growing in serum-containing media. No significant effect on the body weight of mice is observed, and the animals appeared healthy and active throughout the study duration[1]. The quantity of adherent leukocytes in the Pazopanib eye drops group is less than untreated diabetic animals and more than the healthy animals. Average leukocytes adhered to the retinal vasculature in healthy animals is 37.2±7.8, whereas diabetic animals have an average value of 102±15.6, approximately 3-fold higher than healthy animals. Animals treated with 0.5 % w/v Pazopanib suspension demonstrate 69.5±9.5 leukocytes adhered in their retinal vasculature, which is found to be significantly lower than diabetic animals[2].

Name: PI-103, CAS: 371935-74-9, stock 20.9g, assay 98.8%, MWt: 348.36, Formula: C19H16N4O3, Solubility: DMSO : 25 mg/mL (71.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage;PI3K/Akt/mTOR;Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: DNA-PK;DNA-PK;PI3K;Apoptosis;mTOR;Autophagy, Biological_Activity: PI-103 is a potent PI3K and mTOR inhibitor with IC50s of 8 nM, 88 nM, 48 nM, 150 nM, 20 nM, and 83 nM for p110α, p110β, p110δ, p110γ, mTORC1, and mTORC2. PI-103 also inhibits DNA-PK with an IC50 of 2 nM.
IC50 & Target: IC50: 8 nM (p110α), 88 nM (p110β), 48 nM (p110δ), 150 nM (p110γ), 2 nM (DNA-PK), 20 nM (mTORC1), 83 nM (mTORC2), 26 nM (PI3KC2β), 850 nM (ATR), 920 nM (ATM), ~1 μM (PI3KC2α), 2.3 μM (hsVPS34), ~50 μM (PI4KIIIβ)[4]
In Vitro: PI-103 exhibits antiproliferative properties in a panel of human cancer cell lines[1]. PI-103 is essentially cytostatic for cell lines and induced cell cycle arrest in the G1 phase. In blast cells, PI-103 inhibits leukemic proliferation, the clonogenicity of leukemic progenitors and induces mitochondrial apoptosis, especially in the compartment containing leukemic stem cells [2]. PI-103 potently inhibits both the rapamycin-sensitive (mTORC1, IC50=20 nM) and rapamycin-insensitive (mTORC2, IC50=83 nM) complexes of the protein kinase mTOR[4].
In Vivo: PI-103 shows therapeutic activity against a range of human tumor xenografts, exhibiting inhibition of angiogenesis, invasion, and metastasis, as well as direct antiproliferative effects[1]. PI-103 induces immunosuppression promoting in vivo tumor growth and inhibiting apoptosis. Tumors from PI-103-treated mice shows higher levels of cyclin D1 and more proliferating cells[3].

Name: Tandutinib MLN518;CT53518, CAS: 387867-13-2, stock 27.6g, assay 98.8%, MWt: 562.70, Formula: C31H42N6O4, Solubility: DMSO : 50 mg/mL (88.86 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Apoptosis;FLT3;PDGFR;c-Kit, Biological_Activity: Tandutinib (MLN518) is a potent and selective inhibitor of the FLT3 with an IC50 of 0.22 μM, and also inhibits c-Kit and PDGFR with IC50s of 0.17 μM and 0.20 μM, respectively. Tandutinib can be used to treat acute myelogenous leukemia (AML)[1][2]. Tandutinib has the ability to cross the blood-brain barrier[3].
IC50 & Target: IC50: 0.22 μM (FLT3), 0.17 μM (c-Kit) and 0.20 μM (PDGFR)[1]
In Vitro: Tandutinib (0-3 μM; 30 minutes; Ba/F3 cells) treatment inhibits IL-3-independent cell growth and FLT3-ITD autophosphorylation with an IC50 of 10-100 nM in Ba/F3 cells expressing different FLT3-ITD mutants[1]. 
Tandutinib (1 μM; 24-96 hours; Molm-14 and THP-1 AML cells) treatment induces apoptosis in FLT3-ITD-positive AML cells[1]. 
In human FLT3-ITD-positive AML cell lines, Tandutinib inhibits FLT3-ITD phosphorylation (IC50 of ~30 nM). As with Erk2, a constitutively high level of Akt phosphorylation is readily detected and is efficiently blocked by pretreatment of the Molm-14 cells with 100-300 nM Tandutinib[1]. 
Tandutinib inhibits cell proliferation of the FLT3-ITD-positive Molm-13 and Molm-14 with an IC50 of 10 nM. And signaling through the MAP kinase and PI3 kinase pathways[1]. 
In Vivo: Tandutinib (60 mg/kg; oral gavage; daily; for 35 days; athymic nude mice) treatment causes a statistically significant increase in survival that was extended on average by 20 days[1].

Name: Vandetanib ZD6474, CAS: 443913-73-3, stock 15.6g, assay 98.3%, MWt: 475.35, Formula: C22H24BrFN4O2, Solubility: DMSO : 27.5 mg/mL (57.85 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Autophagy, Target: Apoptosis;VEGFR;Autophagy, Biological_Activity: Vandetanib is a potent inhibitor of VEGFR2 with IC50 of 40 nM.
IC50 & Target: IC50: 40 nM (VEGFR2)
In Vitro: Vandetanib inhibits VEGFR3 and EGFR with IC50 of 110 nM and 500 nM, respectively. Vandetanib is not sensitive to PDGFRβ, Flt1, Tie-2 and FGFR1 with IC50 of 1.1-3.6 μM, while almost has no activity against MEK, CDK2, c-Kit, erbB2, FAK, PDK1, Akt and IGF-1R with IC50 above 10 μM. Vandetanib inhibits VEGF-, EGF- and bFGF-stimulated HUVEC proliferation with IC50 of 60 nM, 170 nM and 800 nM, with no effect on basal endothelial cell growth. Vandetanib inhibits tumor cell growth with IC50 of 2.7 μM (A549) to 13.5 μM (Calu-6)[1]. Odanacatib is a weak inhibitor of antigen presentation, measured in a mouse B cell line (IC50=1.5±0.4 μM), compared to the Cat S inhibitor LHVS (IC50=0.001 μM) in the same assay. Odanacatib also shows weak inhibition of the processing of the MHC II invariant chain protein Iip10 in mouse splenocytes compared to LHVS (minimum inhibitory concentration 1-10 μM versus 0.01 μM, respectively)[2]. Vandetanib suppresses phosphorylation of VEGFR-2 in HUVECs and EGFR in hepatoma cells and inhibits cell proliferation[4].
In Vivo: Vandetanib (15 mg/kg, p.o.) has a superior anti-tumor effect than gefitinib in the H1650 xenograft model, and suppresses tumor growth with IC50 of 3.5±1.2 μM[3]. In tumor-bearing mice, vandetanib (50 or 75 mg/kg) suppresses phosphorylation of VEGFR-2 and EGFR in tumor tissues, significantly reduces tumor vessel density, enhances tumor cell apoptosis, suppresses tumor growth, improves survival, reduces number of intrahepatic metastases, and upregulates VEGF, TGF-α, and EGF in tumor tissues[4].

Name: Y-27632, CAS: 146986-50-7, stock 23.2g, assay 98.2%, MWt: 247.34, Formula: C14H21N3O, Solubility: DMSO : 50 mg/mL (202.15 mM; Need ultrasonic); H2O : 5 mg/mL (20.22 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: ROCK;ROCK;ROCK, Biological_Activity: Y-27632 is an ATP-competitive inhibitor of ROCK-I and ROCK-II, with Ki of 220 nM and 300 nM for ROCK-I and ROCK-II, respectively, which primes human induced pluripotent stem cells (hIPSCs) to selectively differentiate towards mesendodermal lineage via epithelial-mesenchymal transition-like modulation.
IC50 & Target: Ki: 220/300 nM (ROCK-I/II)[1]
In Vitro: Y-27632 inhibits the ROCK family of kinases 100 times more potently than other kinases including protein kinase C, cAMP-dependent kinase and myosin light chain kinase. Y-27632 prolongs the lag time and delays the appearance of BrdU-labeled cells in a concentration-dependent manner, delays of about 1 and 4 h are noticed in the Swiss 3T3 cells treated with 10 and 100 μM Y-27632, respectively[1]. Y-27632 promotes neuronal differentiation of adipose tissue-derived stem cells (ADSCs). Compared to 1.0 and 2.5 µM Y-27632 induced groups, percentages of neuroal-like cells achieved a peak in the 5.0 µM Y-27632 induced group[2].
In Vivo: Y-27632 (5 and 10 mg/kg) significantly prolongs the onset time of myoclonic jerks when compare with saline group. Y-27632 (5 and 10 mg/kg) significantly prolongs the onset time of clonic convulsions when compare with saline group[3]. Treatment with Dimethylnitrosamine (DMN) causes a significant decrease in rat body and liver weight (DMN-S group) compared with control animals (S-S group). Oral Y27632 (30 mg/kg) essentially prevents this DMN-induced rat body and liver weight loss (DMN-Y group)[4].

Name: Enzastaurin LY317615, CAS: 170364-57-5, stock 11.4g, assay 98.7%, MWt: 515.61, Formula: C32H29N5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 8.33 mg/mL (16.16 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Apoptosis;TGF-beta/Smad;Epigenetics;Autophagy, Target: Apoptosis;PKC;PKC;Autophagy, Biological_Activity: Enzastaurin is a potent PKCβ selective inhibitor with IC50 of 6 nM, 6- to 20-fold selectivity against PKCα, PKCγ and PKCε.
IC50 & Target: IC50: 6 nM (PKCβ)
In Vitro: Enzastaurin increases apoptosis in malignant lymphocytes of CTCL. When combined with GSK3 inhibitors, enzastaurin demonstrates an enhancement of cytotoxicity levels. Treatment with a combination of enzastaurin and the GSK3 inhibitor AR-A014418 leads to increased levels of β-catenin total protein and β-catenin-mediated transcription. Blocking of β-catenin-mediated transcription or small hairpin RNA (shRNA) knockdown of β-catenin induces the same cytotoxic effects as that of enzastaurin plus AR-A014418. Additionally, treatment with enzastaurin and AR-A014418 decreases the mRNA levels and surface expression of CD44[1].
Enzastaurin application results in a marked dose-dependent inhibition of growth in all MM cell lines investigated, including MM.1S, MM.1R, RPMI 8226 (RPMI), RPMI-Dox40 (Dox40), NCI-H929, KMS-11, OPM-2, and U266, with IC50 from 0.6-1.6 μM. Enzastaurin direct impacts human tumor cells, inducing apoptosis and suppressing proliferation in cultured tumor cells. Enzastaurin also suppresses the phosphorylation of GSK3βser9, ribosomal protein S6S240/244, and AKTThr308 while having no direct effect on VEGFR phosphorylation[3].
In Vivo: Treatment of xenografts with Enzastaurin and radiation produces greater reductions in density of microvessels than either treatment alone. The decrease in microvessel density corresponds to delayed tumor growth[2].

Name: Obatoclax (Mesylate) GX15-070 (Mesylate), CAS: 803712-79-0, stock 5.6g, assay 98.6%, MWt: 413.49, Formula: C21H23N3O4S, Solubility: DMSO : 6.25 mg/mL (15.12 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Autophagy;Apoptosis, Target: Autophagy;Bcl-2 Family, Biological_Activity: Obatoclax Mesylate (GX15-070 Mesylate) is an inhibitor of the BCL-2 family proteins. Obatoclax Mesylate (GX15-070 Mesylate) binds to BCL-2 with a Ki of 220 nM.
IC50 & Target: Ki: ~220 nM (Bcl-2)[5]
In Vitro: Obatoclax (0, 0.5, 1, 2.5, 5, and 10 μM) effectively abrogates the growth of OCI-AmL3 cells, and similar results are seen in HL60, KG1, and U937 cells. Obatoclax also displays low-dose antiproliferative properties that are accompanied by a S/G2 cell cycle block. Obatoclax (10 μM) induces apoptosis proceeds through the intrinsic apoptotic pathway after neutralization of Mcl-1. Obatoclax synergizes with AraC and ABT-737 in inducing apoptosis in AmL cell lines. Obatoclax (250 nM) induces apoptosis and selectively inhibits colony formation of primary AmL cells[1]. Obatoclax induces cell death, with IC50 of 3.18 μM, 0.85 μM, and 0.76 μM for K1, BCPAP, and KTC-1 cells, respectively. Obatoclax also enhances cytotoxicity of RG7204 through inducing mixed cell death forms, loss of MOMP, suppression of mitochondrial respiration, and cellular glycolysis. Obatoclax regulates both the induction and degradation phases of authophagy, and promotes Mcl-1/Beclin-1 dependent autophagy in K1 cells[2]. Obatoclax inhibits cell proliferation and induces G1 cell-cycle arrest in a panel of human colorectal cancer cell lines, and the IC50 of cell proliferation at 72 h are 25.85, 40.69, and 40.01 nM for HCT116, HT-29, and LoVo cells, respectively. Obatoclax (0, 25, 50, 100, 200 nM) downregulates cyclin D1 to induce G1-phase arrest and consequent antiproliferation. Obatoclax (200 nM) targets cyclin D1 for proteasome-mediated degradation[3]. Obatoclax (500 nM, 1 μM) induces necrotic cell death and induces a block in autophagy, unrelated to cell death at 500 nM. Obatoclax localizes to lysosomes, affects lysosome structure and properties, but does not cause massive lysosomal permeabilization[4].
In Vivo: The LY3009120 monotherapy or Obatoclax+RG7204 (20 mg/kg/day for combination) retards tumor growth more thoroughly in subcutaneous xenograft model of thyroid cancer[2]. Obatoclax (5 mg/kg, i.p.) effectively reduces tumor growth in mice[4].

Name: Masitinib AB1010, CAS: 790299-79-5, stock 22.5g, assay 98.4%, MWt: 498.64, Formula: C28H30N6OS, Solubility: DMSO : ≥ 26 mg/mL (52.14 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Src;Apoptosis;PDGFR;FGFR;c-Kit;FAK, Biological_Activity: Masitinib (AB1010) is a potent, orally bioavailable, and selective inhibitor of c-Kit (IC50=200 nM for human recombinant c-Kit). It also inhibits PDGFRα/β (IC50s=540/800 nM), Lyn (IC50= 510 nM for LynB), Lck, and, to a lesser extent, FGFR3 and FAK. Masitinib (AB1010) has anti-proliferative, pro-apoptotic activity and low toxicity[1][2][4].
IC50 & Target: IC50: 200 nM (Kit), 540 nM (PDGFRα), 800 nM (PDGFRβ), 510 nM (LynB)[1]
In Vitro: Masitinib is a competitive inhibitor against ATP at concentrations ≤500 nM. Masitinib also potently inhibits recombinant PDGFR and the intracellular kinase Lyn, and to a lesser extent, fibroblast growth factor receptor 3. In contrast, masitinib demonstrates weak inhibition of Abl and c-Fms. Masitinib more strongly inhibits degranulation, cytokine production, and bone marrow mast cell migration than imatinib. In Ba/F3 cells expressing human wild-type Kit, masitinib inhibits SCF (stem cell factor)-induced cell proliferation with an IC50 of 150 nM, while the IC50 for inhibition of IL-3-stimulated proliferation is at approximately >10 µM. In Ba/F3 cells expressing PDGFRα, masitinib inhibits PDGF-BB-stimulated proliferation and PDGFRα tyrosine phosphorylation with IC50 of 300 nM. Masitinib also causes inhibition of SCF-stimulated tyrosine phosphorylation of human Kit in mastocytoma cell-lines and BMMC. Masitinib inhibits Kit gain-of-function mutants, including V559D mutant and Δ27 mouse mutant with IC50 of 3 and 5 nM in Ba/F3 cells. Masitinib inhibits the cell proliferation of mastocytoma cell lines including HMC-1α155 and FMA3 with IC50 of 10 and 30 nM, respectively[1]. Masitinib inhibits cell growth and PDGFR phosphorylation in two novel ISS cell lines, which suggest that Masitinib displays activity against both primary and metastatic ISS cell line and may aid in the clinical management of ISS[2].
In Vivo: Masitinib inhibits tumour growth and increases the median survival time in Δ27-expressing Ba/F3 tumor models at 30 mg/kg, without cardiotoxicity or genotoxicity[1]. 
Masitinib (12.5 mg/kg/d, p.o.) increases overall TTP (time-to-tumor progression) compared with placebo in dogs[3].

Name: SB-431542, CAS: 301836-41-9, stock 7.4g, assay 99%, MWt: 384.39, Formula: C22H16N4O3, Solubility: DMSO : ≥ 40 mg/mL (104.06 mM); Ethanol : 11.17 mg/mL (29.06 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: SB-431542 is a potent and selective inhibitor of ALK5/TGF-β type I Receptor with an IC50 value of 94 nM.
IC50 & Target: IC50: 94 nM (ALK5)[2]
In Vitro: SB-431542 (1 μM) significantly reduces the TGF-β-induced nuclear accumulation of Smad proteins in A498 cells. SB-431542 inhibits TGF-β1-induced collagen Iα1 and PAI-1 mRNA with IC50 values of 60 and 50 nM, respectively. In addition, SB-431542 inhibits TGF-β1-induced fibronectin mRNA and protein with IC50 values of 62 and 22 nM, respectively[1]. SB-431542 (10 μM) is a selective inhibitor of TGF-β signaling but has no effect on BMP signaling in NIH 3T3 cells[2]. TRKI, SB-431542, inhibits TGF-beta-induced transcription, gene expression, apoptosis, and growth suppression. SB-431542 attenuates the tumor-promoting effects of TGF-beta, including TGF-beta-induced EMT, cell motility, migration and invasion, and vascular endothelial growth factor secretion in human cancer cell lines. SB-431542 induces anchorage independent growth of cells that are growth-inhibited by TGF-beta, whereas it reduces colony formation by cells that are growth-promoted by TGF-beta[3]. SB-431542 (0.3 μM) inhibits cell proliferation induced by TGF-β in MG63 cells[4].
In Vivo: SB-431542 (10 mg/kg, i.p.) decreases lung metastasis but does not significantly alter growth of the primary tumor 4T1 xenograft[5].

Name: Luminespib NVP-AUY922;VER-52296, CAS: 747412-49-3, stock 33.7g, assay 98.7%, MWt: 465.54, Formula: C26H31N3O5, Solubility: DMSO : ≥ 62 mg/mL (133.18 mM), Clinical_Informat: Phase 2, Pathway: Apoptosis;Autophagy;Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: Apoptosis;Autophagy;HSP;HSP, Biological_Activity: Luminespib (NVP-AUY922) is a potent HSP90 inhibitor with IC50s of 7.8 and 21 nM for HSP90α and HSP90β, respectively.
IC50 & Target: IC50: 7.8 nM (HSP90α), 21 nM (HSP90β), 535 nM (GRP94), 85 nM (TRAP-1)[1]
In Vitro: Luminespib is a potent and selective HSP90 inhibitor, with IC50s and Kis of 21 ± 16, 8.2 ± 0.7 nM against HSP90β and of 7.8 ± 1.8, 9.0 ± 5.0 nM for HSP90α. Luminespib shows weak activity against GRP94 and TRAP-1 wich IC50s of 535 ± 51 nM (Ki, 108 nM) and 85 ± 8 nM (Ki, 53 nM), respectively. Luminespib exhibits inhibitory effect on proliferation of various human tumor cell lines (2.3-49.6 nM), induces cell cycle arrest and apoptosis and depletes client proteins in human cancer cells (80 nM)[1]. Luminespib (100 nM) significantly reduces CD40L fibroblast-induced changes in immunophenotype and STAT3 signaling but with no effect on the viability of chronic lymphocytic leukemia (CLL) cells. Luminespib (500 nM) in combination with NSC 118218 more effectively induces apoptosis in cells in co-culture than either drug alone, and overcomes fibroblast-derived resistance to Hsp90 inhibitor[2]. Luminespib shows great inhibition of pancreatic cancer cells with IC50 of at 10 nM. Luminespib (10 nM) reduces the expression and the epidermal growth factor (EGF)-mediated activation of EGFR and substantially disrupts EGF signaling in terms of diminishing downstream phosphorylation of ERKThr202/Tyr204. Luminespib (10 nM) significantly blocks pancreatic cancer cell migration and invasion both in the absence and presence of EGF[3].
In Vivo: Luminespib (50, 75 mg/kg, i.p.) significantly inhibits tumor growth rate, reducing the mean weights of tumors on day 11 in human tumor xenografts[2]. Luminespib (50 mg/kg/week, 3×25 mg/kg/week) significantly reduces tumor growth rates and lowers tumor weights in the L3.6pl pancreatic cancer cell-bearing mice model[3].

Name: PHA-665752, CAS: 477575-56-7, stock 28.4g, assay 98.9%, MWt: 641.61, Formula: C32H34Cl2N4O4S, Solubility: DMSO : 50 mg/mL (77.93 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Autophagy, Target: c-Met/HGFR;Apoptosis;Autophagy, Biological_Activity: PHA-665752 is a selective, ATP-competitive, and active-site inhibitor of the catalytic activity of c-Met kinase (Ki=4 nM; IC50=9 nM). PHA-665752 exhibits >50-fold selectivity for c-Met compared with a panel of diverse tyrosine and serine-threonine kinases. PHA-665752 induces apoptosis and cell cycle arrest, and exhibits cytoreductive antitumor activity[1][2].
IC50 & Target: Ki: 4 nM[1] 
IC50: 9 nM (c-Met)[1]
In Vitro: PHA-665752 is a potent and ATP-competitive inhibitor of c-Met kinase activity with a Ki of 4 nM and an IC50 of 9 nM[1]. 
PHA-665752 exhibits >50-fold selectivity for c-Met enzyme compared with the majority of kinases evaluated[1]. 
PHA-665752 shows potent inhibition of c-Met RTK autophosphorylation in NIH3T3 cells engineered to express high levels of c-Met and hepatocyte growth factor (HGF)[1]. 
PHA-665752 inhibits HGF-stimulated or constitutive phosphorylation of mediators of downstream of c-Met such as Gab-1, ERK, Akt, STAT3, PLC-γ, and FAK in multiple tumor cell lines[1]. 
PHA-665752 (0-1.25 μM; 18 hours) potently inhibits HGF and c-Met-driven phenotypes such as cell growth (proliferation and survival), cell motility, invasion, and/or morphology of a variety of tumor cells[1]. 
PHA-665752 (0-1.25 μM; 72 hours) induces apoptosis in both the presence and absence of HGF at concentrations that inhibited tyrosine phosphorylation of c-Met in GTL-16 cells[1]. 
PHA-665752 (0.0125-0.2 μM; 4 hours) potent inhibits HGF-induced c-Met phosphorylation in A549 cells[1]. 
In Vivo: PHA-665752 (7.5-30 mg/kg/day; i.v. ; for 9 days) exhibits statistically significant dose-dependent tumor growth inhibition of 68%, 39%, and 20% of vehicle control at the 30 mg/kg/day, 15 mg/kg/day, and 7.5 mg/kg/day doses, respectively[1]. 
PHA-665752 shows a potent cytoreductive activity in a gastric carcinoma xenograft model[1].

Name: HA14-1, CAS: 65673-63-4, stock 1.1g, assay 98.2%, MWt: 409.23, Formula: C17H17BrN2O5, Solubility: DMSO : ≥ 50 mg/mL (122.18 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: HA14-1 is a Bcl-2/Bcl-XL antagonist. HA14-1 binds the designated pocket on Bcl-2 with the IC50 of ≈9 μM in competing with the Bcl-2 binding of Flu-BakBH3, and inhibits its function.
IC50 & Target: IC50: ≈9 μM (Bcl-2)[1] 
Bcl-XL[2]
In Vitro: HA14-1 is a nonpeptidic ligand of a Bcl-2 surface pocket. HA14-1 induces the activation of Apaf-1 and caspases, possibly by binding to Bcl-2 protein and inhibiting its function. The interaction of HA14-1 with the Bcl-2 surface pocket appeared to be specific for the chemical structure of HA14-1 as a series of synthetic analogs derived from HA14-1 containing various modifications are found to have widely different Bcl-2 binding activities. To examine the effect of HA14-1 on cell viability, HL-60 cells are treated with various concentrations of HA14-1 for 4 h. HA14-1 induces the death of HL-60 cells in a dose-dependent manner. At 50 μM, HA14-1 causes the lost of viability in more than 90% of the cells[1]. HA14-1 is a Bcl-2/Bcl-xL antagonist[2].
In Vivo: Swiss nude mice are challenged with BeGBM cells (104 injected s.c.). HA14-1 (400 nmol) in 100 μL free RPMI 1640-50% DMSO, or the carrier alone, is given at the site of injection once weekly from day 2 following cell injection. HA14-1 treatment does not have any significant effect on the growth of glioblastoma tumors in immunodeficient mice as monitored twice weekly by measuring the volume of the expanding tumors. Moreover, no gross organ toxicity or weight loss can be detected in mice receiving such treatment. To analyze whether HA14-1 treatment might enhance the efficiency of another antitumoral treatment, Swiss nude mice challenged with human glioblastoma multiforme cells are also given i.p. low doses of Etoposide (2.5 mg/kg in 200 μL of 0.9% NaCl 5 days a week from day 2 following cell injection) together with HA14-1 or mock treatment. Whereas Etoposide treatment is insufficient by itself to restrain the growth of glioblastoma cells, its combination with HA14-1 leads to a significant restrain on tumor growth as judged by the ability of the combined treatment to increase the doubling time of the tumor volume[3].

Name: SB 216763, CAS: 280744-09-4, stock 32.6g, assay 98.1%, MWt: 371.22, Formula: C19H12Cl2N2O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (269.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR;Autophagy, Target: GSK-3;GSK-3;Autophagy, Biological_Activity: SB 216763 is potent and selective and ATP-competitive glycogen synthase kinase-3 (GSK-3) inhibitor, with an IC50 value of 34.3 nM for GSK-3α and GSK-3β, respectively.
IC50 & Target: IC50: 34.3 nM (GSK-3α), 34.3 nM (GSK-3β)[5]
In Vitro: SB-216763 (10-20 µM) induces β-catenin mediated-transcription in a dose-dependent manner in HEK293 cells. SB-216763 (10, 15 and 20 µM) can maintain mESCs with a pluripotent-like morphology in long-term culture. SB-216763 (10 µM) can maintain J1 mESCs in a pluripotent state for more than a month[2]. SB-216763 inhibits GSK-3 with IC50 of 34 nM[3]. SB-216763 is equally effective at inhibiting human GSK-3α and GSK-3β[5].
In Vivo: SB216763 (20 mg/kg, i.v.) significantly improves the survival of BLM-treated mice. Mice randomized to receive BLM plus SB216763 shows a noteworthy reduction, compared with BLM-treated mice. SB216763 (20 mg/kg, i.v.) reduces the magnitude of BLM-induced alveolitis[1]. SB 216763 (0.2 mg/kg, i.v.) with either 17β-E100 or Geni100 reverses the ceiling effect because these agents significantly reduce infarct size when the rabbits' hearts are submitted to 30-min CAO[4].

Name: SB 203580 RWJ 64809, CAS: 152121-47-6, stock 16.5g, assay 98.4%, MWt: 377.43, Formula: C21H16FN3OS, Solubility: DMSO : 100 mg/mL (264.95 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy;Autophagy, Target: p38 MAPK;Autophagy;Mitophagy, Biological_Activity: SB 203580 (RWJ 64809) is a selective and ATP-competitive p38 MAPK inhibitor. SB 203580 (RWJ 64809) inhibits SAPK2a/p38 and SAPK2b/p38β2, with IC50s of 50 nM and 500 nM, respectively. LCK, GSK3β and PKBα are also inhibited by SB 203580 (RWJ 64809), but the IC50s are 100-500-fold higher than that for SAPK2a/p38[1].
In Vitro: SB 203580 (preincubated with 0-30 μM for 1 h and cultured for 24 h in the presence of 20 ng/mL IL-2) prevents the IL-2-induced proliferation of primary human T cells, murine CT6 T cells, or BAF F7 B cells with an IC50 of 3-5 μM[1]. 
SB203580 blocks PKB phosphorylation (IC50 3-5 μM). SB203580 inhibitsthe phosphorylation of Ser473 in a dose-dependent manner in both CT6 and activated human T cells and IL-2-responsive BA/F3 F7 B cells[1].
In Vivo: SB203580 (5 mg/kg/day; intra peritoneal injected daily for 16 consecutive days, in female atymic Nu/Nu mice) treatment, p38WT tumors show a significantly smaller tumor burden when compared with p38TM tumors that were treated in parallel[1].

Name: SB 202190, CAS: 152121-30-7, stock 7.5g, assay 98.2%, MWt: 331.34, Formula: C20H14FN3O, Solubility: DMSO : ≥ 40 mg/mL (120.72 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Apoptosis;Autophagy;Apoptosis, Target: p38 MAPK;Apoptosis;Autophagy;Ferroptosis, Biological_Activity: SB 202190 is a cell-permeable p38 MAP kinase inhibitor with IC50s of 50 nM and 100 nM for p38α and p38β2, respectively. SB 202190 binds to the ATP pocket of the active recombinant human p38 kinase with a Kd of 38 nM.
IC50 & Target: IC50: 50 nM (p38), 100 nM (p38β2)[1]
In Vitro: Treatment of cells with SB 202190 (SB202190) significantly inhibits both basal and anti-Fas antibody-induced MAPKAPK 2 activity in a dose-dependent manner as measured in immune complex kinase assays with GST-hsp27 as a substrate. Jurkat cells are treated with SB202190 or left untreated. After 24 h, cells are harvested, and the activity of CPP32-like caspases in cell extracts is measured by cleavage of the fluorescent peptide DEVD-AMC, which is a specific substrate of CPP32-like caspases. The cleavage of DEVD-AMC is significantly increased in cells treated with SB202190 but not in the control[2].
In Vivo: In HCT-116-derived colorectal tumors, administration of SB 202190 (SB202190), Bay 43-9006 or a combination of both give similar results in terms of measurement of external tumor size (around 58% growth reduction compare with control tumors). SB202190 induces a 28% reduction of tumor growth, compare with a 31% reduction promoted by Bay 43-9006, while combination of both drugs reduce tumor growth by 55%[3]. Compare to the model group, the SB202190 group exhibits significantly shorter escape latencies in the Morris water maze hidden platform trials (P<0.01) and longer times in the original platform quadrant during probe trials (P<0.01). The SB202190 group also shows significantly reduced neuronal apoptosis in the hippocampus compared to VaD model rats (P<0.01) as well as higher (antiapoptotic) Bcl-2 expression and lower (proapoptotic) caspase-3 expression (P<0.01 for both). In conclusion, blockade of the p38 MAPK signaling pathway by SB202190 following permanent 2-OV reduced apoptosis of hippocampal neurons and rescued spatial learning and memory deficits[4].

Name: PD153035 (Hydrochloride) SU-5271 (Hydrochloride);AG1517 (Hydrochloride);ZM 252868 (Hydrochloride), CAS: 183322-45-4, stock 34.6g, assay 98.1%, MWt: 396.67, Formula: C16H15BrClN3O2, Solubility: DMSO : 5.125 mg/mL (12.92 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: PD153035 Hydrochloride (SU-5271 Hydrochloride) is a potent EGFR inhibitor with Ki and IC50 of 6 and 25 pM, respectively.
IC50 & Target: IC50: 25 pM (EGFR)[1]
Ki: 6 pM (EGFR)[1]
In Vitro: PD153035 inhibits EGF-stimulated receptor autophosphorylation in A431 human epidermoid carcinoma cells, with an IC50 of 14 nM[1]. PD153035 has little effect on PDGFR, FGFR, CSF-1 receptor, the insulin receptor, or on src tyrosine kinases at concentrations as high as 50 μM. PD153035 rapidly suppresses autophosphorylation of the EGF receptor at low nanomolar concentrations in fibroblasts or in human epidermoid carcinoma cells and selectively blocks EGF-mediated cellular processes including mitogenesis, early gene expression, and oncogenic transformation[2]. PD153035 causes a dose-dependent growth inhibition of EGF receptor-positive cell lines, beginning at less than micromolar concentrations, and the IC50 is less than 1 pM in most cases[3].
In Vivo: PD153035 levels in the plasma and tumor rise to 50 and 22 μM within 15 minutes following a single i.p. dose of 80 mg/kg. While the plasma levels of PD 153035 falls below 1 μM by 3 hours, in the tumors it remains at micromolar concentrations for at least 12 hours. The tyrosine phosphorylation of the EGF receptor is rapidly suppressed by 80-90% in the tumors[4].

Name: PD153035 SU-5271;AG1517;ZM 252868, CAS: 153436-54-5, stock 14.7g, assay 98.2%, MWt: 360.21, Formula: C16H14BrN3O2, Solubility: DMSO : 33.33 mg/mL (92.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: PD153035 (SU-5271; AG1517; ZM 252868) is a potent EGFR inhibitor with Ki and IC50 of 6 and 25 pM, respectively.
IC50 & Target: IC50: 25 pM (EGFR)[1]
Ki: 6 pM (EGFR)[1]
In Vitro: PD153035 (SU 5271) inhibits EGF-stimulated receptor autophosphorylation in A431 human epidermoid carcinoma cells, with an IC50 of 14 nM[1]. PD153035 (SU 5271) has little effect on PDGFR, FGFR, CSF-1 receptor, the insulin receptor, or on src tyrosine kinases at concentrations as high as 50 μM. PD153035 (SU 5271) rapidly suppresses autophosphorylation of the EGF receptor at low nanomolar concentrations in fibroblasts or in human epidermoid carcinoma cells and selectively blocks EGF-mediated cellular processes including mitogenesis, early gene expression, and oncogenic transformation[2]. PD153035 (SU 5271) causes a dose-dependent growth inhibition of EGF receptor-positive cell lines, beginning at less than micromolar concentrations, and the IC50 is less than 1 pM in most cases[3].
In Vivo: PD153035 (SU 5271) levels in the plasma and tumor rise to 50 and 22 μM within 15 minutes following a single i.p. dose of 80 mg/kg. While the plasma levels of PD153035 (SU 5271) falls below 1 μM by 3 hours, in the tumors it remains at micromolar concentrations for at least 12 hours. The tyrosine phosphorylation of the EGF receptor is rapidly suppressed by 80-90% in the tumors[4].

Name: SU11274 PKI-SU11274, CAS: 658084-23-2, stock 24.4g, assay 98%, MWt: 568.09, Formula: C28H30ClN5O4S, Solubility: DMSO : ≥ 100 mg/mL (176.03 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Autophagy, Target: c-Met/HGFR;Apoptosis;Autophagy, Biological_Activity: SU11274 is a selective Met inhibitor with IC50 of 10 nM, but has no effects on PGDFRβ, EGFR or Tie2.
IC50 & Target: IC50: 10 nM (Met)[1]
In Vitro: SU11274 exhibits greater than 50-fold selectivity for Met versus Flk and more than 500 times selectivity versus other tyrosine kinases such as FGFR-1, c-src, PDGFbR, and EGFR. SU11274 inhibits the phosphorylation of key regulators of the PI3K pathway, including AKT, FKHR, or GSK3β. SU11274 treatment inhibits the growth of TPR-MET-transformed BaF3 cells in a dose-dependent manner with IC50 of < 3 μM in the absence of interleukin 3, without growth inhibition of BaF3 cells transformed by other oncogenic tyrosine kinases, including BCR-ABL, TEL-JAK2, TEL-ABL, and TEL-PDGFβR. In addition to cell growth, SU11274 treatment significantly inhibits the migration of BaF3. TPR-MET cells by 44.8% and 80% at 1 μM and 5 μM, respectively. SU11274 inhibits HGF-dependent phosphorylation of Met as well as HGF-dependent cell proliferation and motility with an IC50 of 1-1.5 μM. In H69 and H345 cells which have functional Met receptor, SU11274 inhibits the HGF-induced cell growth with IC50 of 3.4 μM and 6.5 μM, respectively. SU11274 induces G1 cell cycle arrest with cells in G1 phase increased from 42.4% to 70.6% at 5 μM, and induces caspase-dependent apoptosis by 24% at 1 μM[2]. SU11274 inhibits cell viability in c-Met-expressing non-small cell lung cancer (NSCLC) cells with IC50 values of 0.8-4.4 μM, and abrogates hepatocyte growth factor-induced phosphorylation of c-Met and its downstream signaling[3].

Name: Iniparib BSI-201;NSC-746045;IND-71677, CAS: 160003-66-7, stock 0g, assay 98.9%, MWt: 292.03, Formula: C7H5IN2O3, Solubility: DMSO : 100 mg/mL (342.43 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: Iniparib (BSI-201) is an irreversible inhibitor of PARP1, used in the research of triple negative breast cancer.
IC50 & Target: PARP1[3]
In Vitro: Iniparib nonselectively modifies cysteine-containing proteins in tumor cells[1]. Iniparib (100 μM) weakly inhibits SSB repair, and the inhibition can be reversed by knockdown of PARP1[2]. Iniparib in combination with cisplatin is cytotoxic to Myc/MDA-231 with EMT changes[3].

Name: KU-55933, CAS: 587871-26-9, stock 21.4g, assay 98.6%, MWt: 395.49, Formula: C21H17NO3S2, Solubility: DMSO : 80 mg/mL (202.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Autophagy;Cell Cycle/DNA Damage;PI3K/Akt/mTOR, Target: Autophagy;ATM/ATR;ATM/ATR, Biological_Activity: KU-55933 is a potent ATM inhibitor with an IC50 and Ki of 12.9 and 2.2 nM, respectively, and is highly selective for ATM as compared to DNA-PK, PI3K/PI4K, ATR and mTOR.
IC50 & Target: IC50: 12.9 nM (ATM)[1]
In Vitro: KU-55933 (10 μM) blocks the ionizing radiation-induced p53 serine 15 phosphorylation. KU-55933 has a dose-dependent effect in inhibiting this ATM-dependent phosphorylation event with an estimated IC50 of 300 nM. KU-55933 ablates the ionizing radiation-induced phosphorylation of these ATM substrates. KU-55933 specifically inhibits ATM but not the other DNA damage-activated PIKKs, ATR, and DNA-PK[1]. KU-55933 induces pATM, p53, E2F1 and pATR, noticeably upregulates the nuclear fraction of E2F1 at the 0.5 h time point[2]. Metformin increases ATM and AMPK phosphorylation, as well as SHP protein level in primary hepatocytes, and this stimulatory effect of metformin is repressed by a specific ATM kinase inhibitor KU-55933[3].

Name: PF-04217903, CAS: 956905-27-4, stock 3.6g, assay 98.3%, MWt: 372.38, Formula: C19H16N8O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 20 mg/mL (53.71 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR, Biological_Activity: PF-04217903 is a selective ATP-competitive c-Met inhibitor with IC50 of 4.8 nM, susceptible to oncogenic mutations (no activity to Y1230C mutant).
IC50 value: 4.8 nM [1]
Target:
in vitro: Being more selective than staurosporine or PF-02341066, PF-04217903 displays >1000-fold selectivity for c-Met over a panel of 208 kinases, although more susceptible to oncogenic mutations of c-Met that attenuate potency than PF-02341066. In addition to WT c-Met, PF-04217903 displays similar potency to inhibit the activity of c-Met-H1094R, c-Met-R988C, and c-Met-T1010I with IC50 of 3.1 nM, 6.4 nM, and 6.7 nM, respectively, but has no inhibitory activity against c-Met-Y1230C with IC50 of >10 μM [1]. PF-04217903 in combination with sunitinib significantly inhibits endothelial cells, but not the tumor cells B16F1, Tib6, EL4, and LLC [2] PF-04217903 significantly inhibits the clonogenic growth of LXFA 526L and LXFA 1647L with IC50 values of 16 nM, and 13 nM, respectively, yielding an additive effect when in combination with cetuximab [3].
in vivo: Although unable to inhibit tumor growth in the sunitinib-sensitive B16F1 and Tib6 tumor models, the combination of PF-04217903 and sunitinib significantly inhibits tumor growth in sunitinib-resistant EL4, and LLC tumor models compared with sunitinib or PF-04217903 alone by significantly blocking vascular expansion, indicating a functional role for HGF/c-Met axis in the sunitinib-resistant tumors [2].

Name: Brivanib BMS-540215, CAS: 649735-46-6, stock 8.8g, assay 98.1%, MWt: 370.38, Formula: C19H19FN4O3, Solubility: DMSO : ≥ 50 mg/mL (135.00 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Autophagy, Target: VEGFR;Autophagy, Biological_Activity: Brivanib is an ATP-competitive inhibitor against VEGFR2 with IC50 of 25 nM, and has moderate potency against VEGFR-1 and FGFR-1, but >240-fold against PDGFR-β.
IC50 & Target: IC50: 25 nM (VEGFR2)

In Vitro: Brivanib inhibits VEGFR1 and FGFR-1 with IC50 of 0.38 μM and 0.148 μM. Brivanib is not sensitive to PDGFRβ, EGFR, LCK, PKCα or JAK-3 with IC50 all above 1900 nM. Brivanib could inhibit the proliferation of VEGF-stimulated HUVECs with IC50 of 40 nM, compared to 276 nM in FGF-stimulated HUVECs. On the other hand, brivanib exhibits low activity to tumor cell lines[1]. Brivanib doses ≤20 µM paradoxically enhances FGF-induced LX-2 cell proliferation, whereas higher brivanib doses (≥30 µM) inhibits LX-2 cell proliferation. The inhibitory effect of brivanib on liver fibrosis is not through inhibition of TGF-β1-induced stellate cell activation, and is possibly through inhibition of PDGF-BB-induced stellate cell activation[3].
In Vivo: Brivanib displays antitumor activities in H3396 xenograft in athymic mice. At a dose of 60 and 90 mg/kg (p.o.), brivanib completely inhibits the tumor growth, with TGI of 85% and 97%, respectively[1]. Moreover, brivanib significantly suppresses tumor growth in Hepatocellular carcinoma (HCC) xenografts, which due to the decrease in phosphorylation of VEGFR2. The results show that the tumor weights in 06-0606 xenograft mice are 55% and 13%, compared with the controls at a dose of 50 mg/kg and 100 mg/kg. Brivanib is suggested to be efficient in treatment of HCC[2]. Brivanib (50 mg/kg, p.o.) attenuates liver fibrosis and stellate cell activation induced by BDL in mice. Brivanib inhibits growth factor and growth factor receptor mRNA expression in sham control animals but shows variable effects in bile duct ligated animals[3].

Name: Vatalanib (dihydrochloride) PTK787 dihydrochloride;CGP-797870 dihydrochloride;ZK-222584 dihydrochloride, CAS: 212141-51-0, stock 28.3g, assay 99%, MWt: 419.73, Formula: C20H17Cl3N4, Solubility: DMSO : ≥ 125 mg/mL (297.81 mM), Clinical_Informat: Phase 3, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK, Target: Apoptosis;VEGFR, Biological_Activity: Vatalanib dihydrochloride (PTK787 dihydrochloride) is an inhibitor of VEGFR2/KDR with IC50 of 37 nM.
IC50 & Target: IC50: 37 nM (VEGFR2/KDR)[1]
In Vitro: Vatalanib also inhibits Flk, c-Kit and PDGFRβ with IC50 of 270 nM, 730 nM and 580 nM, respectively. Vatalanib shows the anti-proliferation effect by inhibiting thymidine incorporation induced by VEGF in HUVECs with and IC50 of 7.1 nM, and dose-dependently suppresses VEGF-induced survival and migration of endothelial cells in the same dose range without cytotoxic or antiproliferative effect on cells that do not express VEGF receptors[1]. A recent study shows that Vatalanib significantly inhibits the growth of hepatocellular carcinoma cells and enhances the IFN/5-FU induced apoptosis by increasing proteins levels of Bax and reduced Bcl-xL and Bcl-2[2].
In Vivo: Vatalanib induces dose-dependent inhibition of the angiogenic response to VEGF and PDGF in both a growth factor implant model and a tumor cell-driven angiogenesis model after once-daily oral dosing (25-100 mg/kg). In the same dose range, Vatalanib also inhibits the growth and metastasesof several human carcinomas in nude mice without significant effect on circulating blood cells or bone marrow leukocytes[1].

Name: LY294002 NSC 697286;SF 1101, CAS: 154447-36-6, stock 7.1g, assay 98%, MWt: 307.34, Formula: C19H17NO3, Solubility: DMSO : 41.67 mg/mL (135.58 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage;PI3K/Akt/mTOR;Apoptosis;Autophagy, Target: DNA-PK;DNA-PK;PI3K;Apoptosis;Autophagy, Biological_Activity: LY294002 is a broad-spectrum inhibitor of PI3K with IC50s of 0.5, 0.57, and 0.97 μM for PI3Kα, PI3Kδ and PI3Kβ, respectively[1]. LY294002 also inhibits CK2 with an IC50 of 98 nM[2]. LY294002 is a competitive DNA-PK inhibitorr that binds reversibly to the kinase domain of DNA-PK with an IC50 of 1.4 μM[3].
IC50 & Target: IC50: 0.5 μM (p110α), 0.57 μM (p110δ), 0.97 μM (p110β)[1] ; 98 nM (human CK2), 3.869 μM (human CK2α2)[2]; 1.4 μM (DNA-PK)[3]
In Vitro: LY294002 (0-75 μM; 24 hours and 48 hours) remarkably decreases CNE-2Z cells in a dose-dependent fashion[4]. 
LY294002 (0-75 μM; 24 hours and 48 hours ) induces CNE-2Z cells apoptosis rate in dose-dependent[4]. 
LY294002 (10-75 μM) significantly decreases p-Akt (S473) expression levels and up-regulates caspase-9 activity in CNE-2Z cells. Total Akt protein level is not difference with different concentration[4].
In Vivo: Treatment with LY294002 (i.p.,50 mg/kg, 75 mg/kg) significantly reduces mean NPC tumor burden as compared with the control group. Treatment with 10 mg/kg or 25 mg/kg LY294002 is less effective in decreasing tumor burden. Mean NPC tumor burden treated with LY294002 is remarkably decreased in a dose-dependent manner, whereas mean body weight is no obvious difference between control and treated groups (LY294002, 10 mg/kg, 25 mg/kg, 50 mg/kg, and 75 mg/kg)[4].

Name: Danusertib PHA-739358, CAS: 827318-97-8, stock 18.4g, assay 98.3%, MWt: 474.55, Formula: C26H30N6O3, Solubility: DMSO : 50 mg/mL (105.36 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage;Epigenetics;Autophagy, Target: Aurora Kinase;Aurora Kinase;Autophagy, Biological_Activity: Danusertib is a pyrrolo-pyrazole and aurora kinase inhibitor with IC50 of 13, 79, and 61 nM for Aurora A, B, and C, respectively.
IC50 & Target: IC50: 13 nM (Aurora A), 79 nM (Aurora B), 61 nM (Aurora C)[1]
In Vitro: Danusertib (0.01 to 50 μM) significantly decreases viability of C13 and A2780cp cells. The IC50s are 10.40 and 1.83 μM for C13 cells, and 19.89 and 3.88 μM for A2780cp cells after 24- and 48-h treatment. Danusertib induces cell cycle arrest in G2/M phase in C13 and A2780cp cells. Danusertib treatment results in a marked increase in the percentage of cells arrested in G2/M phase and an accumulation of polyploidy in C13 and A2780cp cells. Danusertib demotes the expression of CDK1/CDC2 and cyclin B1 but promotes the expression of p21 Waf1/Cip1, p27 Kip1, and p53. Danusertib induces autophagy in C13 and A2780cp cells with the involvement of PI3K/Akt/mTOR signaling pathway[1]. PHA-739358 strongly inhibits proliferation of all leukemic cell lines tested, with IC50 values ranging from 0.05 μM to 3.06 μM. PHA-739358 induces antiproliferative effects in BaF3-p210 cells, including IM-resistant M351T, E255K, and T315I mutants. PHA-739358 (5 μM) reduces phosphorylation of CrkL in BaF3-p210 wt cells and IM-resistant mutants[2]. Danusertibsertib leads to cell-cycle arrest and completely inhibits cell proliferation of the GEP-NET cells in vitro[3].
In Vivo: PHA-739358 (15 mg/kg twice a day, i.p.) and IM are well tolerated, and significantly inhibit proliferation of K562 cells andvirtually suppressed tumor growth during the 10-day treatment period[2]. In a subcutaneous murine xenograft model, danusertibsertib (2×15 mg/kg/d, i.p.) significantly reduces tumor growth in vivo compared with controls or mice treated with streptozotocine/5-fluorouracil[3].

Name: Foretinib XL880;GSK1363089;GSK089;EXEL-2880, CAS: 849217-64-7, stock 5.8g, assay 98.8%, MWt: 632.65, Formula: C34H34F2N4O6, Solubility: DMSO : ≥ 38 mg/mL (60.06 mM), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;VEGFR, Biological_Activity: Foretinib is an ATP-competitive inhibitor of HGFR and VEGFR, with IC50 of 0.4 nM and 0.9 nM for Met and KDR, less potent against Ron, Flt-1/3/4, Kit, PDGFRα/β and Tie-2, and has little activity to FGFR1 and EGFR.
IC50 & Target: IC50: 0.4 nM (Met), 0.9 nM (KDR)
In Vitro: Foretinib inhibits HGF receptor family tyrosine kinases with IC50 values of 0.4 nM for Met and 3 nM for Ron. Foretinib also inhibits KDR, Flt-1, and Flt-4 with IC50 values of 0.9 nM, 6.8 nM and 2.8 nM, respectively. Foretinib inhibits colony growth of B16F10, A549 and HT29 cells with IC50 of 40 nM, 29 nM and 165 nM, respectively[1]. A recent study indicates Foretinib affects cell growth differently in gastric cancer cell lines MKN-45 and KATO-III. Foretinib inhibits phosphorylation of MET and downstream signaling molecules in MKN-45 cells, while targets GFGR2 in KATO-III cells[2].
In Vivo: Foretinib (100 mg/kg, p.o.) results in substantial inhibition of phosphorylation of B16F10 tumor Met and ligand (e.g., HGFor VEGF)-induced receptor phosphorylation of Met in liver and Flk-1/KDR in lung, which both persist through 24 hours. Foretinib (30-100 mg/kg, once daily, p.o.) results in reduction in tumor burden. The lung surface tumor burden is reduced by 50% and 58% following treatment with 30 and 100 mg/kg Foretinib, respectively. Foretinib treatment of mice bearing B16F10 solid tumors also results in dose-dependent tumor growth inhibition of 64% and 87% at 30 and 100 mg/kg, respectively. For both studies, administration of Foretinib is well tolerated with no significant body weight loss[1]. Foretinib is developed to target abnormal signaling of HGF through Met and simultaneously target several receptors tyrosine kinase involved in tumor angiogenesis. Foretinib causes tumor hemorrhage and necrosis in human xenografts within 2 to 4 hours, and maximal tumornecrosis is observed at 96 hours (after five daily doses), resulting in complete regression[3].

Name: SGX-523, CAS: 1022150-57-7, stock 14.4g, assay 98.5%, MWt: 359.41, Formula: C18H13N7S, Solubility: DMSO : ≥ 3.6 mg/mL (10.02 mM), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR, Biological_Activity: SGX-523 is a selective Met inhibitor with IC50 of 4 nM, no activity to BRAFV599E, c-Raf, Abl and p38α.
IC50 value: 4 nM [1]
Target: Met
in vitro: SGX-523 belongs to the class of c-Met/hepatocyte growth factor receptor (HGFR) tyrosine kinase inhibitors. SGX-523 stabilizes MET in a unique inactive conformation that is inaccessible to other protein kinases, suggesting an explanation for its selectivity. SGX523 potently inhibits the purified MET catalytic domain but not the closely related receptor tyrosine kinase RON. SGX523 indicates ATP-competitive inhibition with higher apparent affinity for the less active, unphosphorylated form of MET [MET-KD(0P), with a Ki of 2.7 nM] versus the more active phospho-enzyme [MET-KD(3P), with a Ki of 23 nM], a phenomenon consistent with preferential binding to an inactive enzyme conformation. SGX523 inhibits MET-mediated signaling, cell proliferation and cell migration at nanomolar concentrations but had no effect on signaling dependent on other protein kinases, including the closely related RON, even at micromolar concentrations [1].
in vivo: SGX523 significantly retards the growth of preestablished GTL16 tumors when administered orally at doses of ≥10 mg/kg twice daily. SGX523 potently inhibits U87MG tumor growth; at 30 mg/kg dosed twice daily, SGX523 leads to clear regression of U87MG tumors. SGX523, dosed twice daily at 30 mg/kg, also retards the growth of H441 tumors with concomitant reduction in tumor MET autophosphorylation levels. SGX523 inhibition of MET in vivo is associated with the dose-dependent inhibition of growth of tumor xenografts derived from human glioblastoma, lung and gastric cancers, confirming the dependence of these tumors on MET catalytic activity [1].

Name: TW-37, CAS: 877877-35-5, stock 0.5g, assay 98.3%, MWt: 573.70, Formula: C33H35NO6S, Solubility: DMSO : ≥ 42 mg/mL (73.21 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: TW-37 is a potent Bcl-2 inhibitor with Ki values of 260, 290 and 1110 nM for Mcl-1, Bcl-2 and Bcl-xL, respectively.
IC50 & Target: Ki: 290 nM (Bcl-2), 1110 nM (Bcl-xL)[1] 
Ki: 260 nM (Mcl-1)[2]
In Vitro: TW-37 (TW37) is a novel nonpeptide small-molecule inhibitor designed using a structure-based design strategy. TW-37 targets the BH3-binding groove in Bcl-2 where proapoptotic Bcl-2 proteins, such as Bak, Bax, and Bid bind. In fluorescence polarization-based binding assays using recombinant Bcl-2 and Bcl-xL proteins, TW-37 binds to Bcl-2 and Bcl-xL with Ki values of 290 and 1110 nM, respectively. TW-37 has an IC50 of 1.8 μM for endothelial cells but shows no cytotoxic effects for fibroblasts at concentrations up to 50 μM. The mechanism of TW-37-induced endothelial cell death is apoptosis, in a process mediated by mitochondrial depolarization and activation of caspase-9 and caspase-3. The effect of TW-37 on endothelial cell apoptosis is not prevented by coexposure to the growth factor milieu secreted by tumor cells. Inhibition of the angiogenic potential of endothelial cells (i.e., migration and capillary sprouting assays) and expression of the angiogenic chemokines CXCL1 and CXCL8 are accomplished at subapoptotic TW-37 concentrations (0.005-0.05 μM)[1]. TW-37 is a potent Bcl-2 and Mcl-1 inhibitor. In fluorescence polarization-based binding assays using recombinant Bcl-2, Bcl-xL, and Mcl-1 proteins, TW-37 binds to Bcl-2, Bcl-xL, and Mcl-1 with Ki values of 290, 1,110 and 260 nM, respectively[2].
In Vivo: A murine model of humanized vasculature is used to investigate the biological effect of TW-37 (TW37) on human microvascular endothelial cell in vivo. Using this model, a significant decrease is observed in total blood vessel number (P<0.05) comparing both 3 and 30 mg/kg TW-37 against vehicle control. In addition to reduction in total number of blood vessels, an unusual number of occluded vessels are occurring in the treated groups. The levels of vessel occlusion are assessed by counting completely blocked vessels and determining their number as a percentage of total vessel number. TW-37 concentration mediates a significant increase in the number of occluded vessels when compared with control[1].

Name: Abiraterone CB-7598, CAS: 154229-19-3, stock 18.1g, assay 98.6%, MWt: 349.51, Formula: C24H31NO, Solubility: Ethanol : 5.4 mg/mL (15.45 mM; Need ultrasonic); DMSO : 5 mg/mL (14.31 mM; Need ultrasonic); DMF : 8.75 mg/mL (25.04 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Abiraterone is a potent and irreversible CYP17A1 inhibitor with antiandrogen activity, which inhibits both the 17α-hydroxylase and 17,20-lyase activity of the cytochrome p450 enzyme CYP17 with IC50s of 2.5 nM and 15 nM, respectively.
IC50 & Target: IC50:17α-hydroxylase (2.5 nM), 17,20-lyase (15 nM)[6]
In Vitro: Significant inhibition of proliferation of the AR-positive prostate cancer cell lines LNCaP and VCaP with doses of Abiraterone ≥5 μM is confirmed[2]. Abiraterone shows IC50 values of 15 nM and 2.5 nM for the 17,20-lyase and 17α-hydroxylase (CYP17 is a bifunctional enzyme with both 17α-hydroxylase and 17,20-lyase activity). Abiraterone inhibits human 17,20-lyase and 17α-hydroxylase with IC50 of 27 and 30 nM respectively[3]. Abiraterone inhibits recombinant human 3βHSD1 and 3βHSD2 activity with competitive Ki values of 2.1 and 8.8 μM. 10 μM Abiraterone is sufficient to completely block synthesis of 5α-dione and DHT in both cell lines.Treatment with abi significantly inhibited CRPC progression in the robustly growing subset, effectively putting a ceiling on tumor growth over 4 weeks of treatment (P<0.00001). [3H]-dehydroepiandrosterone (DHEA) depletion and Δ4-androstenedione (AD) accumulation are inhibited by Abiraterone in LNCaP, with an IC50<1 μM[4].
In Vivo: The 0.5 mmol/kg/d Abiraterone treatment dose is previously shown to yield serum concentrations of about 0.5 to 1 μM. Xenograft tumor growth in the control group is widely variable, with some tumors growing slowly and only a subset of tumors exhibiting robust growth[4]. Following i.v. administration (5 mg/kg) the clearance (Cl) and volume of distribution (Vd) are found to be 31.2 mL/min/kg and 1.97 L/kg, respectively. The AUC0-∞ (area under the plasma concentration-time curve from time zero to infinity time point) is found to be 2675 ng*h/mL. The terminal half-life (t1/2) is 0.73 h. Because of high clearance, Abiraterone (ART) is quantifiable only until 2 h following i.v. administration[5].

Name: 3-Aminobenzamide PARP-IN-1, CAS: 3544-24-9, stock 1.7g, assay 98.8%, MWt: 136.15, Formula: C7H8N2O, Solubility: H2O : ≥ 11.11 mg/mL (81.60 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: 3-Aminobenzamide (PARP-IN-1) is a potent inhibitor of PARP with IC50 of appr 50 nM in CHO cells, and acts as a mediator of oxidant-induced myocyte dysfunction during reperfusion.
IC50 & Target: IC50: 50 nM (PARP)[1]
In Vitro: 3-Aminobenzamide (PARP-IN-1) (>1 μM) causes more than 95% inhibition of PARP activity without significant cellular toxicity. INO-1001 significantly sensitizes CHO cells by blocking most of the DNA repair occurring between radiation fractions[1]. 3-Aminobenzamide significantly improves endothelial function by enhancing the acetylcholine-induced, endothelium-dependent, nitric oxide mediated vasorelaxation after exposure with 400 μM H2O2[2].
In Vivo: In a db/db (Leprdb/db) mouse model, 3-Aminobenzamide ameliorates diabetes-induced albumin excretion and mesangial expansion, and also decreases diabetes-induced podocyte depletion[3]. 3-Aminobenzamide (1.6 mg/kg via intracerebral injection) prevents NAD+ depletion and improves water maze performance after controlled cortical impact (CCI) in mice[4].

Name: GDC-0879, CAS: 905281-76-7, stock 18.3g, assay 98.2%, MWt: 334.37, Formula: C19H18N4O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (149.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: Raf, Biological_Activity: GDC-0879 is a potent and selective B-Raf inhibitor with an IC50 of 0.13 nM.
IC50 & Target: IC50: 0.13 nM (B-Raf)[1]
In Vitro: GDC-0879 also inhibits pERK with an IC50 of 63 nM[1]. GDC-0879 represents a novel potent and selective B-Raf inhibitor that is being evaluated as a potential antitumor agent. GDC-0879 exhibits potent inhibition of Raf/MEK/ERK signaling pathway in V600E B-Raf mutant cell lines with low cellular pMEK1 inhibition IC50 estimates of 59 and 29 nM in A375 melanoma and Colo205 colorectal carcinoma cells, respectively[2].
In Vivo: The pharmacokinetic parameters of GDC-0879 after oral administration of 15, 25, 50, 100, and 200 mg/kg in MCT in mice are estimated as follows: ka=8.20 h-1, ke=0.59 h-1, and apparent volume of distribution=6.19 L/kg[2].

Name: Brivanib (alaninate) BMS-582664, CAS: 649735-63-7, stock 24.8g, assay 98.1%, MWt: 441.46, Formula: C22H24FN5O4, Solubility: DMSO : ≥ 125 mg/mL (283.15 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Autophagy, Target: VEGFR;Autophagy, Biological_Activity: Brivanib alaninate is an ATP-competitive inhibitor against VEGFR2 with an IC50 of 25 nM; has moderate potency against VEGFR-1 and FGFR-1, but more than 240-fold against PDGFRβ.
IC50 & Target: IC50: 25 nM (VEGFR2)[1]
In Vitro: Brivanib inhibits VEGFR1 and FGFR-1 with IC50 of 0.38 μM and 0.148 μM. Brivanib is not sensitive to PDGFRβ, EGFR, LCK, PKCα or JAK-3 with IC50 all above 1900 nM. Brivanib could inhibit the proliferation of VEGF-stimulated HUVECs with IC50 of 40 nM, compared to 276 nM in FGF-stimulated HUVECs. On the other hand, brivanib exhibits low activity to tumor cell lines[1]. Brivanib doses ≤20 µM paradoxically enhances FGF-induced LX-2 cell proliferation, whereas higher brivanib doses (≥30 µM) inhibits LX-2 cell proliferation. The inhibitory effect of brivanib on liver fibrosis is not through inhibition of TGF-β 1-induced stellate cell activation, and is possibly through inhibition of PDGF-BB-induced stellate cell activation[3].
In Vivo: Brivanib displays antitumor activities in H3396 xenograft in athymic mice. At a dose of 60 and 90 mg/kg (p.o.), brivanib completely inhibits the tumor growth, with TGI of 85% and 97%, respectively[1]. Moreover, brivanib significantly suppresses tumor growth in Hepatocellular carcinoma (HCC) xenografts, which due to the decrease in phosphorylation of VEGFR2. The results show that the tumor weights in 06-0606 xenograft mice are 55% and 13%, compared with the controls at a dose of 50 mg/kg and 100 mg/kg. Brivanib is suggested to be efficient in treatment of HCC[2]. Brivanib (50 mg/kg, p.o.) attenuates liver fibrosis and stellate cell activation induced by BDL in mice. Brivanib inhibits growth factor and growth factor receptor mRNA expression in sham control animals but shows variable effects in bile duct ligated animals[3].

Name: Andarine GTx-007;S-4, CAS: 401900-40-1, stock 23.5g, assay 98.5%, MWt: 441.36, Formula: C19H18F3N3O6, Solubility: DMSO : ≥ 100 mg/mL (226.57 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: Andarine (S-4) is an investigational selective androgen receptor modulator (SARM) and an active partial agonist.

Name: Tanespimycin 17-AAG;NSC 330507;CP 127374, CAS: 75747-14-7, stock 12.5g, assay 98.7%, MWt: 585.69, Formula: C31H43N3O8, Solubility: DMSO : ≥ 55 mg/mL (93.91 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Apoptosis;Autophagy;Metabolic Enzyme/Protease;Cell Cycle/DNA Damage;Autophagy, Target: Apoptosis;Autophagy;HSP;HSP;Mitophagy, Biological_Activity: Tanespimycin (17-AAG) is a potent HSP90 inhibitor with an IC50 of 5 nM, having a 100-fold higher binding affinity for tumour cell derived HSP90 than normal cell derived HSP90. Tanespimycin (17-AAG) depletes cellular STK38/NDR1 and reduces STK38 kinase activity. Tanespimycin (17-AAG) also downregulates the stk38 gene expression.
IC50 & Target: IC50: 5 nM (HSP90)[5]
In Vitro: Tanespimycin causes the degradation of HER2, Akt, and both mutant and wild-type AR and the retinoblastoma-dependent G1 growth arrest of prostate cancer cells. Tanespimycin inhibits prostate cancer cell lines with IC50s ranged from 25-45 nM (LNCaP, 25 nM; LAPC-4, 40 nM; DU-145, 45 nM; and PC-3, 25 nM)[1]. Tanespimycin (0.1-1 μM) induces a nearly complete loss of ErbB2 on ErbB2-overexpressing breast cancer cells[2]. Tanespimycin inhibits cell growth and induces G2/M cell cycle arrest and apoptosis in CCA cells together with the down-regulation of Bcl-2, Survivin and Cyclin B1, and the up-regulation of cleaved PARP[3].
In Vivo: Tanespimycin (25-200 mg/kg, i.p.) causes a dose-dependent decline in AR, HER2, and Akt expression in prostate cancer xenografts. Tanespimycin treatment at doses sufficient to induce AR, HER2, and Akt degradation results in the dose-dependent inhibition of androgen-dependent and -independent prostate cancer xenograft growth without toxicity[1]. Tanespimycin (60 mg/kg) with Rapamycin (30 mg/kg) inhibits A549 and MDA-MB-231 tumor growth and effects tumor cures in MDA-MB-231 tumor-bearing animals by tail vein injection[4].

Name: Alvespimycin (hydrochloride) 17-DMAG hydrochloride;KOS-1022;BMS 826476, CAS: 467214-21-7, stock 30.2g, assay 98.2%, MWt: 653.21, Formula: C32H49ClN4O8, Solubility: DMSO : ≥ 50 mg/mL (76.55 mM), Clinical_Informat: Phase 2, Pathway: Apoptosis;Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: Apoptosis;HSP;HSP, Biological_Activity: Alvespimycin hydrochloride (17-DMAG hydrochloride; KOS-1022; BMS 826476) is a potent inhibitor of Hsp90, binding to Hsp90 with EC50 of 62±29 nM.
IC50 & Target: EC50: 62 nM±29 nM (Hsp90)[1]
In Vitro: Alvespimycin hydrochloride (17-DMAG hydrochloride; KOS-1022; BMS 826476) inhibits the growth of the human cancer cell lines SKBR3 and SKOV3, which overexpress Hsp90 client protein Her2, and causes down-regulation of Her2 as well as induction of Hsp70 consistent with Hsp90 inhibition, for Her2 degradation with EC50 of 8±4 nM and 46±24 nM in SKBR3 and SKOV3 cells, respectively; for Hsp70 induction with EC50 of 4±2 nM and 14±7 nM in SKBR3 and SKOV3 cells, respectively[1]. Compared with the vehicle control, 17-DMAG exerts dose-dependent apoptosis (P<0.001 averaged across 24- and 48-hour time points) at concentrations of 50nM to 500nM, which represent pharmacologically attainable doses. Similar to many other agents, 17-DMAG also demonstrates time-dependent apoptosis (P <0.001, averaged across all doses) in chronic lymphocytic leukemia (CLL) cells with extended exposure from 24 to 48 hours. In addition, 17-DMAG is much more potent after 24 and 48 hours of treatment than 17-AAG[2].
In Vivo: The tumors are grown for two months before the start of i.p. injections every four days over one month with 0, 50, 100 and 200 mg/kg dipalmitoyl-radicicol or 0, 5, 10 and 20 mg/kg 17-DMAG. Despite sample heterogeneity, the HSP90 inhibitor-treated animals have significantly lower tumour volumes than the vehicle control-treated animals. HSP90 inhibitors have been shown to cause liver toxicity in an animal model of gastrointestinal cancer. Nevertheless, the reduction in tumor size using dipalmitoyl-radicicol is statistically significant at 100 mg/kg, while 17-DMAG at either 10 or 20 mg/kg elicited a significant reduction in tumor size[3].

Name: Barasertib-HQPA AZD2811; INH-34; AZD1152-HQPA, CAS: 722544-51-6, stock 19.9g, assay 98.5%, MWt: 507.56, Formula: C26H30FN7O3, Solubility: DMSO : ≥ 22 mg/mL (43.34 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: Barasertib-HQPA (AZD2811) is a highly selective Aurora B inhibitor with an IC50 of 0.37 nM in a cell-free assay, and shows 3700-fold selectivity for Aurora B over Aurora A.
IC50 & Target: IC50: 0.37 nM (Aurora B)[2]
In Vitro: Barasertib-HQPA (AZD2811) displays >3000-fold selectivity for Aurora B as compared with Aurora A which has an IC50 of 1.368 μM.Barasertib-HQPA (AZD2811) has even less activity against 50 other serine-threonine and tyrosine kinases including FLT3, JAK2, and Abl. Barasertib-HQPA (AZD2811) inhibits the proliferation of hematopoietic malignant cells such as HL-60, NB4, MOLM13, PALL-1, PALL-2, MV4-11, EOL-1, THP-1, and K562 cells with IC50 of 3-40 nM, displaying appr 100-fold potency than another Aurora kinase inhibitor ZM334739 which has IC50 of 3-30 μM. Barasertib-HQPA (AZD2811) inhibits the clonogenic growth of MOLM13 and MV4-11 cells with IC50 of 1 nM and 2.8 nM, respectively, as well as the freshly isolated imatinib-resistant leukemia cells with IC50 values of 1-3 nM, more significantly compared with bone marrow mononuclear cells with IC50 values of >10 nM. Barasertib-HQPA (AZD2811) induces accumulation of cells with 4N/8N DNA content, followed by apoptosis in a dose- and time-dependent manner[2]. Barasertib-HQPA (AZD2811) treatment induces defective cell survival, polyploidy, and cell death in LNCaP cell line. AZD1152-HQPA also decreases expression of AR[3].
In Vivo: AZD1152 (10-150 mg/kg/day) significantly inhibits the growth of a variety of human solid tumor xenografts, including colon, breast, and lung cancers, in a dose-dependent manner[1]. Administration of AZD1152 (25 mg/kg) alone markedly suppresses the growth of MOLM13 xenografts, confirmed by the observation of necrotic tissue with infiltration of phagocytic cells[2].

Name: Sorafenib (Tosylate) Bay 43-9006 (Tosylate), CAS: 475207-59-1, stock 29.9g, assay 98.1%, MWt: 637.03, Formula: C28H24ClF3N4O6S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 31 mg/mL (48.66 mM), Clinical_Informat: Launched, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;MAPK/ERK Pathway;Protein Tyrosine Kinase/RTK;Autophagy;Apoptosis, Target: Apoptosis;VEGFR;Raf;FLT3;Autophagy;Ferroptosis, Biological_Activity: Sorafenib Tosylate (Bay 43-9006 Tosylate) is a potent multikinase inhibitor, with IC50s of 6 nM, 20 nM, and 22 nM for Raf-1, B-Raf, and VEGFR-3, respectively.
IC50 & Target: IC50: 6 nM (Raf-1), 20 nM (VEGFR-3), 22 nM (BRAF), 57 nM (PDGFR-β), 58 nM (Flt3), 68 nM (c-KIT), 90 nM (VEGFR-2)[1]
In Vitro: Sorafenib Tosylate also inhibits BRAFwt (IC50=22 nM), BRAFV599E (IC50=38 nM), VEGFR-2 (IC50=90 nM), VEGFR-3 (IC50=20 nM), PDGFR-β (IC50=57 nM), c-KIT (IC50=68 nM), and Flt3 (IC50=58 nM) in biochemical assays[1]. Sorafenib-induced phosphorylation of c-Met, p70S6K and 4EBP1 is significantly reduced when 10-0505 cells are co-treated with anti-human anti-HGF antibody, suggesting that treatment with Sorafenib Tosylate leads to increased HGF secretion and activation of c-Met and mTOR targets[2].
In Vivo: Sorafenib Tosylate (10, 30, 50 and 100 mg/kg, orally) treatment inhibits the tumor growth of 06-0606 and 10-0505 xenografts in a dose-dependent manner (P<0.01). The growth rate of 06-0606 and 10-0505 xenografts is also significantly reduced by Sorafenib. The weights of 06-0606 tumors in mice that are treated with Sorafenib 50 mg/kg and 100 mg/kg are approximately 13% and 5% of the controls, respectively. 50 mg dose of Sorafenib significantly inhibits tumor growth in mice with lines 5-1318, 26-1004 and 10-0505 (P<0.01). For 50 mg dose, the T/C ratio, where T and C are the median weight (mg) of Sorafenib- and vehicle-treated tumors at the end of the treatment, respectively, for 06-0606, 26-1004, 5-1318, and 10-0505 xenografts is 0.13, 0.10, 0.12 and 0.49, respectively[2]. The survival rate is 73.3 % in Diethyl nitrosamine (DENA) group and 83.3 % in Sorafenib group compared to 100 % in the normal control group. DENA group shows a significant increase in liver index (1.51-fold increase, p<0.05) compared to normal control group, while treatment with Sorafenib shows significant decrease (p<0.05) in liver index when compared to DENA group. The liver index in Sorafenib group significantly decreases to lower than its value in the normal control[3].

Name: Pomalidomide CC-4047, CAS: 19171-19-8, stock 30g, assay 98.1%, MWt: 273.24, Formula: C13H11N3O4, Solubility: DMSO : ≥ 100 mg/mL (365.98 mM), Clinical_Informat: Launched, Pathway: Apoptosis;PROTAC, Target: Apoptosis;Ligand for E3 Ligase, Biological_Activity: Pomalidomide is the third-generation immunomodulatory agent, functions through interacting with the E3 ligase cereblon and induces degradation of essential Ikaros transcription factors.
IC50 & Target: E3 ligase cereblon[5]
In Vitro: Pomalidomide also inhibits Whole Blood TNF-α with IC50 of 25 nM[1]. Exposure of lymphoma cells to Pomalidomide (CC-4047) leads to 40% decrease in cell proliferation when compared with vehicle-treated controls. Pomalidomide inhibits by 40% the DNA synthesis of Raji cells (P=0.036)[2]. In both CD4+ and CD8+ cells, Pomalidomide (CC-4047) is the most potent IL-2-elevator, followed by CC-6032 and CC-5013. Pomalidomide is significantly more potent than CC-5013 at elevating IL-2, IL-5, and IL-10, and slightly more potent than CC-5013 at elevating IFN-γ[3].
In Vivo: The administration of Pomalidomide (CC-4047) for two consecutive days before mAb therapy enhances the antitumor activity of Rituximab and doubled the median survival of lymphoma-bearing mice. Statistically, significant differences are observed between animals treated with Rituximab versus Pomalidomide+Rituximab. The median survival time of animals treated with Pomalidomide and Rituximab is longer (median survival, 74 days; 95% CI, 70-78) than those treated with Rituximab monotherapy (median survival, 38 days; 95% CI, 26-50; log-rank test, P=0.002). The administration of CC-5013 or Pomalidomide for two consecutive days leads to a significant increase in the number of circulating NK cells as shown by flow cytometry analysis, in lymphoma-bearing SCID mice[2]. Following a 50 mg/kg PO administration of Pomalidomide (POM) to rats, unbound concentrations in blood reach a Cmax value of 1100±82 ng/mL at 4.6±2.4 hours, with a concomitant AUC(0-10) value of 6800±2000 ng•hr/mL. Unbound POM in the brain, however, has a Cmax value of 430±63 ng/mL at 4.1±1.5 hours and an AUC(0-10) value of 2700±740 ng•hr/mL, giving an unbound AUCbrain to AUCblood ratio of 0.39±0.03. These values are consistent with excellent blood-brain-barrier penetration. The results obtained in this study are consistent with those seen in a concurrent study looking at whole brain POM content following its oral administration to mice[4].

Name: Serdemetan JNJ-26854165, CAS: 881202-45-5, stock 23.9g, assay 98.8%, MWt: 328.41, Formula: C21H20N4, Solubility: DMSO : 50 mg/mL (152.25 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis;Metabolic Enzyme/Protease;Apoptosis, Target: Apoptosis;E1/E2/E3 Enzyme;MDM-2/p53, Biological_Activity: Serdemetan(JNJ-26854165) acts as a HDM2 ubiquitin ligase antagonist and also induces early apoptosis in p53 wild-type cells, inhibits cellular proliferation followed by delayed apoptosis in the absence of functional p53.
IC50 value: HDM2 ubiquitin ligase
Target:
in vitro: JNJ 26854165 is a novel tryptamine derivative which activates p53 and acts as a HDM2 ubiquitin ligase antagonist. JNJ 26854165 inhibits cell growth and induces apoptosis in leukemia cell lines with IC50 values of 0.24, 0.33, 0.32 and 0.44 μM at 72 hours for OCI-AML-3, MOLM-13, NALM-6 and REH cells, respectively. In addition, JNJ 26854165 accelerates proteasome-mediated degradation of p21 and antagonizes the transcriptional induction of p21 by p53. It also induces S-phase delay and upregulates E2F1 expression in p53 mutant cells, resulting in preferential apoptosis of S-phase cells. JNJ 26854165 is an oral Mdm2 inhibitor which can inhibit the interaction of Mdm2-p53 complex with the proteasome and increase p53 levels by binding to RING domain of Mdm2. A recent study shows that JNJ 26854165 inhibits clonogenic survival in four human cancer cell lines: H460, A549, p53-WT-HCT116, and p53-null-HCT116.
in vivo:JNJ 26854165 leads to significant differences in EFS distribution in 17 of the 36 (47%) evaluable solid tumor xenografts and in 5 of 7 (71%) of the evaluable ALL xenografts using a dose of 20 mg/kg administered via oral gavage daily for 5 days, repeated for 6 weeks.

Name: WZ4002, CAS: 1213269-23-8, stock 20.1g, assay 98.7%, MWt: 494.97, Formula: C25H27ClN6O3, Solubility: DMSO : ≥ 100 mg/mL (202.03 mM), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: WZ4002 is a mutant selective EGFR inhibitor with IC50s of 2, 8, 3 and 2 nM for EGFRL858R, EGFRL858R/T790M, EGFRE746_A750 and EGFRE746_A750/T790M, respectively.
IC50 & Target: IC50: 2 nM (EGFRL858R), 8 nM (EGFRL858R/T790M), 3 nM (EGFRE746_A750), 2 nM (EGFRE746_A750/T790M)[1]
In Vitro: WZ4002 increases cellular potency correlated with inhibition of EGFR, AKT and ERK1/2 phosphorylation in NSCLC cell lines and EGFR phosphorylation in NIH-3T3 cells expressing different EGFRT790M mutant alleles. WZ4002 inhibits EGFR kinase activity of recombinant L858R/T790M protein more potently than of WT EGFR[1].
In Vivo: In a pharmacodynamic study WZ4002 effectively inhibits EGFR, AKT and ERK1/2 phosphorylation which is associated with a significant increase in TUNEL positive and a significant decrease in Ki67 positive cells compared to vehicle alone treated mice. In a 2 week efficacy study, WZ4002 treatment results in significant tumor regressions compared to vehicle alone in both T790M containing murine models. Histological evaluation of the lungs following treatment confirms significant resolution of the tumor nodules with only few small residual nodules and nodule remnants that has evidence of treatment effect with decreased cellularity and increased fibrosis consistent with remodeling/scarring[1].

Name: BIIB021 CNF2024, CAS: 848695-25-0, stock 17.5g, assay 98.1%, MWt: 318.76, Formula: C14H15ClN6O, Solubility: DMSO : ≥ 45 mg/mL (141.17 mM), Clinical_Informat: Phase 2, Pathway: Autophagy;Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: Autophagy;HSP;HSP, Biological_Activity: BIIB021 is an orally available, fully synthetic inhibitor of HSP90 with Ki and EC50 of 1.7 nM and 38 nM, respectively.
IC50 & Target: Ki: 1.7 nM (HSP90)[1]
In Vitro: BIIB021 binds in the ATP-binding pocket of Hsp90, interferes with Hsp90 chaperone function, and results in client protein degradation and tumor growth inhibition. BIIB021 inhibits tumor cell (BT474, MCF-7, N87, HT29, H1650, H1299, H69 and H82) proliferation with IC50 from 0.06-0.31 μM. BIIB021 induces the degradation of Hsp90 client proteins including HER-2, Akt, and Raf-1 and up-regulated expression of the heat shock proteins Hsp70 and Hsp27[1]. BIIB021 inhibits Hodgkin's lymphoma cells (KM-H2, L428, L540, L540cy, L591, L1236 and DEV) with IC50 from 0.24-0.8 μM. BIIB021 shows low activity in lymphocytes from healthy individuals. BIIB021 inhibits the constitutive activity of NF-κB despite defective IκB. BIIB021 induces the expression of ligands for the activating NK cell receptor NKG2D on Hodgkin's lymphoma cells resulting in an increased susceptibility to NK cell-mediated killing[2]. BIIB021 enhances the in vitro radiosensitivity of HNSCCA cell lines (UM11B and JHU12) with a corresponding reduction in the expression of key radioresponsive proteins, increases apoptotic cells and enhances G2 arrest[3]. BIIB021 is considerably more active than 17-AAG against adrenocortical carcinoma H295R. The cytotoxic activity of BIIB021 is not influenced by loss of NQO1 or Bcl-2 overexpression, molecular lesions that do not prevent client loss but are nonetheless associated with reduced cell killing by 17-AAG. BIIB021 is also active in 17-AAG resistant cell lines (NIH-H69, MES SA Dx5, NCI-ADR-RES, Nalm6)[4].
In Vivo: Oral administration of BIIB021 leads to tumor growth inhibition in many tumor xenograft models including N87, BT474, CWR22, U87, SKOV3 and Panc-1[1]. BIIB021 effectively inhibits growth of L540cy tumor at a dose of 120 mg/kg[2]. BIIB021 significantly enhances antitumor growth effect of radiation in JHU12 xenograft[3].

Name: PD98059, CAS: 167869-21-8, stock 18.1g, assay 98%, MWt: 267.28, Formula: C16H13NO3, Solubility: DMSO : 16 mg/mL (59.86 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Autophagy;MAPK/ERK Pathway, Target: Autophagy;MEK, Biological_Activity: PD98059 is a selective, cell permeable inhibitor of the MEK. PD98059 binds to the inactive form of MEK, thereby preventing the activation of MEK1 (IC50=2-7 µM) and MEK2 (IC50=50 µM) by upstream kinases. PD98059 causes G1 arrest by blocking p53-dependent p21 induction.
IC50 & Target: IC50: 2-7 μM (MEK1), 50 μM (MEK2)[1]
In Vitro: PD98059 (20 μM; 24 hours) causes G1-phase cell cycle arrest in OCI-AML-3 cells[4]. 
PD98059 (10 μM; 22 hours) results in concentration-dependent reductions in the dually phosphorylated forms of ERK1 and ERK2[1].
In Vivo: PD98059 (10 mg/kg; i.p.; 1 and 6 hours after Zymosan) significantly reduces the level of p-ERK1/2 in zymosan-injected mice[3].

Name: Regorafenib BAY 73-4506, CAS: 755037-03-7, stock 39.9g, assay 98.2%, MWt: 482.82, Formula: C21H15ClF4N4O3, Solubility: DMSO : ≥ 260 mg/mL (538.50 mM), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;MAPK/ERK Pathway;Protein Tyrosine Kinase/RTK;Autophagy;Protein Tyrosine Kinase/RTK, Target: VEGFR;Raf;PDGFR;Autophagy;RET, Biological_Activity: Regorafenib is a multi-target inhibitor for VEGFR1/2/3, PDGFRβ, Kit, RET and Raf-1 with IC50s of 13/4.2/46, 22, 7, 1.5 and 2.5 nM, respectively.
IC50 & Target: IC50: 13 nM (VEGFR1), 4.2 nM (VEGFR2), 46 nM (VEGFR3), 22 nM (PDGFRβ), 7 nM (Kit), 1.5 nM (RET), 2.5 nM (Raf-1)
In Vitro: Regorafenib potently inhibits VEGFR2 autophosphorylation in NIH-3T3/VEGFR2 cells with an IC50 of 3 nM. In HAoSMCs, regorafenib inhibits PDGFR-β autophosphorylation after stimulation with PDGF-BB, with an IC50 of 90 nM. Regorafenib inhibits the proliferation of VEGF165-stimulated HUVECs, with an IC50 of 3 nM[1]. Regorafenib causes a concentration-dependent decrease in Hep3B cell growth, having an IC50 of 5 μM. Regorafenib subsequently increases the levels of phospho-c-Jun, a JNK target, but not total c-Jun in Hep3B cells[3].
In Vivo: Regorafenib effectively inhibits growth of the Colo-205 xenografts in the dose range of 10-100 mg/kg reaching a TGI of 75% at day 14 at the 10 mg/kg dose. In the MDA-MB-231 model, regorafenib is highly efficacious at a dose as low as 3 mg/kg, resulting in a significant TGI of 81%, which increases to 93% at doses of 10 and 30 mg/kg, where tumor stasis is reached[1].

Name: PIK-90, CAS: 677338-12-4, stock 35.4g, assay 98.6%, MWt: 351.36, Formula: C18H17N5O3, Solubility: DMSO : 1.75 mg/mL (4.98 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage;PI3K/Akt/mTOR, Target: DNA-PK;DNA-PK;PI3K, Biological_Activity: PIK-90 is a DNA-PK and PI3K inhibitor, which inhibits p110α, p110γ and DNA-PK with IC50s of 11, 18 and 13 nM, respectively.
IC50 & Target: IC50: 13 nM (DNA-PK), 11 nM (p110α), 350 nM (p110β), 58 nM (p110δ), 18 nM (p110γ), 47 nM (PI3KC2α), 64 nM (PI3KC2β), 830 nM (hsVPS34), 830 nM (PI4KIIIα), 3.1 μM (PI4KIIIβ) , 15 μM (ATR), 610 nM (ATM),1.05 μM (mTORC1)[1]
In Vitro: PIK-90 also inhibits p110β, p110δ, PI3KC2α, PI3KC2β, hsVPS34, PI4KIIIα, PI4KIIIβ, ATR, ATM and mTORC1 with IC50s of 350 nM, 58 nM, 47 nM, 64 nM, 830 nM, 830 nM, 3.1 μM, 15 μM, 610 nM and 1.05 μM, respectively[1]. To determine the effects of PIK-90 on chronic lymphocytic leukemia (CLL) cell viability, CLL cells from different patients are incubated with various concentrations of PIK-90 (1 μM and 10 μM) for 24, 48, and 72 hours. PIK-90 reveals the strong apoptosis-inducing effects at both concentrations and at all different time points. Using a concentration of 10 μM, PIK-90 reduces the viability of CLL cells to 51.1% plus or minus 6.6% at 24 hours, whereas 1 μM PIK-90 reduces the viability to 77.8% plus or minus 6.4%[2].
In Vivo: To test the efficacy of Roscovitine and PIK-90 in vivo, GBM43 cells are implanted s.c. into nude mice. Mice with established tumors are randomized into four treatment groups: vehicle (PBS:H2O), Roscovitine, PIK-90, or PIK-90 plus Roscovitine. After 12 d of treatment, both Roscovitine and PIK-90 show clear single-agent efficacy, with tumor size in mice treated with Roscovitine and PIK-90 in combination significantly smaller than either vehicle or monotherapy-treated controls. Roscovitine is less effective than PIK-90 in blocking proliferation (levels of Ki-67), whereas combination therapy shows essentially additive antiproliferative effects[3].

Name: U0126 U0126-EtOH, CAS: 1173097-76-1, stock 29.2g, assay 98.2%, MWt: 426.56, Formula: C20H22N6OS2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 49 mg/mL (114.87 mM), Clinical_Informat: No Development Reported, Pathway: Autophagy;MAPK/ERK Pathway;Autophagy;Anti-infection, Target: Autophagy;MEK;Mitophagy;Virus Protease, Biological_Activity: U0126 is a non-ATP competitive MEK inhibitor, with IC50 of 70 nM and 60 nM for MEK1 and MEK2, respectively.
IC50 & Target: IC50: 70/60 nM (MEK1/2)[1]
In Vitro: Treatment with U0126 efficiently reduces progeny virus titers of all tested strains in A549 cells. While nM concentrations of U0126 are efficient to reduce H1N1v and H5N1 (MB1), μM concentrations of U0126 are required to reduce the virus titer of H5N1 (GSB) and H7N7. The EC50 values for U0126 against H1N1v are 1.2±0.4 μM in A549 cells and 74.7±1.0 μM in MDCKII cells[2].Rat hepatocarcinoma cells (FAO) stimulated by fetal calf serum (FCS) exhibits a significant proportion in S phase (32.62%) whereas U0126 strongly decreases the proportion of cells in S phase (9.92%) and increases the proportion of cells in G0-G1 phase and to a lesser extent in G2/M[3].
In Vivo: Mice are treated daily with U0126 (i.p., 10.5 mg/kg). In control experiment, tumor sizes are constant or slightly increase all over the kinetic. At the opposite, in all U0126 experiments, engraftment and early tumor growth are significantly decreased. Furthermore, a 60-70% reduction in the volume of tumors treated with U0126 is obtained 9 days after injection and thereafter[3]. Rats are subjected to 120?minutes transient middle cerebral artery occlusion (tMCAO) and thereafter treated with the U0126 (i.p., 30 mg/kg) at 0 and 24 hours of reperfusion. After treatment with U0126, the vasoconstriction to S6c is markedly reduced[4].

Name: OSI-930, CAS: 728033-96-3, stock 29.9g, assay 98.5%, MWt: 443.44, Formula: C22H16F3N3O2S, Solubility: DMSO : 50 mg/mL (112.75 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Apoptosis;VEGFR;c-Fms;c-Kit, Biological_Activity: OSI-930 is a potent inhibitor of Kit, KDR and CSF-1R with IC50 of 80 nM, 9 nM and 15 nM, respectively; also potent to Flt-1, c-Raf and Lck and low activity against PDGFRα/β, Flt-3 and Abl.
IC50 value: 9 nM(VEGFR2); 15 nM(CSF1R); 80 nM (Kit activated) [1]
Target: VEGFR2/Kit/CSF1R
in vitro: OSI-930 inhibits the cell proliferation in the HMC-1 cell line with IC50 of 14 nM without significant effect on growth of the COLO-205 cell line that does not express a constitutively active mutant receptor tyrosine kinase. Moreover, OSI-930 also induces apoptosis in HMC-1 cell line with EC50 of 34 nM [1]. A recent study shows that OSI-930 inactivates purified, recombinant cytochrome P450 (P450) 3A4 with a Ki of 24 μM in a time- and concentration-dependent mode [2].
in vivo: OSI-930, administrated at the maximally efficacious dose of 200 mg/kg by oral gavage, exhibits potent antitumor activity in a broad range of preclinical xenograft models including HMC-1, NCI-SNU-5, COLO-205 and U251 xenograft models [1].

Name: AG14361, CAS: 328543-09-5, stock 22.9g, assay 98.2%, MWt: 320.39, Formula: C19H20N4O, Solubility: DMSO : ≥ 32 mg/mL (99.88 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: AG14361 is a potent PARP-1 inhibitor, with a Ki of < 5 nM, and in permeabilized SW620 and intact SW620 cells, the IC50s are 29 nM and 14 nM, respectively.
IC50 & Target: Ki: < 5 nM (PARP-1)[1] 
IC50: 29 nM (PARP-1, in permeabilized SW620 cells), 14 nM (PARP-1, in intact SW620 cells)[1]
In Vitro: AG14361 is a potent PARP-1 inhibitor, with a Ki of < 5 nM, and in permeabilized SW620 and intact SW620 cells, the IC50s are 29 nM and 14 nM, respectively. AG14361 inhibits the proliferation of human cancer cells, such as A549, LoVo, and SW620 cells, with GI50s of 14 μM, 11.2 μM and 20 μM, respectively. Furthermore, AG14361 in combination with NSC 362856 markedly reduces the GI50 value of NSC 362856 in LoVo and A549 cells, but does not exert such an effect in SW620 cells[1]. AG14361 suppresses breast cancer cells with IC50s of 17 μM and 25 μM for 92 J-wt-BRCA1 and 92 J-sh-BRCA1 cells, respectively. AG14361 induces caspase 3/7 activation and cell cycle abnormalities, and also inhibits NF-κB signaling[2]. AG14361 (0.4 μM) enhances the growth-inhibitory and cytotoxic effects of topoisomerase I poisons, with no obvious effect on the formation and reversal of cleavable complexes, and increases the persistence of camptothecin-induced DNA single-strand breaks[3].
In Vivo: AG14361 (5 and 15 mg/kg, i.p.) has no toxicity and does not inhibit the growth of tumor. However, AG14361 markedly enhances NSC 362856 activity against LoVo xenografts and delays tumor growth when combined with NSC 362856. AG14361 (15 mg/kg, i.p.) treatment before irradiation dramaticly increases the sensitivity to radiation therapy of mice bearing LoVo xenografts[1]. AG14361 (30 mg/kg) synergizes lestaurtinib activity on inhibiting breast cancer tumors in allografts[2].

Name: 2-Methoxyestradiol 2-ME2;NSC-659853, CAS: 362-07-2, stock 39g, assay 98.8%, MWt: 302.41, Formula: C19H26O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (330.68 mM), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis;Autophagy;Metabolic Enzyme/Protease, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis;Autophagy;Endogenous Metabolite, Biological_Activity: 2-Methoxyestradiol (2-ME2), an orally active endogenous metabolite of 17β-estradiol (E2), is an apoptosis inducer and an angiogenesis inhibitor with potent antineoplastic activity. 2-Methoxyestradiol also destablize microtubules.
IC50 & Target: IC50: 1.2 μM (tubulin/microtubule, in living interphase MCF7 cells)[1]
In Vitro: 2-Methoxyestradiol (2-ME) (5-100 μM) inhibits assembly of purified tubulin in a concentration-dependent manner, with maximal inhibition (60%) at 200 μM 2-Methoxyestradiol (2ME2). In living interphase MCF7 cells at the IC50 for mitotic arrest (1.2 μM), 2-Methoxyestradiol significantly suppresses the mean microtubule growth rate, duration and length, and the overall dynamicity, consistent with its effects in vitro, and without any observable depolymerization of microtubules. 2-Methoxyestradiol induces G2-M arrest and apoptosis in many actively dividing cell types while sparing quiescent cells. 2-Methoxyestradiol binds to tubulin at or near the colchicine site, it inhibits microtubule assembly, and high concentrations have been shown to depolymerize microtubules in cells[1]. 
2-Methoxyestradiol (2-ME) decreases the HIF-1α and HIF-2α nuclear staining in cells cultured under hypoxia. 2-Methoxyestradiol is an anti-angiogenic, anti-proliferative and pro-apoptotic agent that suppresses HIF-1α protein levels and its transcriptional activity. A significant decrease in the growth rate is found in the 10 µM 2-Methoxyestradiol-treated A549 cells in comparison with the DMSO-treated cells (66.2±7.2 and 101.2±2.3%, respectively; p=0.04) at 96 h. A significant increase in apoptosis is observed in cells treated with 10 µM 2-Methoxyestradiol in a normoxic condition in comparison with cells under lower O2 concentration (5.8±0.2%; p=0.003)[2].
In Vivo: To investigate the effect of 2-Methoxyestradiol (2-ME2) on uveitis development, C57BL/6 mice are randomly assigned into two groups and immunized with IRBP peptide. 2ME2 group starts 2-Methoxyestradiol (15 mg/kg) intraperitoneally from day 0 to day 13 while control group is given with vehicle. The disease score of 2-Methoxyestradiol (2ME2) group is 0.30±0.30, significantly lower than that of control group 2.09±0.28 (p<0.05), each group containing 5 mice[3]. 
Treatment with 2-Methoxyestradiol (60-600 mg/kg/d) results in a dose-dependent inhibition of tumor growth. The percentage of cells with strong pimonidazole-positive staining (+++) is significantly decreased in the 2-Methoxyestradiol-treated group (36.0% for 60 mg/kg/d and 0% for 200 and 600 mg/kg/d) compare with the vehicle-treated group (86.5%). This may be attributed to the dramatic inhibition of tumor growth in a dose-dependent manner following 2-Methoxyestradiol treatment[4].

Name: Amuvatinib MP470;HPK 56, CAS: 850879-09-3, stock 13.4g, assay 98.7%, MWt: 447.51, Formula: C23H21N5O3S, Solubility: DMSO : 50 mg/mL (111.73 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;Apoptosis;FLT3;PDGFR;RAD51;c-Kit;RET, Biological_Activity: Amuvatinib (MP470) is an orally bioavailable multi-targeted tyrosine kinase inhibitor with potent activity against mutant c-Kit, PDGFRα, Flt3, c-Met and c-Ret. Amuvatinib (MP470) is also a DNA repair suppressor through suppression of DNA repair protein RAD51, thereby disrupting DNA damage repair[1][2][3]. Antineoplastic activity[4].
In Vitro: Amuvatinib (MP470) inhibits c-Kit (D816V), c-Kit (D816H), c-Kit (V560G), c-Kit (V654A), PDGFRα (D842V), and PDGFRα (V561D) with IC50s of 950 nM, 10 nM, 34 nM, 127 nM, 81 nM, and 40 nM, respectively[4]. 
Amuvatinib (MP470), a novel receptor tyrosine kinase (RTK) inhibitor has shown growth inhibitory activity against a variety of cancer cell lines. Amuvatinib (0.1-10 μM, 4 days incubation) is effective on LNCaP and PC-3 cells with IC50s of ~4 μM and 8 μM, respectively. When Erlotinib (10 μM) is combined with varying doses of Amuvatinib, the IC50 of Amuvatinib decreases to 2 μM on LNCaP cells[5]. 
Akt activity (as measured by phosphorylation on Ser473) is significantly reduced by 10 μM Amuvatinib (treated for 30 hours) alone but is not reduced by Erlotinib or Imatinib Mesylate (IM). Moreover, Amuvatinib plus Erlotinib completely abolished Akt phosphorylation in LNCaP cells with an unchanged total protein level of Akt[5].
In Vivo: Four LNCaP xenograft arms each with 12 mice are dosed intraperitoneally with DMSO (control) or Erlotinib 80 mg/kg or Amuvatinib (MP470) 50 mg/kg or Erlotinib 80 mg/kg plus Amuvatinib 50 mg/kg daily for 2 weeks and then observed for a further 11 days. Individual therapy with Amuvatinib or Erlotinib shows modest tumor growth inhibition (TGI), while Amuvatinib plus Erlotinib has a marked effect on TGI (45-65%). However, due to the high doses of Amuvatinib used, only five or one mouse remained alive in the combination arm at the end of treatment or at the end of the study, respectively. Therefore the Amuvatinib dose is reduced to 10 mg/kg or 20 mg/kg for the combination treatment. TGI in the group receiving 10 mg/kg Amuvatinib+80 mg/kg Erlotinib is not significantly different from the control group. However, mice receiving 20 mg/kg Amuvatinib+80 mg/kg Erlotinib have a significant TGI compared to the control group (p=0.01)[5].

Name: JNJ-7706621, CAS: 443797-96-4, stock 38.5g, assay 98.9%, MWt: 394.36, Formula: C15H12F2N6O3S, Solubility: DMSO : ≥ 125 mg/mL (316.97 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage;Cell Cycle/DNA Damage;Epigenetics, Target: Apoptosis;CDK;Aurora Kinase;Aurora Kinase, Biological_Activity: JNJ-7706621 is a potent aurora kinase inhibitor, and also inhibits CDK1 and CDK2, with IC50s of 9, 3, 11, and 15 nM for CDK1, CDK2, Aurora-A and Aurora-B, respectively.
IC50 & Target: IC50: 3 nM (CDK2), 9 nM (CDK1), 11 nM (Aurora-A), 15 nM (Aurora-B)[4]
In Vitro: JNJ-7706621 shows antiproliferative activity against various human tumor cells with IC50s of 284, 254, and 447 nM for HeLa, HCT116, and A375, respectively[1]. JNJ-7706621 inhibits other centrosomal proteins such as TOG, Nek2, and TACC3 in early mitotic phase, but does not prevent localization of Aurora A to the spindle poles. Treatment of nocodazole-synchronized cells with JNJ-7706621 can override mitotic arrest by preventing spindle checkpoint signaling, resulting in failure of chromosome alignment and segregation[2]. JNJ-7706621 suspensions inhibits cell viability of HeLa cells with IC50s of 2.1 and 0.9 μg/mL at 24 and 48 h. The IC50 of the JNJ-7706621-loaded nanoparticles are 35 and 2.7 μg/mL and the IC50 of the JNJ-7706621-loaded micelles are 6.3 and 1.6 μg/mL[3]. JNJ-7706621 shows inhibition of Aurora-A and Aurora-B but has no activity at the highest concentration tested on the Plk1 or Wee1 serine/threonine kinases. JNJ-7706621 also shows potent growth inhibition in vitro on all human cancer cell types with IC50 values ranging from 112 to 514 nM[4].
In Vivo: JNJ-7706621 (100 mg/kg, i.p.) exhibits 95% tumor growth inhibition in A375 (human melanoma) tumor xenograft model[1]. JNJ-7706621-loaded micelles inhibit tumor growth, and delay the tumor growth more efficiently than the control JNJ-7706621 suspension[3]. JNJ-7706621 (100 and 125 mg/kg) is efficacious in a human tumor xenograft model under intermittent dosing regimens[4].

Name: Avagacestat BMS-708163, CAS: 1146699-66-2, stock 27.9g, assay 98.8%, MWt: 520.89, Formula: C20H17ClF4N4O4S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (191.98 mM), Clinical_Informat: Phase 2, Pathway: Stem Cell/Wnt;Neuronal Signaling;Stem Cell/Wnt;Neuronal Signaling, Target: γ-secretase;γ-secretase;Notch;Notch, Biological_Activity: Avagacestat (BMS-708163) is a potent inhibitor of γ-secretase, with IC50s of 0.27 nM and 0.30 nM for Aβ42 and Aβ40 inhibition; Avagacestat (BMS-708163) also inhibits NICD (Notch IntraCellular Domain) with IC50 of 0.84 nM and shows weak inhibition of CYP2C19, with IC50 of 20 μM.
IC50 & Target: IC50: 0.27 nM (γ-secretase, Aβ42), 0.30 nM (γ-secretase, Aβ40), 20 μM (CYP2C19)[1], 0.84 nM (NICD)[2]
In Vitro: Avagacestat (BMS-708163) exhibits weaker potency for inhibition of Notch processing, IC50=58±23 nM, as compared to its inhibition potency for APP cleavage[1]. Avagacestat (BMS-708163) (10 µM) combined with gefitinib significantly attenuates the colony growth of PC9/AB2 cells, increases the expression of active caspase 3 and PARP and reduces the expression of Ki-67 in PC9/AB2 cells. Avagacestat (BMS-708163) induces apoptosis and enhances cell cycle arrest at the G1 phase in PC9/AB2 cells. Avagacestat (BMS-708163) treatment effectively downregulates the expression of Notch1, HES1, PI3K and Akt in PC9/AB2 cells[3].
In Vivo: Avagacestat (BMS-708163) significantly reduces both plasma and brain Aβ40 levels relative to control at 10 and 100 mg/kg for the entire dosing interval, demonstrates significant Aβ40 lowering for 8 h after an oral dose of 1 mg/kg, and significantly lowers CSF Aβ40 levels in rats, when measured 5 h after single oral doses ranging from 3 to 100 mg/kg[1]. Avagacestat (BMS-708163) (10 mg/kg) monotherapy has a minor inhibitory effect on PC9/AB2 tumor growth compared with gefitinib alone. BMS-708163 monotherapy results in a slight increase in caspase 3 expression as well as a mild decrease in Ki-67 expression in vivo. In the xenograft lung cancer samples treated with Avagacestat (BMS-708163) plus gefitinib, there are a marked increase in caspase 3 expression and a reduction in Ki-67 staining[3].

Name: CHIR-99021 CT99021, CAS: 252917-06-9, stock 10.2g, assay 98.7%, MWt: 465.34, Formula: C22H18Cl2N8, Solubility: DMSO : 16.67 mg/mL (ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR;Autophagy, Target: GSK-3;GSK-3;Autophagy, Biological_Activity: CHIR-99021 (CT99021) is a GSK-3α/β inhibitor with an IC50 of 10 and 6.7 nM, showing 500-fold selectivity over its closest homologs CDC2 and ERK2, as well as other protein kinases.
IC50 & Target: IC50: 10 nM/6.7 nM (GSK-3α/β)[1]
In Vitro: CHIR-99021 inhibits human GSK-3β with Ki values of 9.8 nM[1]. CHIR-99021 is a small organic molecule that inhibits GSK3α and GSK3β by competing for their ATP-binding sites.In vitro kinase assays reveal that CHIR-99021 specifically inhibits GSK3β (IC50=~5 nM) and GSK3α (IC50=~10 nM), with little effect on other kinases[2]. In the presence of CHIR-99021 the viability of the ES-D3 cells is reduced by 24.7% at 2.5 μM, 56.3% at 5 μM, 61.9% at 7.5 μM and 69.2% at 10 μM CHIR-99021 with an IC50 of 4.9 μM[3].
In Vivo: In ZDF rats, a single oral dose of CHIR-99021 (16 mg/kg or 48 mg/kg) rapidly lowers plasma glucose, with a maximal reduction of nearly 150 mg/dl 3-4 h after administration[1]. CHIR99021 (2 mg/kg) given once, 4 h before irradiation, significantly improves survival after 14.5 Gy abdominal irradiation (ABI). CHIR99021 treatment significantly blocks crypt apoptosis and accumulation of p-H2AX+ cells, and improves crypt regeneration and villus height. CHIR99021 treatment increases Lgr5+ cell survival by blocking apoptosis, and effectively prevents the reduction of Olfm4, Lgr5 and CD44 as early as 4 h[4].

Name: PD173074, CAS: 219580-11-7, stock 13g, assay 98.9%, MWt: 523.67, Formula: C28H41N7O3, Solubility: DMSO : ≥ 52 mg/mL (99.30 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Apoptosis;VEGFR;FGFR, Biological_Activity: PD173074 is a potent FGFR1 inhibitor with an IC50 of 25 nM and also inhibits VEGFR2 with an IC50 of 100-200 nM, showing 1000-fold selectivity for FGFR1 over PDGFR and c-Src.
IC50 & Target: IC50: 25 nM (FGFR1), 100-200 nM (VEGFR2)
In Vitro: PD 173074 inhibits autophosphorylation of FGFR1 in a dose-dependent manner with an IC50 in the range 1-5 nM. PD 173074 is an ATP-competitive inhibitor of FGFR1 with an inhibitory constant (Ki) of 40 nM[1]. PD 173074 and SU 5402 produce concentration-dependent reductions in FGF-2 enhancement of granule neuron survival, with IC50 values of 8 nM and 9 μM, respectively. PD 173074 does not inhibit neurotrophic and neuritogenic actions of FGF-2 signalling molecules in cerebellar granule neurons. PD 173074 and SU 5402 concentration-dependently inhibits the neurite growth response, when tested on FGF-2-treated granule neurons growing on polylysine/laminin, with IC50s of 22 nM and 25 μM, respectively[2]. PD173074 effectively antagonizes the effect of FGF-2 on proliferation and differentiation of OL progenitors in culture. Mitogen-activated protein kinase (MAPK) activation, a downstream event after activation of either FGFR or PDGFR, is also blocked by PD173074 in OL progenitors stimulated with FGF-2 but not PDGF[3].
In Vivo: PD 173074 (1 mg/kg, i.p.) exhibits dose-dependent inhibition of FGF-induced neovascularization and angiogenesis in mice[1]. D173074 (25 mg/kg, p.o.) significantly inhibits tumor growth in mice[4].

Name: WYE-354, CAS: 1062169-56-5, stock 27.3g, assay 98.9%, MWt: 495.53, Formula: C24H29N7O5, Solubility: DMSO : ≥ 26 mg/mL (52.47 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: Apoptosis;mTOR;Autophagy, Biological_Activity: WYE-354 is an ATP-competitive mTOR inhibitor with an IC50 of 5 nM. WYE-354 also inhibits PI3Kα and PI3Kγ with IC50s of 1.89 μM and 7.37 μM, respectively. WYE-354 inhibits both mTORC1 and mTORC2.
IC50 & Target: IC50: 5 nM (mTOR), 1.89 μM (PI3Kα), 7.37 μM (PI3Kγ)[1] 
mTORC1, mTORC2[1]
In Vitro: In the DELFIA measuring His6-S6K1 T389 phosphorylation, WYE-354 inhibits recombinant mTOR enzyme with an IC50 of 5 nM[1]. Cell viability is analyzed by MTS assay. G-415 and TGBC-2TKB cell lines are treated with increasing concentrations of WYE-354 (0.1, 1, 5 and 10 μM) for 24, 48, and 72 hours. WYE-354 significantly reduces cell viability starting at a 1 μM concentration after a 24 hours exposure, in both studied cell lines (P<0.001). A decrease in cell viability is not observed at a dose of 100 nM, except for the TGBC-2TKB cell line after 72 hours of treatment[2].
In Vivo: The effect of Rapamycin and WYE-354 on tumor growth is evaluated in xenograft GBC tumor models. 2×106 or 5×106 cells of G-415 or TGBC2TKB, respectively, are xenotransplanted into NOD-SCID mice subcutaneously. When tumors reach an average volume of 100 mm3, the mice are treated either with Rapamycin or WYE354. Rapamycin is administered i.p. at a concentration of 10 mg/kg, daily for 5 days per week for 3 weeks, while WYE-354 is administrated at a daily i.p. dose of 50 mg/kg for 5 days. Mice are sacrificed 30 days after the initiation of the treatments and an autopsy is performed that include removal of the entire tumor area. Mice treated with WYE-354 exhibit 68.6% and 52.4% reduction in average tumor size (P<0.01; P<0.01), as well as 82.9% and 45.5% (P<0.01; ns) reduction in tumor weight, respectively[2].

Name: IC-87114, CAS: 371242-69-2, stock 16.5g, assay 98.4%, MWt: 397.43, Formula: C22H19N7O, Solubility: DMSO : 10 mg/mL (25.16 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: IC-87114 is a potent and selective PI3Kδ inhibitor with IC50 of 0.5 μM.
IC50 & Target: IC50: 0.5 μM (PI3Kδ)[1]
In Vitro: IC-87114 (IC87114), an analog of the original inhibitor, is synthesized and tested for PI3Kδ selectivity relative to the other class I PI3Ks. The IC50 of IC87114 for PI3Kδ inhibition is 0.5 μM whereas the IC50 values for PI3Kα, PI3Kβ, and PI3Kγ are >100, 75, and 29 μM, respectively. Thus IC87114 is 58-fold more selective for PI3Kδ relative to PI3Kγ, and over 100-fold selective relative to PI3Kα and PI3Kβ. IC87114 selectively antagonizes PI3Kδ over at least a concentration range of 0.3-10 μM[1]. IC-87114 (10 μM) is also used to selectively inhibit PI3Kδ catalytic activity to address this question. IC87114 (10 μM) effectively inactivates Akt in macrophages after treatment for 1 hour (n=6; P<0.001 versus control). The effect of IC-87114 (IC87114) is next detected ton AP-1 DNA-binding activity. The electrophoretic mobility shift assay assay demonstrates that DNA-binding activity of AP-1 is significantly increased after the treatment with TNF-α (10 ng/mL; P<0.001) and TNF-α (20 ng/mL; P<0.001). IC87114 alone induces AP-1 DNA-binding activity after treatment for 1 hour. Furthermore, there is stronger AP-1 DNA-binding activity after costimulation of IC87114 (10 μM) and TNF-α (0-20 ng/mL) than only treatment with TNF-α (0-20 ng/mL; n=5; P<0.01). IC87114 (10 μM) also effectively inhibits p110δ catalytic activities (Akt phosphorylation) in macrophages with or without TNF-α treatment for 24 hours (n=6; P<0.001)[2].
In Vivo: Treatment with PD 89059 (10 mg/kg), IC-87114 (0.3 mg/kg) and BAY 11-7085 (10 mg/kg), significantly (P<0.05) reduces the OVA- induced inflammatory cell influx into the airways and the histopathological airway remodeling. However, these treatments does not significantly improve OVA induced-AHR (P>0.05). Of note, the observed reduction in the histopathological airway remodeling induced by PD 89059, IC-87114 and BAY 11-7085 are less effective as compared to the reduction seen with AG 1478 and SU6656[3].

Name: AMG-208, CAS: 1002304-34-8, stock 14.6g, assay 98%, MWt: 383.40, Formula: C22H17N5O2, Solubility: DMSO : 7.8 mg/mL (20.34 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR, Biological_Activity: AMG-208 is a potent small molecular c-Met inhibitor with an IC50 of 9.3 nM.
IC50 value: 9.3 nM
Target: c-Met
in vitro: AMG-208 shows the potent inhibition of kinase c-Met activity with IC50 of 9 nM in a cell-free assay. Besides, AMG-208 treatment also leads to the inhibition of HGF-mediated c-Met phosphorylation in PC3 cells with IC50 of 46 nM [1]. Pre-incubation of AMG-208 with human liver microsomes for 30 minutes shows a potent time-dependent inhibition for CYP3A4 metabolic activity with IC50 of 4.1 μM, which is an eightfold decrease relative to the IC50 (32 μM) without preincubation [2]. AMG-208 is identified to be a c-MET and RON dual selective inhibitor [3].
in vivo: In male Sprague Dawley rats, AMG-208 (0.5 mg/kg i.v.) shows a high bioavailability with Cl of 0.37 L/h/kg, Vss of 0.38 L/kg and T1/2 of 1 hour[1].

Name: TG100-115, CAS: 677297-51-7, stock 35g, assay 98.4%, MWt: 346.34, Formula: C18H14N6O2, Solubility: DMSO : 5.45 mg/mL (15.74 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: TG100-115 is a selective PI3Kγ/PI3Kδ inhibitor with IC50s of 83 and 235 nM, respectively.
IC50 & Target: IC50: 83 nM (PI3Kγ), 235 nM (PI3Kδ)[1]
In Vitro: TG100-115 inhibits PI3Kγ and PI3Kδ with IC50s of 83 and 235 nM, respectively, whereas both PI3Kα and PI3Kβ are relatively unaffected (IC50 values >1 μM). As a gauge of general specificity, TG100-115 is also assayed against a 133 protein kinase panel, none of which are inhibited at IC50 values <1 μM. TG100-115 potently inhibits edema and inflammation in response to multiple mediators known to participate in myocardial infarction, including vascular endothelial growth factor and platelet-activating factor; by contrast, endothelial cell mitogenesis, a repair process important to tissue survival after ischemic damage[1].
In Vivo: To correlate these in vivo responses with the molecular target of interest, PI3K pathway signaling is monitored through western blot analyses of Akt phosphorylation (a PI3K-mediated event). VEGF injection i.v. in mice induces a rapid Akt phosphorylation readily detectable in lung lysates, pretreatment with TG100-115 blocks this response. Blockade is seen with TG100-115 doses as low as 0.5 mg/kg and persists over a period of several hours. In initial dose-ranging studies, generally equivalent responses are observed using TG100-115 doses of 0.5-10 mg/kg, and we therefore elected to conduct a statistically powered test at the lowest dose. Animals dosed with TG100-115 as a single 0.5 mg/kg i.v. bolus 30 min after reperfusion developed smaller infarcts vs. vehicle-treated controls. Measuring infarct area as percent of total LV ischemic area, infarct size is reduced by 35% (P=0.04). Viable tissue within the ischemic zone is increased by 37% (P=0.04), directly demonstrating the cardioprotective effect of PI3Kγ/δ inhibition[1].

Name: GSK1059615, CAS: 958852-01-2, stock 26.8g, assay 98.5%, MWt: 333.36, Formula: C18H11N3O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 5 mg/mL (15.00 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR;Apoptosis;PI3K/Akt/mTOR, Target: PI3K;Apoptosis;mTOR, Biological_Activity: GSK1059615 is a dual inhibitor of PI3Kα/β/δ/γ (reversible) and mTOR with IC50 of 0.4 nM/0.6 nM/2 nM/5 nM and 12 nM, respectively.
IC50 & Target: IC50: 0.4 nM (PI3Kα), 0.6 nM (PI3Kβ), 2 nM (PI3Kδ), 5 nM (PI3Kγ), 12 nM (mTOR)
In Vitro: GSK1059615 inhibits PI3Kα, β, γ and δ, with Ki of 0.42 nM, 0.6 nM, 0.47 nM and 1.7 nM, respectively[1]. In T47D and BT474 cancer cells, GSK1059615 inhibits the phosphorylation of Akt at S473, with IC50 of 40 nM[2].
In Vivo: GSK1059615 (25 mg/kg) effectively inhibits tumor growth in xenograft mice models of BT474 or HCC1954 breast cancer cells[1].

Name: MGCD-265 analog, CAS: 875337-44-3, stock 4.5g, assay 98.4%, MWt: 517.60, Formula: C26H20FN5O2S2, Solubility: DMSO : ≥ 100 mg/mL (193.20 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;Apoptosis;VEGFR, Biological_Activity: MGCD-265-analog (structurally related to MGCD-265) is an orally bioavailable multitargeted tyrosine kinase inhibitor with potential antineoplastic activity with IC50 of 29 nM and 10 nM for c-Met and VEGFR2, respectively.
IC50 value:10 nM (VEGFR2), 29 nM(c-Met) [1]
Target:VEGFR, c-Met
in vivo: MGCD-265-analog has a reasonable half-life, 1.2 h in rats and 5.8 h in dogs, and has an acceptable clearance, 0.33 L/(kg h) in rats and 1.1 L/(kg h) in dogs. The steady state volume of distribution was low in rats (0.25 L/kg) and reasonable in dogs (1.5 L/kg), while the oral bio-availability was determined to be 12% and 42% in rats and dogs, respectively. GCD-265-analog performed well in vivo against a panel of different human tumor types, particularly those that are driven by or overexpress c-Met (MNNGHOS and MKN45). Tumor growth inhibition at a dose of 20 mg/kg po once daily ranged from 41% to 94%. MGCD-265-analog was found to show spill-over inhibition of a number of kinases in addition to the intended c-Met/VEGFR2 activity. MGCD-265-analog has significant antitumor activity in vivo.[1]

Name: Rigosertib (sodium) ON-01910 sodium, CAS: 592542-60-4, stock 3.5g, assay 98.9%, MWt: 473.47, Formula: C21H24NNaO8S, Solubility: H2O : ≥ 52 mg/mL (109.83 mM); DMSO : 210 mg/mL (443.53 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: PI3K/Akt/mTOR;Apoptosis;Cell Cycle/DNA Damage, Target: PI3K;Apoptosis;Polo-like Kinase (PLK), Biological_Activity: Rigosertib sodium (ON-01910 sodium) is a multi-kinase inhibitor and a selective anti-cancer agent, which induces apoptosis by inhibition the PI3K/Akt pathway, promotes the phosphorylation of histone H2AX and induces G2/M arrest in cell cycle[1][2]. Rigosertib sodium is a selective and non-ATP-competitive inhibitor of PLK1 with an IC50 of 9 nM[3].
IC50 & Target: IC50: 9 nM (PLK1), 260 nM (PLK2)[1]
In Vitro: Rigosertib is non-ATP-competitive inhibitor of PLK1 with IC50 of 9 nM. Rigosertib also exhibits inhibition of PLK2, PDGFR, Flt1, BCR-ABL, Fyn, Src, and CDK1, with IC50 of 18-260 nM. Rigosertib shows cell killing activity against 94 different tumor cell lines with IC50 of 50-250 nM, including BT27, MCF-7, DU145, PC3, U87, A549, H187, RF1, HCT15, SW480, and KB cells. While in normal cells, such as HFL, PrEC, HMEC, and HUVEC, Rigosertib has little or no effect unless its concentration is greater than 5-10 μM. In HeLa cells, Rigosertib (100-250 nM) induces spindle abnormalities and apoptosis[3]. Rigosertib also inhibits several multidrug resistant tumor cell lines, including MES-SA, MES-SA/DX5a, CEM, and CEM/C2a, with IC50 of 50-100 nM. In DU145 cells, Rigosertib (0.25-5 μM) blocks cell cycle progression in G2/M phase, results in an accumulation of cells containing subG1 content of DNA, and activates apoptotic pathways. In A549 cells, Rigosertib (50 nM-0.5 μM) induces loss of viability and caspase 3/7 activation[4]. Rigosertib sodium (2 μM) induces apoptosis in chronic lymphocytic leukemia (CLL) cells without toxicity against T-cells or normal B-cells. Rigosertib sodium (2 μM) also abrogates the pro-survival effect of follicular dendritic cells on CLL cells and reduces SDF-1-induced migration of leukemic cells[5].
In Vivo: Rigosertib (250 mg/kg, i.p.) markedly inhibits tumor growth in mouse xenograft models of Bel-7402, MCF-7, and MIA-PaCa cells[3]. Rigosertib (200 mg/kg, i.p.) shows inhibition on tumor growth in a mouse xengraft model of BT20 cells[4].

Name: Ki8751, CAS: 228559-41-9, stock 26.5g, assay 98.7%, MWt: 469.41, Formula: C24H18F3N3O4, Solubility: DMSO : ≥ 92 mg/mL (195.99 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: VEGFR, Biological_Activity: Ki8751 is a potent VEGFR2 inhibitor with an IC50 of 0.9 nM.
IC50 & Target: IC50: 0.9 nM (VEGFR2)[1]
In Vitro: Ki8751 inhibits VEGFR-2 phosphorylation at an IC50 value of 0.90 nM, and also inhibits the PDGFR family members such as PDGFRR and c-Kit at 67 nM and 40 nM, respectively. However, Ki8751 does not have any inhibitory activity against other kinases such as EGFR, HGFR, InsulinR and others even at 10000 nM. Ki8751 suppresses the growth of the VEGF-stimulated human umbilical vein endothelial cell (HUVEC) on a nanomolar level[1].
In Vivo: Ki8751 shows significant antitumor activity against five human tumor xenografts such as GL07 (glioma), St-4 (stomach carcinoma), LC6 (lung carcinoma), DLD-1 (colon carcinoma) and A375 (melanoma) in nude mice and also shows complete tumor growth inhibition with the LC-6 xenograft in nude rats following oral administration once a day for 14 days at 5 mg/kg without any body weight loss[1].

Name: Lyn-IN-1 Bafetinib analog, CAS: 887650-05-7, stock 26.2g, assay 98.1%, MWt: 576.62, Formula: C30H31F3N8O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (86.71 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Bcr-Abl, Biological_Activity: Lyn-IN-1 (Bafetinib analog) is a potent and selective dual Bcr-Abl/Lyn inhibitor, extracted from patent WO2014169128A1.

Name: Elesclomol STA-4783, CAS: 488832-69-5, stock 37.1g, assay 98.6%, MWt: 400.52, Formula: C19H20N4O2S2, Solubility: DMSO : ≥ 22 mg/mL (54.93 mM), Clinical_Informat: Phase 3, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Elesclomol is an oxidative stress inducer that induces cancer cell apoptosis.
In Vitro: Elesclomol significantly induces the expression of heat shock stress response genes and metallothionein genes, a signature transcription profile indicative of oxidative stress in Hs294T cells. Elesclomol (100 nM) rapidly induces Hsp70 RNA levels with a 4.8-fold increase at 1 hour and a 160-fold increase at 6 hours in Ramos Burkitt's lymphoma B cells in consistent with the intracellular ROS content which increases by 20% as early as 0.5 hour and 385% at 6 hours, and the induction of Hsp70 can be blocked by antioxidants N-acetylcysteine (NAC) and Tiron pretreatment. Elesclomol increases the number of early and late apoptotic cells with 3.7- and 11-fold through the induction of oxidative stress, which can be completely blocked by NAC, while having little effect on normal cells[1]. Elesclomol significantly inhibits the cell viability of SK-MEL-5, MCF-7, and HL-60 with IC50 of 110 nM, 24 nM and 9 nM, respectively[2]. Elesclomol induces copper-dependent ROS generation and cytoxicity in yeast. Instead of working through a specific cellular protein target, elesclomol interacts with the electron transport chain (ETC), a biologically coherent set of processes occurring in the mitochondrion, to generate high levels of ROS within the organelle and consequently cell death[3].
In Vivo: Although elesclomol (25-100 mg/kg) shows no antitumor activity in nude mouse xenograft models of human breast cancers (MDA435, MCF7 and ZR-75-1), lung cancer (RER) or lymphoma (U937). Elesclomol substantially enhances the efficacy of chemotherapeutic agents such as paclitaxel in these models, both in terms of tumor regression and extended survival of mice[4].

Name: Motesanib (Diphosphate) AMG 706 (Diphosphate), CAS: 857876-30-3, stock 37.7g, assay 98.8%, MWt: 569.44, Formula: C22H29N5O9P2, Solubility: DMSO : ≥ 110 mg/mL (193.17 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;c-Kit, Biological_Activity: Motesanib Diphosphate (AMG 706 Diphosphate) is a potent ATP-competitive inhibitor of VEGFR1/2/3 with IC50s of 2 nM/3 nM/6 nM, respectively, and has similar activity against Kit, and is approximately 10-fold more selective for VEGFR than PDGFR and Ret.
IC50 & Target: IC50: 2 nM (VEGFR1), 3 nM (VEGFR2), 6 nM (VEGFR3)[1]
In Vitro: Motesanib Diphosphate (AMG 706 Diphosphate) has broad activity against the human VEGFR family, and displays over 1000-fold selectivity against EGFR, Src, and p38 kinase.Motesanib Diphosphate (AMG 706 Diphosphate) significantly inhibits VEGF-induced cellular proliferation of HUVECs with an IC50 of 10 nM, while displaying little effect at bFGF-induced proliferation with an IC50 of >3,000 nM. Motesanib Diphosphate (AMG 706 Diphosphate) also potently inhibits PDGF-induced proliferation and SCF-induced c-kit phosphorylation with IC50 of 207 nM and 37 nM, respectively, but not effective against the EGF-induced EGFR phosphorylation and cell viability of A431 cells[1]. Although displaying little antiproliferative activity on cell growth of HUVECs alone, Motesanib Diphosphate (AMG 706 Diphosphate) treatment significantly sensitizes the cells to fractionated radiation[2].
In Vivo: Motesanib Diphosphate (AMG 706 Diphosphate) (100 mg/kg) significantly inhibits VEGF-induced vascular permeability in a time-dependent manner. Oral administration of Motesanib twice daily or once daily potently inhibits, in a dose-dependent manner, VEGF-induced angiogenesis using the rat corneal model with ED50 of 2.1 mg/kg and 4.9 mg/kg, respectively. Motesanib Diphosphate (AMG 706 Diphosphate) induces a dose-dependent tumor regression of established A431 xenografts by selectively targeting neovascularization in tumor cells[1]. Motesanib Diphosphate (AMG 706 Diphosphate) in combination with radiation displays significant anti-tumor activity in head and neck squamous cell carcinoma (HNSCC) xenograft models[2]. Motesanib Diphosphate (AMG 706 Diphosphate) treatment also induces significant dose-dependent reductions in tumor growth and blood vessel density of MCF-7, MDA-MB-231, or Cal-51 xenografts, which can be markedly enhanced when combined with docetaxel or tamoxifen[3].

Name: PHA-680632, CAS: 398493-79-3, stock 29.4g, assay 98.6%, MWt: 501.62, Formula: C28H35N7O2, Solubility: DMSO : ≥ 30 mg/mL (59.81 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: PHA-680632 is an aurora kinase inhibitor with IC50s of 27, 135 and 120 nM for aurora A, B and C, respectively.
IC50 & Target: IC50: 27 nM (Aurora A), 135 nM (Aurora B), 120 nM (Aurora C)[1]
In Vitro: PHA-680632 shows 30- to 200-fold higher IC50s of FLT3, LCK, PLK1, STLK2, VEGFR2, and VEGFR3 compared with Aurora A. PHA-680632 has potent antiproliferative activity in a wide range of cell types. The IC50s are 0.32, 0.41, 0.06, 1.17, 0.56, 0.62, 0.29, 0.11, 1.56, 0.62, 0.07, 0.13, 0.41 μM for C33A, HeLa, HCT116, HT29, LOVO, A549, MCF7, A2780, U2OS, DU145, U937, HL60, NHDF. PHA-680632 can cause polyploidy in tumor cells. PHA-680632 cell treatment induces phenotypes similar to Aurora A or B depletion[1]. PHA680632, inhibits colony formation in different cancer cell lines and induced polyploidy. Aurora-A inhibition by PHA680632 enhances radiation response in cancer cells, especially in p53-deficient cells[2].
In Vivo: PHA-680632 suppresses tumor growth in animal models. PHA-680632 treatment at 45 mg/kg dose results in 85% of TGI without signs of toxicity in the HL60 human acute myelogenous leukemia xenograft model. PHA-680632 treatment at 60 mg/kg i.v. b.i.d. for 5 days results in 78% of TGI without signs of toxicity in the A2780 human ovarian carcinoma model[1]. PHA680632 in association with radiation leads to an additive effect in cancer cells, especially in the p53-deficient cells, but does not act as a radiosensitiser[2].

Name: Neflamapimod VX-745, CAS: 209410-46-8, stock 17.2g, assay 98.8%, MWt: 436.26, Formula: C19H9Cl2F2N3OS, Solubility: DMSO : 13.08 mg/mL (29.98 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: Neflamapimod (VX-745) is a potent, blood-brain barrier penetrant, highly selective inhibitor of p38α inhibitor with an IC50 for p38α of 10 nM and for p38β of 220 nM. Neflamapimod (VX-745) possesses anti-inflammatory activity.
In Vitro: Neflamapimod (VX-745) exhibits PBMC IL-1β and TNFα IC50 values of 45 and 51 nM, respectively. Neflamapimod is also effective in whole blood, blocking IL-1β and TNFα release with IC50 values of 150 and 180 nM, respectively[1]. 
Neflamapimod shows a promising selectivity profile, with 20-fold selectivity for p38α over p38β (Ki=220 nM)[1]. 
Neflamapimod (VX-745) solutions in DMSO/DMEM inhibits the IL-6 production with IC50 of 15±9 nM[2]. 
Neflamapimod (VX-745; 5.0 nM) displays potent activity and 1000-fold selectivity over closely related kinases, including ERK1, JNK1-3 and MK2. Neflamapimod (10 nM-50 μM) increasingly inhibits the anisomycin-induced activity of p38α[3]. 
Neflamapimod (VX-745; 0.06 μM-20 μM) inhibits IL-6 and VEGF secretion in BMSCs. Neflamapimod can inhibit cytokine (TNF-α, IL-6, VEGF)-induced paracrine MM cell growth, survival, and drug resistance in the BM microenvironment. Neflamapimod induces modest growth inhibition of MM.1S, RPMI8226, and U266 cell lines in a dose-dependent fashion, with inhibitory concentration of 50% (IC50) of 10 μM[4].
In Vivo: Neflamapimod (VX-745; 2.5, 5, and 10 mg/kg) improves the inflammatory scores in mice by 27%, 31%, and 44%, respectively[1]. Neflamapimod (VX-745; 1.06 mg/kg) significantly decreases the inflammation score from 2.07±0.29 for the control group to 1.42±0.06[2].

Name: SP600125, CAS: 129-56-6, stock 2.3g, assay 98.7%, MWt: 220.23, Formula: C14H8N2O, Solubility: DMSO : ≥ 45 mg/mL (204.33 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Apoptosis;Autophagy;Apoptosis, Target: JNK;Apoptosis;Autophagy;Ferroptosis, Biological_Activity: SP600125 is a cell-permeable, reversible, and ATP-competitive JNK inhibitor with IC50s of 40, 40 and 90 nM for JNK1, JNK2 and JNK3, respectively.
IC50 & Target: IC50: 40/40/90 nM (JNK1/2/3)[1]
In Vitro: SP600125 is an ATP-competitive inhibitor of JNK2 with a Ki value of 0.19±0.06 μM. SP600125 inhibits the phosphorylation of c-Jun with IC50 of 5 μM to 10 μM in Jurkat T cells. In CD4+ cells, such as Th0 cells isolated from either human cord or peripheral blood, SP600125 blocks cell activation and differentiation and inhibits the expression of inflammatory genes COX-2, IL-2, IL-10, IFN-γ, and TNF-α, with IC50 of 5 μM to 12 μM[1]. In a mouse beta cells MIN6, SP600125 (20 μM) induces the phosphorylation of p38 MAPK and its downstream CREB-dependent promoter activation[2]. In HCT116 cells, SP600125 (20 μM) blocks the G2 phase to mitosis transition and induces endoreplication. This ability of SP600125 is independent of JNK inhibition, but due to its inhibition of CDK1-cyclin B activation upstream of Aurora A and Polo-like kinase 1[3].
In Vivo: Administration of SP600125 at 15 or 30 mg/kg i.v. significantly inhibits TNF-α serum levels, whereas oral administration dose-dependently blocks TNF-α expression with significant inhibition observed at 30 mg/kg per os[1]. SP600125 attenuates LPS-induced ALI in rats in vivo. The expression levels of TNF-α and IL-6 in the BALF in rats in the SP600125 group are significantly decreased[4].

Name: Orantinib SU6668; TSU-68, CAS: 252916-29-3, stock 11.2g, assay 98.3%, MWt: 310.35, Formula: C18H18N2O3, Solubility: DMSO : ≥ 28 mg/mL (90.22 mM), Clinical_Informat: Phase 3, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Apoptosis;VEGFR;PDGFR;FGFR, Biological_Activity: Orantinib (SU6668; TSU-68) is a multi-targeted receptor tyrosine kinase inhibitor with Kis of 2.1 μM, 8 nM and 1.2 μM for Flt-1, PDGFRβ and FGFR1, respectively.
In Vitro: Orantinib (SU6668; 0.03-10 μM) shows inhibitory activity against tyrosine phosphorylation of KDR in VEGF stimulated HUVECs, and also blocks PDGF-stimulated PDGFRβ tyrosine phosphorylation in NIH-3T3 cells overexpressing PDGFRβ. Orantinib (≥10 μM) inhibits acidic FGF-induced phosphorylation of the FGFR1 substrate 2. However, Orantinib (up to 100 μM) has no effect on EGF-stimulated EGFR tyrosine phosphorylation in NIH-3T3 cells overexpressing EGFR. Furthermore, Orantinib inhibits VEGF-driven and FGF-driven mitogenesis of HUVECs with mean IC50 of 0.34 μM and 9.6 μM, respectively[1]. In human myeloid leukemia MO7E cells, Orantinib (SU6668) inhibits the tyrosine autophosphorylation of stem cell factor (SCF) receptor, c-kit, with IC50 of 0.1-1 μM, as well as ERK1/2 phosphorylation. In addition, Orantinib suppresses SCF-induced proliferation of MO7E cells with an IC50 of 0.29 μM, and induces apoptosis[2].
In Vivo: Orantinib (SU6668; 75-200 mg/kg) causes tumor growth inhibition on several tumor types in xenograft models in athymic mice, such as A375, Colo205, H460, Calu-6, C6, SF763T, and SKOV3TP5 cells. Orantinib (75 mg/kg) also inhibits tumor angiogenesis of C6 glioma xenografts[1]. In a tumor model of HT29 human colon carcinoma, Orantinib (200 mg/kg) decreases the average vessel permeability and average fractional plasma volume in the tumor rim and core. Orantinib enhances abnormal stromal development at the periphery of carcinomas[3]. Moreover, Orantinib (TSU-68; 200 mg/kg) augments the effect of chemotherapeutic infusion in a rabbit VX2 liver tumor model[4].

Name: Pimasertib AS703026;MSC1936369B, CAS: 1236699-92-5, stock 19.9g, assay 98.3%, MWt: 431.20, Formula: C15H15FIN3O3, Solubility: DMSO : ≥ 100 mg/mL (231.91 mM), Clinical_Informat: Phase 2, Pathway: MAPK/ERK Pathway, Target: MEK, Biological_Activity: Pimasertib (AS703026) is a highly selective, potent, ATP non-competitive allosteric inhibitor of MEK1/2, used for cancer treatment.
In Vitro: Pimasertib (5, 0.5, and 0.1 μM) specifically blocks ERK1/2 activation in MM cells, cultured alone or with BMSCs. Pimasertib inhibits the growth of MM cell lines in a dose-dependent manner, with IC50s ranging from 0.005 to 2 μM. The IC50s of Pimasertib against INA-6, U266, H929 cells are 10 nM, 5 nM, 200 nM respectively. Pimasertib induces apoptosis and modulates the cell cycle profile. Pimasertib targets MM cells in the BM microenvironment[1]. Pimasertib (10 μmol/L) inhibits ERK pathway, proliferation, and transformation in cetuximab-resistant D-MUT cells[2]. Pimasertib in combination with PLX4032 significantly induces apoptosis of RPMI-7951 cells, whereas each drug used alone does not. Pimasertib synergizes with small interfering RNA-mediated downregulation of BRAF to produce results similar to those of combined treatment with PLX4032 and Pimasertib[3].
In Vivo: Pimasertib (15, 30 mg/kg) significantly inhibits the growth of tumor in the human H929 MM xenograft model in CB17 SCID mice[1]. Pimasertib (10 mg/kg, p.o.) inhibits tumor growth of cetuximab-resistant tumor attributed by K-ras mutation[2].

Name: SB 525334, CAS: 356559-20-1, stock 16.8g, assay 98.5%, MWt: 343.42, Formula: C21H21N5, Solubility: DMSO : ≥ 46 mg/mL (133.95 mM), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: SB 525334 is a potent and selective transforming growth factor β1 receptor (ALK5) inhibitor with an IC50 of 14.3 nM.
IC50 & Target: IC50: 14.3 nM (ALK5)[1]
In Vitro: SB525334 (1 μM; for 15 minutes before stimulating with 0.625 ng/ml of TGF-β1, assesses after 6 days) inhibits TGF-β1-mediated proliferation of familial idiopathic pulmonary arterial hypertension (iPAH) pulmonary artery smooth muscle cells (PASMCs) at an IC50 of 295 nM [2].
In Vivo: SB525334 (3-30 mg/kg; p.o.; daily from days 17 to 35) significantly reverses pulmonary arterial pressure in a rat model of pulmonary arterial hypertension (PAH)[2].

Name: SU 5402, CAS: 215543-92-3, stock 12.2g, assay 98.3%, MWt: 296.32, Formula: C17H16N2O3, Solubility: DMSO : ≥ 30 mg/mL (101.24 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;FGFR, Biological_Activity: SU 5402 is a potent multi-targeted receptor tyrosine kinase inhibitor with IC50 of 20 nM, 30 nM, and 510 nM for VEGFR2, FGFR1, and PDGFRβ, respectively.
IC50 & Target: IC50: 20 nM (VEGFR2), 30 nM (FGFR1), 510 nM (PDGFRβ)[1]
In Vitro: SU 5402 is cocrystallized with the catalytic domain of FGF-R1 (flg-1) and is found to inhibit tyrosine phosphorylation of VEGF-R2 (Flk-1/KDR) and PDGF-R in NIH 3T3 cells with IC50 values of 0.4 and 60.9 μM, respectively[1]. In order to investigate whether phosphorylation of PKM2 and LDHA is mediated in FGFR1-specific manner, FTC-133 are treated with receptor tyrosine kinase inhibitors Dovitinib and SU 5402 (SU-5402). Dovitinib treatment results in significant decrease of phosphorylation status at a concentration of 100 nM after four hours of incubation for both PKM2 and LDHA. No significant changes are seen when administered at concentrations of 1 nM and 10 nM. SU 5402 administration leads to a sigificant decrease of PKM2 and LDHA phosphorylation at a concentration of 20 μM[2].
In Vivo: Inhibition of FGFR1 with SU 5402 (SU5402) administered to ΔF508-CFTR homozygous mice results in partial ΔF508-CFTR rescue, as shown by an increase in saliva secretion, a surrogate "sweat test" assay in mice. As salivary secretion is often sex dependent, only male mice are chosen for these experiments. Our results indicate that treatment of the ΔF508-CFTR mice with SU 5402 restores the saliva secretion level to ~10% of that observed for the wild-type CFTR mice, which suggests that SU 5402 can have therapeutic benefits to Cystic Fibrosis (CF)[3]. The selective FGFR1 inhibitor SU 5402 (SU5402) prevents and/or reverses PH induced by MCT (monocrotaline) in rats. In rats treated with SU 5402 on days 21 to 42 after the MCT injection, evaluations on day 42 show marked decreases in pulmonary artery pressure (PAP), RV/(LV+S), and distal artery muscularization compare with rats treated with the vehicle (saline)[4].

Name: Cabozantinib (S-malate) XL184 (S-malate);BMS-907351 (S-malate), CAS: 1140909-48-3, stock 1.1g, assay 98.8%, MWt: 635.59, Formula: C32H30FN3O10, Solubility: DMSO : ≥ 23 mg/mL (36.19 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK, Target: Apoptosis;VEGFR, Biological_Activity: Cabozantinib S-malate (XL184 S-malate) is a potent multiple receptor tyrosine kinases inhibitor that inhibits VEGFR2, c-Met, Kit, Axl and Flt3 with IC50s of 0.035, 1.3, 4.6, 7 and 11.3 nM, respectively.
IC50 & Target: IC50: 0.035 nM (VEGFR-2 (KDR)), 1.3 nM (c-Met), 4 nM (Ret), 4.6 nM (Kit), 12 nM (Flt-1), 11.3 nM (Flt-2), 6 nM (Flt-3), 14.3 nM (Tie2), 7 nM (AXL)
In Vitro: Cabozantinib (0.1-0.5μM) inhibits the constitutive and inducible MET phosphorylation and its resultant downstream signaling in all MPNST cells. Cabozantinib (> 0.1μM) elicits a significant MPNST cell growth inhibition; higher Cabozantinib doses are needed to inhibit NSC growth. Cabozantinib treatment blocks HGF-induced MPNST motility and invasion (a similar effect of found on NSC)[2]. In cellular assays, cabozantinib inhibits phosphorylation of MET and VEGFR2, as well as KIT, FLT3, and AXL with IC50 values of 7.8, 1.9, 5.0, 7.5, and 42 μM, respectively. Cabozantinib also inhibits tubule formation in response to conditioned media derived from cultures of MDA-MB-231 (IC50=5.1 nM), A431 (IC50=4.1 nM), HT1080 (IC50=7.7 nM), and B16F10 (IC50=4.7 nM) cells[3].
In Vivo: Cabozantinib (60 mg/kg, i.p.) decreases the tumor vascularity with reductions ranging from 67% at 3 mg/kg to 83% at 30 mg/kg for 7 days in animals. Tumors in RIP-Tag2 mice treated for 7 days beginning at age 10 weeks are 40% smaller after XL880 and 35% smaller after Cabozantinib, compared to corresponding values for vehicle[1]. Cabozantinib (30 mg/kg) significantly decreases the microvessel density in mice[2]. Cabozantinib (100 mg/kg, p.o.) inhibits in vivo stimulation of MET phosphorylation by HGF in liver hepatocytes and VEGF-stimulated phosphorylation of FLK1 with inhibition of both targets sustained through 8 hours postdose. Cabozantinib (100 mg/kg, p.o.) disrupts tumor vasculature and promotes tumor and endothelial cell death. Cabozantinib (1-60 mg/kg, p.o.) inhibits tumor growth and promotes tumor regression in vivo[3].

Name: HMN-214 IVX-214, CAS: 173529-46-9, stock 19.8g, assay 98.7%, MWt: 424.47, Formula: C22H20N2O5S, Solubility: DMSO : 25 mg/mL (58.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Polo-like Kinase (PLK), Biological_Activity: HMN-214, an orally bioavailable prodrug of HMN-176, is an inhibitor of polo-like kinase-1 (plk1), with antitumor activity.
IC50 & Target: PLK1[2][4]
In Vitro: HMN-214 is a prodrug of HMN-176. HMN-176 shows potent activities against 22 human tumor cell lines, with a mean IC50s of 118 nM[1]. HMN-176 (3-300 nM) inhibits luciferase expression driven by the MDR1 promoter in a dose dependent manner in HeLa cells. HMN-176 (30-3000 nM) also dose-dependently suppresses complex formation on the Y-box[3]. HMN-214 (3.3 μM) enhances luciferase expression relative to vehicle control with the 1,4C-1,4Bis polymer (11-fold) and PEI (37-fold) in PC3-PSMA cells. HMN-214 (≥ 3.3 μM) significantly reduces cell proliferation, causes considerable changes in cell morphology in MB49 cells[4].
In Vivo: HMN-214 (33 mg/kg, p.o.) converts to HMN-176 in rats. HMN-214 has no effect on the conduction velocity and the amplitude of action potentials in the aciatic and tibial nerves. HMN-214 (20 mg/kg, p.o.) exhibits antitumor activity in mice[1]. HMN-214 (10, 20 mg/kg, p.o.) decreases MDR1 mRNA expression in nude mice bearing KB- and KB-A.1.-derived tumors[3].

Name: PIK-93, CAS: 593960-11-3, stock 39g, assay 98.6%, MWt: 389.88, Formula: C14H16ClN3O4S2, Solubility: DMSO : ≥ 150 mg/mL (384.73 mM), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR;Anti-infection, Target: PI3K;PI4K;Virus Protease, Biological_Activity: PIK-93 is the first potent, synthetic PI4K (PI4KIIIβ) inhibitor with IC50 of 19 nM, and also inhibits PI3Kγ and PI3Kα with IC50 of 16 nM and 39 nM, respectively.
IC50 & Target: IC50: 19 nM (PI4KIIIβ), 39 nM (p110α), 16 nM (p110γ), 590 nM (p110β), 120 nM (p110δ), 140 nM (PI3KC2β), 64 nM (DNA-PK)[1]
In Vitro: PIK-93 inhibits PI3Kγ and PI4KIIIβ, with IC50 values of 16 nM and 19 nM, respectively. PIK-93 also inhibits other members of PI3Ks, including PI3Kα, β, and δ, with IC50 values of 39 nM, 0.59 μM, and 0.12 μM, respectively. PIK-93 shows no obvious inhibitory effect against a panel of other kinases, even at a concentration of 10 μM[1]. In differentiated HL60 (dHL60) cells, PIK-93 (0.5 μM-1 μM) impairs consolidation and stability of the leading edge formed after treatment with uniform f-Met-Leu-Phe (fMLP). PIK-93 alters the localization, but not the amount, of the fMLP-dependent accumulation of total F-actin. In fMLP gradients, PIK-93 reduces the chemotactic index and triples the cells' turning frequency[2]. In COS-7 cells, PIK-93 (250 nM) effectively abrogates the accumulation of CERT-PH domain and FL-Cer in Golgi. PIK-93 of the same concentration also significantly inhibits the conversion of [3H]serine-labeled endogenous ceramide to sphingomyelin. These facts indicate a key role of PI4KIIIβ in ceramide transport between the ER and Golgi, as well as in the regulation of spingomyelin synthesis[3]. In T6.11 cells, PIK-93 (300 nM) reduces carbachol-induced translocation of TRPC6 to the plasma membrane and net Ca2+ entry[4]. A recent report shows that PIK-93 has anti-enterovirus effects, as revealed by its inhibition of both poliovirus (PV) and hepatitis C virus (HCV) replication, with EC50 values of 0.14 µM and 1.9 µM, respectively[5].

Name: Ponatinib AP24534, CAS: 943319-70-8, stock 25.6g, assay 98%, MWt: 532.56, Formula: C29H27F3N6O, Solubility: DMSO : ≥ 50 mg/mL (93.89 mM), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy;Protein Tyrosine Kinase/RTK, Target: Src;VEGFR;Bcr-Abl;PDGFR;Autophagy;FGFR, Biological_Activity: Ponatinib (AP24534) is an orally active multi-targeted kinase inhibitor with IC50s of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM, and 5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively.
IC50 & Target: IC50: 0.37 nM (Abl), 0.24 nM (Lyn), 1.1 nM (PDGFRα), 1.5 nM (VEGFR2), 2.2 nM (FGFR1), 5.4 nM (Src)[1]
In Vitro: Ponatinib (AP24534) potently inhibits native ABL (IC50: 0.37 nM), ABLT315I (IC50: 2.0 nM), and other clinically important ABL kinase domain mutants (IC50: 0.30-0.44 nM). Ponatinib also inhibits SRC (IC50: 5.4 nM) and members of the VEGFR, FGFR, and PDGFR families of receptor tyrosine kinases. Ponatinib potently inhibits proliferation of Ba/F3 cells expressing native BCR-ABL (IC50: 0.5 nM). All BCR-ABL mutants tested remained sensitive to Ponatinib (IC50: 0.5-36 nM) including BCR-ABLT315I (IC50: 11 nM)[1]. 
Ponatinib inhibits the in vitro kinase activity of FLT3, KIT, FGFR1, and PDGFRα with IC50 values of 13, 13, 2, and 1 nM, respectively. Ponatinib inhibits phosphorylation of all 4 RTKs in a dose-dependent manner, with IC50 values between 0.3 to 20 nM. Consistent with these activated receptors being important in driving leukemogenesis Ponatinib also potently inhibits the viability of all 4 cell lines with IC50 values of 0.5 to 17 nM. In contrast, the IC50 for inhibition of RS4;11 cells which express native (unmutated) FLT3, is more than 100 nM[2]. 
In Vivo: In a survival model in which mice are instead injected with Ba/F3 BCR-ABLT315I cells, administration of Dasatinib at doses as high as 300 mg/kg has no effect on survival time. By contrast, treatment with Ponatinib (AP24534) prolongs survival in a dose-dependent manner. Ponatinib dosed orally for 19 days at 5, 15, and 25 mg/kg prolongs median survival to 19.5, 26, and 30 days, respectively compare to 16 days for vehicle-treated mice (p<0.01 for all three dose levels). The anti-tumor activity of Ponatinib (AP24534) is further assessed in a xenograft model in which Ba/F3 BCR-ABLT315I cells are injected subcutaneously into mice. Tumor growth is inhibited by Ponatinib in a dose-dependent manner compare to vehicle-treated mice, with significant suppression of tumor growth upon daily oral dosing at 10 and 30 mg/kg (%T/C = 68% and 20%, respectively; p<0.01 for both dose levels). Daily oral dosing of 50 mg/kg Ponatinib causes significant tumor regression (%T/C = 0.9%, p<0.01), with a 96% reduction in mean tumor volume at the final measurement compared to the start of treatment. Ponatinib is well tolerated at all efficacious dose levels for the duration of the study; maximal decreases in body weight are <5%, <5%, and <12% for the 10, 30, and 50 mg/kg dose groups, respectively, with no signs of overt toxicity[1]. 
Ponatinib (1-25 mg/kg) is administered orally, once daily for 28 days, to mice bearing MV4-11 xenografts. Ponatinib potently inhibits tumor growth in a dose-dependent manner. Administration of 1 mg/kg, the lowest dose tested, leads to significant inhibition of tumor growth (TGI=46%, P<0.01) and doses of 2.5 mg/kg or greater results in tumor regression[2].

Name: Chelerythrine Chloride, CAS: 3895-92-9, stock 26.2g, assay 98.3%, MWt: 383.82, Formula: C21H18ClNO4, Solubility: DMSO : 4.35 mg/mL (11.33 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;TGF-beta/Smad;Epigenetics;Autophagy;Apoptosis, Target: Apoptosis;PKC;PKC;Autophagy;Bcl-2 Family, Biological_Activity: Chelerythrine Chloride is a potent, cell-permeable inhibitor of protein kinase C, with an IC50 of 660 nM. Chelerythrine Chloride inhibits the BclXL-Bak BH3 peptide binding with IC50 of 1.5 μM and displaces Bax from BclXL. Chelerythrine Chloride induces apoptosis and autophagy.
IC50 & Target: IC50: 660 nM (protein kinase C)
In Vitro: Chelerythrine inhibits the BclXL-Bak BH3 peptide binding with IC50 of 1.5 μM and displaces Bax, a BH3-containing protein, from BclXL. Mammalian cells treated with Chelerythrine undergoes apoptosis with characteristic features that suggest involvement of the mitochondrial pathway[1]. Chelerythrine treatment inhibits LPS-induced TNF-α level and NO production in LPS-induced murine peritoneal macrophages through selective inhibition of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) activation. Moreover, the effects of chelerythrine on NO and cytokine TNF-α production can possibly be explained by the role of p38 MAPK and ERK1/2 in the regulation of inflammatory mediators expression[2]. Chelerythrine shows cytotoxic effect on the human monocytic leukaemia cells with LD50 value of 3.46 μM. Two hours after LPS stimulation, cells influenced by sanguinarine and Chelerythrine significantly decline the CCL-2 expression by a factors of 3.5 and 1.9[3]. Chelerythrine chloride significantly enhances the phosphorylation of ERK1/2 in a dose-dependent manner. In addition, chelerythrine chloride inhibits the phosphorylation of p38[4].
In Vivo: Chelerythrine displays significant anti-inflammatory effects in experimentally induced mice endotoxic shock model in vivo through inhibition of LPS-induced tumor necrosis factor-alpha (TNF-α) level and nitric oxide (NO) production in serum[2]. Chelerythrine chloride (5 mg/kg/day, i.p.) induces apoptosis of RCC cells without significant toxicity to mice. Chelerythrine Chloride treatment leads to a dose-dependent accumulation of p53[4].

Name: CCT129202, CAS: 942947-93-5, stock 4g, assay 98.3%, MWt: 497.02, Formula: C23H25ClN8OS, Solubility: DMSO : 1 mg/mL (2.01 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: CCT129202 is an aurora kinase inhibitor with IC50s of 42, 198, and 227 nM for aurora A, B and C, respectively.
IC50 & Target: IC50: 142 nM (Aurora A), 198 nM (Aurora B), 227 nM (Aurora C)[1]
Ki: 49.8 nM (Aurora A)[1]
In Vitro: CCT129202 causes the accumulation of human tumor cells with z4N DNA content, leading to apoptosis. CCT129202 is found to induce apoptosis with GI50 values that ranges between 0.08 and 1.7 μM. CCT120202-treated human tumor cells shows a delay in mitosis, abrogation of nocodazole-induced mitotic arrest, and spindle defects. CCT129202 Causes p21Up-regulation, Rb Hypophosphorylation, and H2F-DependentTK1Down-regulation[1].
In Vivo: Growth of HCT116 xenografts in nude mice is inhibited after i.p. administration of CCT129202. p21, the cyclin-dependent kinase inhibitor, is induced by CCT129202. Up-regulation of p21 by CCT129202 in HCT116 cells led to Rb hypophosphorylation and E2F inhibition, contributing to a decrease in thymidine kinase 1 transcription[1].

Name: CP-673451, CAS: 343787-29-1, stock 15.6g, assay 98.1%, MWt: 417.50, Formula: C24H27N5O2, Solubility: DMSO : ≥ 100 mg/mL (239.52 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: PDGFR, Biological_Activity: CP-673451 is a potent and selective inhibitor of PDGFR with IC50s of 10 and 1 nM for PDGFRα and PDGFRβ, respectively.
IC50 & Target: IC50: 10 nM (PDGFR-α), 1 nM (PDGFR-β)[4]
In Vitro: CP-673451 efficiently suppresses the PDGFR downstream signaling pathway. It inhibits phosphorylation of Akt, GSK-3β, p70S6, and S6 in A549 cells in a concentration-dependent manner. CP-673451 (0.0625-4 μM) significantly reduces the viability of NSCLC cell lines A549 and H1299 in a time- and concentration-dependent manner, with IC50s of 0.49 and 0.61 μM, respectively. CP-673451 (1, 4 μM) induces apoptosis in non-small-cell lung cancer cells. CP-673451 (25, 100, or 400 nM) is effective at inhibiting migration and invasion of NSCLC cells by suppression of lamellipodia formation[1]. CP-673451 and crenolanib show selective lethality toward cells with CA. U2OS cells treated with 1 to 4 μM CP-673451 or crenolanib show a ruffled cell surface as a sign for alterations of the cortical actin cytoskeleton. CP-673451 attenuates PDGF-BB-induced signaling, and significantly enhances the phosphorylation of PDGFR-β downstream effectors, Akt and MEK[2]. CP-673,451 (0.5 μM) regulates cell proliferation through mechanisms involving reduced phosphorylation of GSK-3α and GSK-3β. CP-673,451 impairs rhabdosphere-forming capacity in both RD and RUCH2 cultures[3]. CP-673,451 inhibits PDGFR-β in PAE-β cells with an IC50 value of 6.4 nM. Besides, CP-673,451 incubation in H526 and PAE-β cells results in an IC50 value of 1.1 μM against c-kit[4].
In Vivo: CP-673451 (20 mg/kg) leads to a medium suppression of tumor growth, while high-dose CP-673451 (40 mg/kg) strongly inhibits tumor growth in mice without significant weitht loss[1]. CP-673,451 (10, 33, and 100 mg/kg, p.o., b.i.d) inhibits the growth of Colo205 tumor in a dose-dependent manner, and similar tumor growth inhibition experiments completes on LS174T, H460, and U87MG xenografts, with no signs of morbidity or weight loss[4].

Name: Ralimetinib dimesylate LY2228820 dimesylate, CAS: 862507-23-1, stock 36.7g, assay 98.8%, MWt: 612.74, Formula: C26H37FN6O6S2, Solubility: DMSO : 61 mg/mL (99.55 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: MAPK/ERK Pathway;Apoptosis;Autophagy, Target: p38 MAPK;Apoptosis;Autophagy, Biological_Activity: Ralimetinib dimesylate (LY2228820 dimesylate) is a selective, ATP-competitive inhibitor of p38 MAPK α/β with IC50s of 5.3 and 3.2 nM, respectively. Ralimetinib (LY2228820) selectively inhibits phosphorylation of MK2 (Thr334), with no effect on phosphorylation of p38a MAPK, JNK, ERK1/2, c-Jun, ATF2, or c-Myc.
IC50 & Target: IC50: 5.3 nM (p38 MAPK α), 3.2 nM (p38 MAPK β)[3]
In Vitro: Ralimetinib dimesylate inhibits p38α, as well as the level of phosphoMAPKAPK-2 (pMK2) in RAW 264.7 cells, with IC50 values of 7 nM and 34.3 nM, respectively. Furthermore, Ralimetinib dimesylate inhibits lipopolysaccharide (LPS)-induced TNFα formation in murine peritoneal macrophages, with IC50 of 5.2 nM[1]. In multiple myeloma (MM) cells, including INA6, RPMI-8226, U266, and RPMI-Dox40, Ralimetinib dimesylate (LY2228820) (200 nM-800 nM) significantly blocks p38MAPK signaling, as revealed by its inhibition on phosphorylation of HSP27, a downstream target of p38MAPK, without affecting the expression level of HSP27. Ralimetinib dimesylate (200 nM-400 nM) enhances bortezomib-induced cytotoxicity and apoptosis, but Ralimetinib dimesylate alone doesn't inhibit the growth of MM.1S cells. Ralimetinib dimesylate (200 nM-800 nM) also inhibits secretion of IL-6 and MIP-1α in long-term BM stromal cells (LT-BMSCs), BM mononuclear cells (BMMNCs), peripheral blood (PB) CD138+, CD138- or PB CD14+ cells. Ralimetinib dimesylate (400 nM-800 nM) also blocks osteoclastogenesis from CD14+ cells[2].
In Vivo: In LPS-induced mice, Ralimetinib dimesylate effectively inhibits the formation of TNFα with a threshold minimum 50% effective dose (TMED50) less than 1 mg/kg. In a rat model of collagen-inducedarthritis (CIA), Ralimetinib dimesylate displays potent effects on paw swelling, bone erosion, and cartilage destruction, with a threshold minimum 50% effective dose (TMED50)of 1.5 mg/kg[1]. Ralimetinib dimesylate inhibits tumor phospho-MK2 in a dose-dependent manner (TED50=1.95 mg/kg, TED70=11.17 mg/kg) in mice implanted with B16-F10 melanoma. Ralimetinib dimesylate inhibits MK2 phosphorylation: mouse in vivo TED50=1.01 mg/kg (compound exposure approximately 100 nM) and human ex vivo IC50=0.12 μM with either mouse or human PBMC[3].

Name: Perifosine KRX-0401;NSC 639966;D21266, CAS: 157716-52-4, stock 2.4g, assay 98.2%, MWt: 461.66, Formula: C25H52NO4P, Solubility: H2O : ≥ 153.33 mg/mL (332.13 mM); DMSO : < 1 mg/mL (insoluble or slightly soluble); DMF : < 1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: Apoptosis;Akt;Autophagy, Biological_Activity: Perifosine is an oral Akt inhibitor. All cells are sensitive to the antiproliferative properties of Perifosine with an IC50 of ~0.6-8.9 μM.
IC50 & Target: Akt[1]
In Vitro: The IC50 for growth of Ntv-a/LacZ cell lines is determined by MTT assay. When the cells are cultured for 48 hours in 10% FCS-supplemented media, the IC50 for cells with constitutively active PDGF, Ras, or Akt signaling is similar and found to be ~45 μM[1].Perifosine, a oral-bioavailable alkylphospholipid (ALK), on the cell cycle kinetics of immortalized keratinocytes (HaCaT) as well as head and neck squamous carcinoma cells. Proliferation is assessed by the incorporation of [3H]thymidine into cellular DNA. Exposure to Perifosine (0.1-30 μM) for 24 h results in a dose-dependent inhibition of [3H]thymidine uptake in all cell lines tested. The IC50s for growth are between 0.6 and 8.9 μM, reaching IC80s of ~10 μM. Perifosine blocks cell cycle progression of head and neck squamous carcinoma cells at G1-S and G2-M by inducing p21WAF1, irrespective of p53 function, and may be exploited clinically because the majority of human malignancies harbor p53 mutations. Perifosine (20 μM) induces both G1-S and G2-M cell cycle arrest, together with p21WAF1 expression in both p53 wild-type and p53-/- clones[2].
In Vivo: Mice are identified with tumors by bioluminescence imaging and either treated them with 100 mg/kg Temozolomide, or 30 mg/kg Perifosine, or a combination with 100 mg/kg Temozolomide and 30 mg/kg Perifosine (Temozolomide+Perifosine) for 3 to 5 days. The mice are sacrificed and tumors analyzed histologically for cell proliferation by Ki-67 immunostaining. Ki-67 staining index is significantly reduced in mice treated with either Temozolomide (Ki-67 staining index=5.5±1.2%, n=4, P=0.0019) or Perifosine (Ki-67 staining index=3.2±1.1%, n=3, P=0.001) compared with Control, demonstrating the inhibitory effect on proliferation. Most importantly, the tumors treated with Temozolomide+Perifosine have the lowest Ki-67 staining index (1.7±1.2%, n=3, P=0.0005). The additional treatment with Perifosine results in a significantly lower proliferation rate than Temozolomide alone (P=0.0087)[1]. Perifosine markedly decreases p-Akt from 10 min to 24 hours and subsequently, moderately decreased p-S6 from 1h to 24 h after injection[3].

Name: ENMD-2076 (Tartrate), CAS: 1291074-87-7, stock 3g, assay 98%, MWt: 525.56, Formula: C25H31N7O6, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage;Epigenetics;Protein Tyrosine Kinase/RTK, Target: Src;VEGFR;FLT3;PDGFR;Aurora Kinase;Aurora Kinase;FGFR, Biological_Activity: ENMD-2076 Tartrate is a multi-targeted kinase inhibitor with IC50s of 1.86, 14, 58.2, 15.9, 92.7, 70.8, 56.4 nM for Aurora A, Flt3, KDR/VEGFR2, Flt4/VEGFR3, FGFR1, FGFR2, Src, PDGFRα, respectively.
IC50 & Target: IC50: 1.86 nM (Aurora A), 14 nM (Flt3), 58.2 nM (KDR/VEGFR2), 15.9 nM (Flt4/VEGFR3), 92.7 nM (FGFR1), 70.8 nM (FGFR2), 20.2 nM (Src), 56.4 nM (PDGFRα)[1]
In Vitro: ENMD-2076 is selective toward Aurora A versus Aurora B (IC50=350 nM). ENMD-2076 inhibits HUVEC growth with an IC50 value of 0.15 mM. Against 10 human leukemia cell lines, the IC50 values range from 0.025 to 0.53 mM. Within this panel, MV4:11 cells are the most sensitive cells by a factor of greater than 4. The lymphoma-derived U937 cell line treated with ENMD-2076 shows that the ENMD-2076 induces a dose-dependent increase in G2-M-phase arrest as well as the induction of apoptosis. ENMD-2076 inhibits cellular Flt3 ligand (FL)-induced Flt3 autophosphorylation in THP-1 cells, which have been shown to express FL-responsive wild-type Flt- 3 (18) with an IC50 value of 28 nM. ENMD-2076 inhibits stem cell factor (SCF)-induced Kit autophosphorylation in MO7e cells with an IC50 value of 40 nM. ENMD-2076 inhibits VEGFR2/KDR autophosphorylation with an IC50 value of 7 nM[1].
In Vivo: ENMD-2076 treatment results in statistically significant, dose dependent inhibition of tumor growth or tumor regression. Moreover, there is no correlation between tumor growth rate and antitumor efficacy, which would conceivably be expected for a mitotic kinase inhibitor, as fast growing (e.g., A375 melanoma) and slow-growing (e.g., HT29 colon carcinoma) tumors are similarly inhibited by ENMD-2076. ENMD-2076 is well tolerated at daily doses up to 302 mg/kg (equivalent to 200 mg/kg of the free base), with no weight loss or signs of morbidity noted in any study at this dose with the exception of the A375 model[1].

Name: Quizartinib AC220, CAS: 950769-58-1, stock 24.4g, assay 99%, MWt: 560.67, Formula: C29H32N6O4S, Solubility: DMSO : ≥ 33 mg/mL (58.86 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Autophagy, Target: FLT3;Autophagy, Biological_Activity: Quizartinib (AC220) is a potent Flt3 tyrosine kinase inhibitor with a Kd of 1.6±0.7 nM.
IC50 & Target: Kd: 1.6±0.7 nM (Flt3)[1]
In Vitro: Quizartinib (AC220) is a novel compound expressly optimized as a FLT3 inhibitor for the treatment of acute myeloid leukemia (AML). Quizartinib inhibits FLT3-WT and FLT3-ITD autophosphorylation with IC50 of 4.2±0.3 nM and 1.1±0.1 nM, respectively. Quizartinib inhibits MV4-11 and A375 cells with IC50 of 0.56±0.3 nM and >10 000 nM, respectively. Quizartinib inhibits FLT3 with low nanomolar potency in cellular assays and is highly selective when screened against the majority of the human protein kinome[1].
In Vivo: Quizartinib (AC220) inhibits FLT3 activity in vivo, significantly extends survival in a mouse model of FLT3-ITD AML at doses as low as 1 mg/kg when dosed orally once a day, eradicates tumors in a FLT3-dependent mouse xenograft model at 10 mg/kg, and potently inhibits FLT3 activity in primary patient cells. The oral bioavailability of Quizartinib, determined in rats by comparing oral and intravenous pharmacokinetics at 3 mg/kg, is approximately 40%. A single 10 mg/kg dose of Quizartinib is administered by oral gavage, and mice are killed at 2 time points after dosing, using groups of 4 animals each. Quantitation of total FLT3 and phospho-FLT3 in tumor samples revealed time-dependent inhibition of FLT3 autophosphorylation. FLT3 activity is inhibited by 90% at 2 hours, and 40% at 24 hours after administration. The extent of inhibition therefore correlated well with the expected free Quizartinib plasma levels, based on pharmacokinetic experiments[1].

Name: Vinorelbine KW-2307 base, CAS: 71486-22-1, stock 24g, assay 98.5%, MWt: 778.93, Formula: C45H54N4O8, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Autophagy, Target: Microtubule/Tubulin;Microtubule/Tubulin;Autophagy, Biological_Activity: Vinorelbine is an anti-mitotic agent which inhibits the proliferation of Hela cells with IC50 of 1.25 nM.
In Vitro: Vinorelbine (0.5-5 nM) inhibits cell proliferation by 50% (IC50) at concentrations of 1.25 nM. At concentration of 8 nM vinorelbine, no cells are in anaphase[1]. Vinorelbine time-dependently induces the p53 and p21WAFI/CIP1 expression in androgen-dependent (AD) and- independent (AI) prostate cancer cell lines. Vinorelbine stimulates reporter genes in a concentration-dependent manner[2].
In Vivo: After vinorelbine treatment, the first neutropenicepisode occurred after the first (4 dogs), second (1), or sixth(1) vinorelbine treatment in the dogs[3]. Vinorelbine is tolerated at a weekly interval in tumor-bearing cats, with an MTD of 11.5 mg/m2[4].

Name: Hesperadin, CAS: 422513-13-1, stock 17.4g, assay 98.3%, MWt: 516.65, Formula: C29H32N4O3S, Solubility: DMSO : ≥ 100 mg/mL (193.55 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Epigenetics;Autophagy;Anti-infection;Anti-infection, Target: Aurora Kinase;Aurora Kinase;Autophagy;Influenza Virus;Parasite, Biological_Activity: Hesperadin is an ATP-competitive inhibitor of aurora B kinase with an IC50 of 250 nM.
IC50 & Target: IC50: 250 nM (Aurora B)[1]
In Vitro: Hesperadin also inhibits other kinases such as AMPK, Lck, MKK1, MAPKAP-K1, CHK1, and PHK at 1 µM drug concentration. Hesperadin causes polyploidy in HeLa cells. Hesperadin-treated HeLa cells show alignment and segregation defects, but sister chromatid separation is intact. Hesperadin causes defects in mitosis and cytokinesis. Hesperadin inhibits Aurora B. Immunofluorescence microscopy reveals that Hesperadin-treated cells in which chromosomes are stretched toward opposite poles, i.e., which have entered anaphase, fail to assemble a central spindle and to properly localize the human centralspindlin subunits CYK-4 and MKLP1[1]. Hesperadin inhibits multiple human clinical isolates of influenza A and B viruses with single to submicromolar efficacy, including oseltamivir-resistant strains. Mechanistic studies reveal that hesperadin inhibits the early stage of viral replication by delaying the nuclear entry of viral ribonucleoprotein complex, thereby inhibiting viral RNA transcription and translation as well as viral protein synthesis[2]. Hesperadin inhibits cell cell proliferation due to appearance of multiple mitotic defects caused by Aurora B activity reduction and elimination of checkpoint proteins--such as hBUBR1 and CENP-E--from kinetochores of mitotic chromosomes[3].

Name: BIX02188, CAS: 334949-59-6, stock 5.4g, assay 98.4%, MWt: 412.48, Formula: C25H24N4O2, Solubility: DMSO : ≥ 45 mg/mL (109.10 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;MAPK/ERK Pathway, Target: ERK;ERK;MEK, Biological_Activity: BIX02188 is a potent MEK5-selective inhibitor with an IC50 of 4.3 nM. BIX02188 inhibits ERK5 catalytic activity, with an IC50 of 810 nM.
IC50 & Target: IC50: 4.3 nM (MEK5), 810 nM (ERK5)[2]
In Vitro: BIX02188 is a potent inhibitor of catalytic function of purified, active MEK5 enzyme. In activated HeLa cells, BIX02188 blocks phosphorylation of ERK5, without affecting phosphorylation of ERK1/2, JNK and p38 MAP kinases. To characterize the effects of BIX02188 in cultured endothelial cells (EC), H2O2 is used to activate BMK1. Bovine lung microvascular endothelial cells (BLMECs) are pretreated with 0.1-10 μM BIX02188 for 30 min, and then stimulated with 300 μM H2O2. BMK1 is dramatically activated by H2O2, with peak at 20 min. Phosphorylated BMK1 is inhibited by BIX02188 in a dose-dependent manner, with an IC50=0.8±1.0 μM, and maximal inhibition at concentrations >3 μM. To examine the specificity of BIX02188, The effect of 0.1-10 μM BIX02188 is measured on the activity of ERK1/2 and JNK. There is no significant inhibition of ERK1/2 and JNK at these concentrations. These observations confirm the selectivity of BIX02188 for MEK5-induced BMK1 phosphorylation[1]. BIX02188 inhibits MEK5 and ERK5 activity, with IC50s of 4.3 nM and 810 nM, respectively. BIX02188 does not inhibit closely related kinases MEK1, MEK2, ERK2, and JNK2. BIX02188 inhibits ERK5 phosphorylation in a dose dependent manner[2]. To assess the proliferation of podocytes in response to the pro-fibrotic stimulus of TGFβ1, podocytes are pre-incubated in the presence and absence of BIX02188 (10 μM) for 60 min after which cells are co-treated with TGFβ1 (2.5 ng/mL) for 48 h to provide adequate time for proliferation to occur and a colorimetric cell proliferation assay is employed where metabolic activity is directly proportional to cell number. Inhibition of Erk5 activation with BIX02188 incubation reduces podocyte cell number. TGFβ1 stimulation increases podocyte cell number which is prevented following BIX02188 co-treatment[3].

Name: BIX02189, CAS: 1265916-41-3, stock 25.1g, assay 98.6%, MWt: 440.54, Formula: C27H28N4O2, Solubility: DMSO : ≥ 49.4 mg/mL (112.14 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;MAPK/ERK Pathway, Target: ERK;ERK;MEK, Biological_Activity: BIX02189 is a potent and selective MEK5 inhibitor with an IC50 of 1.5 nM. BIX02189 also inhibits ERK5 catalytic activity with an IC50 of 59 nM.
IC50 & Target: IC50: 1.5 nM (MEK5), 59 nM (ERK5)[1]
In Vitro: BIX02189 blocks phosphorylation of ERK5, without affecting phosphorylation of ERK1/2 in sorbitol-stimulated HeLa cells. BIX02189 inhibits ERK5 phosphorylation in a dose dependent manner[1]. Fluvastatin reduces advanced glycation endproduct (AGE)-induced vascular smooth muscle cells (VSMCs) proliferation. To confirm this effect, VSMCs are treated with AGEs in the presence or absence of Fluvastatin and then subject to MTT assay. AGEs are found to dose-dependently induce cell proliferation, and this is significantly suppressed by Fluvastatin. In addition to MTT assay, the similar results are got with cell counting. This suppressive effect of Fluvastatin is prevented when VSMCs are pretreated with BIX02189. Whether ERK5 activation can reduce proliferation is also examined by using Ad-CA-MEK5α encoding a constitutively active mutant form of MEK5α (an upstream kinase of ERK5). AGE-induced proliferation determined by both MTT assay and cell counting is significantly diminished in the presence of Ad-CA-MEK5α, and Nrf2 depletion using siRNA restored AGE-induced proliferation[2].
In Vivo: Mice are treated with either 10 mg/kg of BIX02189 (in 25% DMSO) or vehicle control (same volume of 25% DMSO) by intraperitoneal injection. The nuclear localization of Nrf2 is inhibited in aortic endothelial cells from mice treated with BIX02189[3].

Name: Vemurafenib PLX4032;RG7204;RO5185426, CAS: 918504-65-1, stock 35g, assay 98.3%, MWt: 489.92, Formula: C23H18ClF2N3O3S, Solubility: DMSO : 6.2 mg/mL (12.66 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: MAPK/ERK Pathway;Autophagy, Target: Raf;Autophagy, Biological_Activity: Vemurafenib (PLX4032; RG7204) is a first-in-class, selective, potent inhibitor of B-RAF kinase, with IC50s of 31 and 48 nM for RAFV600E and c-RAF-1, respectively.
IC50 & Target: IC50: 31 nM (BRAFV600E), 48 nM (c-RAF-1)
In Vitro: Vemurafenib (PLX4032) selectively blocks the RAF/MEK/ERK pathway in BRAF mutant cells[1]. RG7204 is a potent inhibitor of proliferation in those expressing RAFV600E but not BRAFWT in 17 melanoma cell lines. Vemurafenib (RG7204) induces MEK and ERK phosphorylation at high concentrations in CHL-1 cells[2]. Ectopic expression of EGFR in melanoma cells is sufficient to cause resistance to PLX4032[3].
In Vivo: Vemurafenib (PLX4032, 20, 25, 75 mg/kg, p.o.) causes dose-dependent inhibition of tumor growth, with higher exposures resulting in tumor regression of BRAF mutant xenografts[1]. RG7204 (12.5, 25, and 75 mg/kg, p.o.) significantly inhibits tumor growth and induced tumor regression in mice bearing LOX tumor xenografts[2].

Name: AZD8330 ARRY-424704;ARRY-704, CAS: 869357-68-6, stock 23.7g, assay 98.5%, MWt: 461.23, Formula: C16H17FIN3O4, Solubility: DMSO : ≥ 100 mg/mL (216.81 mM), Clinical_Informat: Phase 1, Pathway: MAPK/ERK Pathway, Target: MEK, Biological_Activity: AZD8330 (ARRY-424704) is a potent, uncompetitive MEK1/MEK2 inhibitor, with an IC50 of 7 nM.
IC50 & Target: IC50: 7 nM (MEK1/MEK2)[1]
In Vitro: AZD8330 is a selective allosteric MEK1/ MEK2 inhibitor. Exposing human osteosarcoma cell lines MOS, U2OS, and 143B to a concentration of 0.5 μM of Trametinib, AZD8330 or TAK-733 for 6 hours, leads to loss of ERK phosphorylation indicating effective MEK inhibition.The activity of these three inhibitors is tested using concentration ranges in six osteosarcoma cell lines: MOS, U2OS, KPD, ZK58, 143b and Saos-2. All three inhibitors decrease viability of MOS and U2OS and strongly affect 143b. By contrast, viability of KPD, ZK58 and Saos-2 is not affected by any of the three inhibitors[2].
In Vivo: In tumour xenograft models, AZD8330 demonstrates dose-dependent tumour growth inhibition of approximately 90% at tolerated doses (1.0 mg/kg once daily [OD])[1].

Name: AT7867, CAS: 857531-00-1, stock 7g, assay 98.3%, MWt: 337.85, Formula: C20H20ClN3, Solubility: DMSO : 10 mg/mL (29.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK;PI3K/Akt/mTOR;MAPK/ERK Pathway, Target: PKA;PKA;Akt;Ribosomal S6 Kinase (RSK), Biological_Activity: AT7867 is a potent ATP-competitive inhibitor of Akt1/Akt2/Akt3 and p70S6K/PKA with IC50s of 32 nM/17 nM/47 nM and 85 nM/20 nM, respectively.
IC50 & Target: IC50: 32 nM/17 nM/47 nM (Akt1/Akt2/Akt3), 85 nM/20 nM (p70S6K/PKA)[1]
In Vitro: The inhibition of AKT2 by AT7867 is shown to be ATP-competitive with a Ki of 18nM. AT7867 also displays potent activity against the structurally related AGC kinases p70S6K and PKA, but shows a clear window of selectivity against kinases from other kinase sub-families. In vitro growth inhibition studies show that AT7867 blocks proliferation in a number of human cancer cell lines. AT7867 appears to be most potent at inhibiting proliferation in MES-SA uterine, MDA-MB-468 and MCF-7 breast, and HCT116 and HT29 colon lines (IC50 values range from 0.9-3 μM), and least effective in the two prostate lines tested (IC50 values range from 10-12 μM) [1].
In Vivo: In vivo: Following oral administration at 20 mg/kg, the elimination of AT7867 from plasma appears to be similar to that observed after i.v. administration. Plasma levels of AT7867 remain above 0.5 μM for at least 6 hours following an oral dose of 20 mg/kg. Assuming linear pharmacokinetics following i.v. administration, the bioavailability by the oral route is calculated to be 44%. In vivo pharmacodynamic (PD) biomarker studies are therefore performed with this model. Following pharmacokinetic and tolerability studies, doses of AT7867 (90 mg/kg p.o. or 20 mg/kg i.p.) are administered to athymic mice bearing MES-SA tumors and the phosphorylation status of GSK3β and S6RP in tumors is monitored over time. Clear inhibition of phosphorylation of the two markers of pathway activity is seen at 2 and 6 hours following treatment with AT7867. By 24 hours, total levels of both GSK3β and S6RP are greatly reduced[1].

Name: Doramapimod BIRB 796, CAS: 285983-48-4, stock 15.8g, assay 98.1%, MWt: 527.66, Formula: C31H37N5O3, Solubility: DMSO : ≥ 100 mg/mL (189.52 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: MAPK/ERK Pathway;MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Raf;Autophagy, Biological_Activity: Doramapimod (BIRB 796) is an orally active, highly potent p38 MAPK inhibitor, which has an IC50 for p38α=38 nM, for p38β=65 nM, for p38γ=200 nM, and for p38δ=520 nM. Doramapimod (BIRB 796) has picomolar affinity for p38 kinase (Kd=0.1 nM). Doramapimod (BIRB 796) also inhibits B-Raf with an IC50 of 83 nM.
IC50 & Target: IC50: 4 nM (p38α), 83 nM (B-Raf)[1]
In Vitro: Doramapimod (BIRB 796) is usually associated with inflammation because of its role in T-cell proliferation and cytokine production[1]. 
Doramapimod (BIRB 796) blocks the stress-induced phosphorylation of the scaffold protein SAP97, further establishing that this is a physiological substrate of SAPK3/p38γ. The binding of Doramapimod to the p38 MAPKs or JNK1/2 is impairing their phosphorylation by the upstream kinase MKK6 or MKK4[3].
In Vivo: The mean xenograft weigh of Doramapimod (BIRB 796) is lighter than control. The inhibition rate of Doramapimod is 1.93%[4]. 
The Doramapimod (BIRB 796) treatment slightly reduces blood pressure (166±7 mm Hg at week 7; P<0.05), whereas SD rats are normotensive (123±3 mm Hg). Despite the reduction in blood pressure, untreated and Doramapimod-treated dTGRs have similar heart weight and cardiac hypertrophy indices (heart-to-tibia ratio), which are significantly higher compare with nontransgenic SD rats (310±6 versus 307±6 versus 206±5 mg/cm, respectively; P<0.05)[5].

Name: KRN-633, CAS: 286370-15-8, stock 17.9g, assay 98.2%, MWt: 416.86, Formula: C20H21ClN4O4, Solubility: DMSO : ≥ 8 mg/mL (19.19 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: VEGFR, Biological_Activity: KRN-633 is a potent VEGFR inhibitor with IC50s of 170, 160 and 125 nM for VEGFR1, VEGFR2 and VEGFR3, respectively.
IC50 & Target: IC50: 170 nM (VEGFR1), 160 nM (VEGFR2), 125 nM (VEGFR3)[1]
In Vitro: KRN-633 inhibits tyrosine phosphorylation of VEGFR-1, VEGFR2, c-Kit, and PDGFR-β (IC50=11.7, 1.16, 8.01, 130 nM) in human umbilical vein endothelial cells. KRN-633 also inhibits the VEGF-driven proliferation of HUVECs (IC50=14.9 nM). KRN-633 suppresses capillary tube formation of endothelial cells[1].
In Vivo: KRN-633 inhibits tumor growth in several tumor xenograft models with diverse tissue origins, including lung, colon, and prostate, in athymic mice and rats. KRN-633 also causes the regression of some well-established tumors and those that have regrown after the cessation of treatment. KRN-633 is well tolerated and has no significant effects on body weight or the general health of the animals. Histologic analysis of tumor xenografts treated with KRN-633 reveals a reduction in the number of endothelial cells in non-necrotic areas and a decrease in vascular permeability[1].

Name: KU-60019, CAS: 925701-46-8, stock 14.2g, assay 98.2%, MWt: 547.67, Formula: C30H33N3O5S, Solubility: DMSO : ≥ 30 mg/mL (54.78 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;PI3K/Akt/mTOR, Target: ATM/ATR;ATM/ATR, Biological_Activity: KU-60019 is an improved ATM kinase-specific inhibitor with IC50 of 6.3 nM.
IC50 & Target: IC50: 6.3 nM (ATM)[1]
In Vitro: KU-60019 is an improved analogue of KU-55933. KU-55933 has an IC50 of 13 nM and Ki of 2.2 nM in vitro and is highly specific for the ATM kinase using a panel of 60 protein kinases. KU-60019 is an improved inhibitor of the ATM kinase with an IC50 of 6.3 nM, approximately half that of KU-55933. The IC50 values for DNA-PKcs and ATR are 1.7 and >10 μM, respectively, almost 270-and 1600-fold higher than for ATM. KU-60019 is 10-fold more effective than KU-55933 at blocking radiation-induced phosphorylation of key ATM targets in human glioma cells. In human U87 glioma cells, KU-55933 completely inhibits phosphorylation of p53 (S15) at 10 μM but not at 3 μM, whereas γ-H2AX levels are only partly reduced with 10 μM 1 h after irradiation. By comparison, 3 μM KU-60019 completely inhibits p53 phosphorylation and partial inhibits at 1 μM[1].
In Vivo: Despite PTEN-deficient control tumors reaching a 4-fold increase in size before PTEN wild-type controls, KU-60019-treated PTEN-deficient tumors display a statistically significant slowing in growth. This growth inhibition is especially evident at the start of the experiment (days 5-12) just after KU-60019 is administered (days 1-5)[2].

Name: PD318088, CAS: 391210-00-7, stock 36.3g, assay 98.2%, MWt: 561.09, Formula: C16H13BrF3IN2O4, Solubility: DMSO : ≥ 100 mg/mL (178.22 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MEK, Biological_Activity: PD318088 is an allosteric MEK inhibitor.
IC50 & Target: MEK[1][2]

Name: PHT-427, CAS: 1191951-57-1, stock 19.7g, assay 98.7%, MWt: 409.61, Formula: C20H31N3O2S2, Solubility: DMSO : 50 mg/mL (122.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR, Target: Apoptosis;Akt, Biological_Activity: PHT-247 is an inhibitor of the pleckstrin homology (PH) domain of Akt, and it is also an inhibitor of PDPK1 with Kis of 2.7 µM and 5.2 µM and for Akt and PDPK1, respectively.
IC50 & Target: Ki: 2.7 µM (Akt), 5.2 µM (PDPK1)[1]
In Vitro: The effects of PHT-427 on cell signaling are investigated by RPPA using a panel of 86 antibodies to phospho- and non-phosphorylated signaling protein related to PtdIns-3-K/PDPK1/Akt signaling in PC-3 prostate cells where PtdIns-3-K/PDPK1/Akt signaling is activated because of homozygous PTEN mutation. After 16 hours, a reduction is observed in phospho-Ser241-PDPK1 phospho-Thr308-Akt by both 10 µM PH-427 and 0.1 µM Wortmannin. Finally, phospho-Ser657-protein kinase C (PKC) and total SGK1 are decreased by treatment with both PHT-427 and Wortmannin. These results suggest that at 10 µM PHT-427 inhibits both Akt and PDKP1. The BxPC-3 and MiaPaCa-2 pancreatic cancer cell lines are probed by Western blotting following up to 24 hr exposure to 10 µM PHT-427, which is below the IC50 for cell growth inhibition of around 30 µM, to determine the effects of PHT-427 on of the PtdIns-3-K/PDPK1/Akt signaling pathway components[1].
In Vivo: Mice with BxPC-3 pancreatic, MCF-7 breast or A-549 NSCL cancer xenografts are administered PHT-427, or its analogs with a C-4, C-6 or C-8 alkyl chain by oral gavage twice a day for 10 days. The results show that PHT-427 has the greatest antitumor activity with the C-8 chain analog having less activity, and analogs with a C-4 or C-6 chain very little activity. All further antitumor studies are conducted using compound PHT-427. Plasma levels of PHT-427 following oral administration to mice of a dose of 200 mg/kg show rapid absorption, without a lag phase, Cmax is 8.2 µg/mL 1 hr following dosing, and the elimination half-life is 1.4 hr with a terminal PHT-427 concentration of 0.1 µg/mL 10 hr after dosing. The plasma concentration of PH-427 is above the level which gave inhibition of Akt and PDPK1 signaling in cells of 10 µM (4 µg/mL) for at least 3 hr[1].

Name: TWS119, CAS: 601514-19-6, stock 7.8g, assay 98.8%, MWt: 318.33, Formula: C18H14N4O2, Solubility: DMSO : ≥ 50 mg/mL (157.07 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR;Autophagy, Target: GSK-3;GSK-3;Autophagy, Biological_Activity: TWS119 is a specific inhibitor of GSK-3β, with an IC50 of 30 nM, and activates the wnt/β-catenin pathway.
IC50 & Target: IC50: 30 nM (GSK-3β)[1]
In Vitro: TWS119 induces neuronal differentiation in P19 EC cells and primary mouse ESCs. TWS119 binds to GSK-3β with KD of 126 nM, and modulates the activity of the complex, triggering downstream transcriptional events that lead the neuronal induction[1]. TWS119 (< 4 μM) significantly enhances the proliferation and survival of γδT cells via activation of the mammalian target of rapamycin (mTOR) pathway, upregulation of the expression of anti-apoptotic protein Bcl-2 and inhibition of cleaved caspase-3. TWS119 (0-8 μM) induces the generation of CD62L+γδT or CCR5+γδT cell phenotypes. TWS119 (0.5, 1.0 and 2 μM) increases the expression level of granzyme B in a dose-dependent manner. TWS119 also enhances the cytolytic activity of γδT cells against tumour cells in vitro[3].
In Vivo: TWS119 (30 mg/kg, i.p.) improves the neurologic function and decreases neurologic deficit dcore in rtPA-treated MCAO rats. TWS119 effectively relieves cerebral edema, and reduces cerebral infarction in rats treated with rtPA. TWS119 also effectively decreases blood-brain barrier permeability in rtPA-Treated MCAO Rats and attenuates rtPA-induced hemorrhage in ischemic brain tissue. Futhermore, TWS119 activates the Wnt/β-Catenin signaling pathway and increases the expression of Claudin-3 and ZO-1[2].

Name: Fasudil (Hydrochloride) HA-1077 (Hydrochloride);AT-877 (Hydrochloride), CAS: 105628-07-7, stock 11.4g, assay 99%, MWt: 327.83, Formula: C14H18ClN3O2S, Solubility: DMSO : ≥ 31 mg/mL (94.56 mM); H2O : 55 mg/mL (167.77 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK;Membrane Transporter/Ion Channel;TGF-beta/Smad;Epigenetics;TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage;Autophagy;Anti-infection;Neuronal Signaling, Target: PKA;PKA;Calcium Channel;PKC;PKC;ROCK;ROCK;ROCK;Autophagy;HIV;Calcium Channel, Biological_Activity: Fasudil Hydrochloride (HA-1077 Hydrochloride; AT877 Hydrochloride), is a nonspecific ROCK inhibitor and also has inhibitory effect on protein kinases, with an Ki of 0.33 μM for ROCK1, IC50s of 0.158 μM and 4.58 μM, 12.30 μM, 1.650 μM for ROCK2 and PKA, PKC, PKG, respectively[1]. Fasudil Hydrochloride is also a potent Ca2+ channel antagonist and vasodilator[2].
IC50 & Target: Ki: 0.33 μM (ROCK1), 1.0 μM (PKA), 9.3 μM (PKC), 55 μM (MLCK)[8]
In Vitro: Fasudil Hydrochloride (100 μM) inhibits cell spreading, the formation of stress fibers, and expression of α-SMA with concomitant suppression of cell growth in rat HSCs and human HSC-derived TWNT-4 cells[4].
Fasudil Hydrochloride (50-100 μM; 24 hours) inhibits the LPA-induced phosphorylation of ERK1/2, JNK, and p38 detected by western blotting in rat HSCs and human HSC-derived TWNT-4 cells[4].
Fasudil Hydrochloride (25-100 μM; 24 hours) suppresses transcription of collagen and TIMP, stimulates transcription of MMP-1 in human HSC-derived TWNT-4 cells[4].
In Vivo: Fasudil (30 μg) increases CBF by 50% via intra-coronary injection to dogs. Fasudil (0.01, 0.03, 0.1 and 0.3 mg/kg, bolus, i.v.) decreases MBP and increases HR, VBF, CBF, RBF, and FBF. Fasudil (1.0 ng/mL) increases cardiac output. Fasudil via i.v. produces a significant fall in MBP, left ventricular systolic pressure and total peripheral resistance with an increase in HR and cardiac output, but without obvious effect on right atrial pressure, dP/dt or left ventricular minute work in dogs[3]. Fasudil exhibits protectable effects on cardiovascular disease and reduces the activation of JNK and attenuates mitochondrial-nuclear translocation of AIF under ischemic injury[6]. Fasudil (100 mg/kg/day, p.o.) significantly reduces incidence and mean maximum clinical score of EAE in SJL/J mice immunized with PLP p139-151. Fasudil inhibits the proliferative response of splenocytes to the antigen in mice. Fasudil decreases inflammation, demyelination, axonal loss and APP positivein spinal cord of Fasudil-treated mice via p.o. administration[7].

Name: VER-82576 NVP-BEP800, CAS: 847559-80-2, stock 0.9g, assay 98.6%, MWt: 480.41, Formula: C21H23Cl2N5O2S, Solubility: DMSO : 6.2 mg/mL (12.91 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: VER-82576 (NVP-BEP800) is a potent, orally available and selective Hsp90 inhibitor, with an IC50 of 58 nM for Hsp90β; VER-82576 also slightly blocks Grp94 and Trap-1, with IC50s of 4.1 and 5.5 μM, respectively.
IC50 & Target: IC50: 58 nM (Hsp90β), 4.1 μM (Grp94), 5.5 μM (Trap-1)[1]
In Vitro: VER-82576 (NVP-BEP800) is a potent and selective Hsp90 inhibitor, with an IC50 of 58 nM for Hsp90β and is >70-fold selective against Grp94 and Trap-1, with IC50s of 4.1 ± 1.1 and 5.5 ± 0.48 μM. VER-82576 potently inhibits the proliferation of tumor cells, with GI50s ranging from 38 nM in A375 cells to 1050 nM in PC3 cells, with an average GI50 of 245 nM. VER-82576 (250-1250 nM) depletes client proteins in human cancer cell lines in vitro[1]. VER-82576 (NVP-BEP800; 200 nM) shows no significant effect on the ionizing radiation (IR) dose-response curves of A549 cells, and is less toxic to SNB19 cells. VER-82576 in combination with IR results in more severe DNA damage in both A549 and SNB19 cell lines than each treatment alone and also protracts the kinetics of DNA damage repair in SNB19 cells[2]. VER-82576 (NVP-BEP800; 0.05, 0.1 or 0.2 μM) dose-dependently decreases the viability and induces apoptosis of glioblastoma cells. VER-82576 (0.2 μM) suppresses the expression of IKKβ protein but does not alter the levels of IKKβ mRNA in T98G cells. VER-82576 (0.2 μM) suppresses the expression of heat shock protein 70[3].
In Vivo: VER-82576 (NVP-BEP800; 15 or 30 mg/kg, p.o.) shows antitumor activities in A375 cancer xenografts and BT-474 xenograft-bearing mice[1].

Name: BMS 777607 BMS 817378, CAS: 1025720-94-8, stock 22.8g, assay 98%, MWt: 512.89, Formula: C25H19ClF2N4O4, Solubility: DMSO : ≥ 39 mg/mL (76.04 mM), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;TAM Receptor, Biological_Activity: BMS 777607 is a Met-related inhibitor for c-Met, Axl, Ron and Tyro3 with IC50s of 3.9 nM, 1.1 nM, 1.8 nM and 4.3 nM, respectively, and 40-fold more selective for Met-related targets than Lck, VEGFR-2, and TrkA/B, with more than 500-fold greater selectivity versus all other receptor and non receptor kinases.
IC50 & Target: IC50: 3.9 nM (c-Met), 1.1 nM (Axl), 1.8 nM (Ron), 4.3 nM (Tyro3)
In Vitro: BMS 777607 is a selective ATP-competitive Met kinase inhibitor which potently blocks the autophosphorylation of c-Met with IC50 of 20 nM in GTL-16 cell lysates, and demonstrates selective inhibition of proliferation in Met-driven tumor cell lines, such as GTL-16 cell line, H1993 and U87[1]. BMS 777607 inhibits hepatocyte growth factor (HGF)-triggered c-Met autophosphorylation with IC50 of < 1 nM in PC-3 and DU145 prostate cancer cells. BMS 777607 has little effect on tumor cell growth, but exhibits inhibitory effect on HGF-induced cell scattering in PC-3 and DU145 cells, with almost complete inhibition at 0.5 μM. BMS 777607 also suppresses stimulated cell migration and invasion in a dose-dependent fashion (IC50 < 0.1 μM) in both cell lines[2]. Application of BMS 777607 (appr 10 μM) to the highly metastatic murine KHT cells for 2 hours potently eliminates basal levels of autophosphorylated c-Met with IC50 of 10 nM without affecting the total c-Met, leading to dose-dependent inhibition of phosphorylation of downstream signaling molecules including ERK, Akt, p70S6K and S6. Treatment with BMS 777607 (appr 1 μM) for 24 hours potently inhibits the KHT cell scatter, motility and invasion at doses in the nanomolar range which consists with MET gene knockdown, and modestly affects cell proliferation and colony formation[3].

In Vivo: Oral administration of BMS 777607 (6.25-50 mg/kg) significantly reduces tumor volumes of the GTL-16 human tumor xenografts in athymic mice with no observed toxicity[1]. Administration of BMS 777607 (25 mg/kg/day) decreases the number of KHT lung tumor nodules (28.3%), improves the morphological hemorrhage, and significantly impairs the metastatic phenotype in the 6-8 week-old female C3H/HeJ mice injected with rodent fibrosarcoma KHT cells without apparent systemic toxicity compared to the control treatment. A low dose of BMS 777607 (10 mg/kg) also offers a mild but not significant inhibition of lung nodule formation compared to the vehicle control[3].

Name: GSK1292263, CAS: 1032823-75-8, stock 14.1g, assay 98.8%, MWt: 456.56, Formula: C23H28N4O4S, Solubility: DMSO : ≥ 30 mg/mL (65.71 mM), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: GPR119;GPR119, Biological_Activity: GSK1292263 is a novel GPR119 receptor agonist used for the treatment of type 2 diabetes.
IC50 value:
Target: GPR119
in vitro: GSK-1292263 is selected from 1538 compounds by using Hypo1, the Fit-Value and Estimate of GSK-1292263 that is aligned in Hypo1 are 8.8 and 7.7 (nM), respectively [1].
in vivo: GSK-1292263 administrated at a single dose of 3-30 mg/kg in the absence of nutrients correlates with increased levels of circulating gastrointestinal peptides, including glucagon-like peptide 1 (GLP-1), gastric inhibitory polypeptide (GIP), peptide YY (PYY) and glucagon in male Sprague-Dawley rats, the increase is enhanced following administration of glucose in the oral glucose tolerance test (OGTT). GSK-129226 significant increases in the peak insulin response and insulin AUC(0-15 min) of 30-60% compared with values in the vehicle control cohort in the intravenous glucose tolerance test in rats, this insulin upregulation correlated with a significant increase in the glucose disposal rate. GSK-1292263 is associated with a statistically significant increase in insulin immunoreactivity in pancreatic sections in a 6-week study performed in Zucker diabetic fatty rats, compared with insulin immunoreactivity in samples obtained from rats receiving vehicle control. GSK-1292263 administrated at dose of 10 or 30 mg/kg or vehicle control at 2 hours prior to insulin infusion in hyperinsulinemic-euglycemic clamps stimulates glucagon secretion without increasing blood glucose levels Sprague-Dawley rats [2].

Name: R406, CAS: 841290-81-1, stock 30.8g, assay 98.3%, MWt: 628.63, Formula: C28H29FN6O8S, Solubility: DMSO : ≥ 61 mg/mL (97.04 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Syk, Biological_Activity: R406 is a competitive Syk inhibitor for ATP binding with a Ki of 30 nM, potently inhibits Syk kinase activity in vitro with an IC50 of 41 nM, measured at an ATP concentration corresponding to its Km value.
IC50 & Target: Ki: 30 nM (Syk)[1]
 IC50: 41 nM (Syk)[1]
In Vitro: R406 also exhibits antagonistic activity for adenosine A3 receptor with an IC50 estimated to be 93 nM[1]. In Ramos B lymphoma cells, B-cell receptor (BCR) crosslinking induces robust phosphorylation of B-cell linker protein (BLNK), which is ablated by addition of the Syk inhibitor R406. Additionally, R406 significantly reduces constitutive Syk signaling in EBV+ cell lines derived from patients with Post-transplant lymphoproliferative disorder (PTLD), termed SLCL. Therefore, R406 inhibits Syk activation[2].
In Vivo: Prophylactic treatment of mice with R406 administers 1 h before immune complex challenge reduces the cutaneous reverse passive Arthus reaction by approximately 72 and 86% at 1 and 5 mg/kg, respectively, compared with the vehicle control. The net optical density reading of extravasated dye extracted after treatment with R406 at 1 or 5 mg/kg R406 is reduced from 0.14 (vehicle) to 0.04 or 0.02, respectively (p<0.01)[1].

Name: PI3K-IN-1 XL-147 derivative 1, CAS: 1349796-36-6, stock 23.7g, assay 98.5%, MWt: 599.66, Formula: C31H29N5O6S, Solubility: DMSO : 27.5 mg/mL (45.86 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: PI3K-IN-1 (XL-147 derivative 1) is a potent inhibitor of PI3K, more information can be found in patent WO2012103524 A2 and WO2013147649 A2.

Name: KW-2449, CAS: 1000669-72-6, stock 32.7g, assay 98.4%, MWt: 332.40, Formula: C20H20N4O, Solubility: DMSO : ≥ 50 mg/mL (150.42 mM), Clinical_Informat: Phase 1, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage;Epigenetics;Protein Tyrosine Kinase/RTK, Target: Apoptosis;Bcr-Abl;FLT3;Aurora Kinase;Aurora Kinase;FGFR, Biological_Activity: KW-2449 is a multi-targeted kinase inhibitor of FLT3, ABL, ABLT315I and Aurora kinase with IC50s of 6.6, 14, 4 and 48 nM, respectively.

IC50 & Target: IC50: 6.6 nM (FLT3), 14 nM (ABL), 4 nM (ABLT315I), 48 nM (Aurora kinase)[1]
In Vitro: KW-2449 shows growth inhibitory activities against FLT3/ITD-, FLT3/D835Y-, and wt-FLT3/FL-expressing 32D cells, MOLM-13 and MV4;11 with GI50 values of 0.024, 0.046, 0.014, 0.024, and 0.011 μM, respectively. KW-2449 suppresses the phosphorylations of FLT3 (P-FLT3) and its downstream molecule phospho-STAT5 (P-STAT5) in MOLM-13 cells in a dose-dependent manner. KW-2449 increases the percentage of cells in the G1 phase of the cell cycle and reciprocally reduced the percentage of cells in the S phase, resulting in the increase of apoptotic cell population[1].
In Vivo: Oral administration of KW-2449 shows dose-dependent and significant tumor growth inhibition in FLT3-mutated xenograft model with minimum bone marrow suppression. In FLT3 wild-type human leukemia, it induces the reduction of phosphorylated histone H3, G2/M arrest, and apoptosis. In imatinib-resistant leukemia, KW-2449 contributes to release of the resistance by the simultaneous down-regulation of BCR/ABL and Aurora kinases. Furthermore, the antiproliferative activity of KW-2449 is confirmed in primary samples from AML and imatinib-resistant patients. The inhibitory activity of KW-2449 is not affected by the presence of human plasma protein, such as α1-acid glycoprotein[1].

Name: RAF265 CHIR-265, CAS: 927880-90-8, stock 5.9g, assay 98.9%, MWt: 518.41, Formula: C24H16F6N6O, Solubility: DMSO : ≥ 26 mg/mL (50.15 mM); Ethanol : 10 mg/mL (19.29 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;MAPK/ERK Pathway;Autophagy, Target: Apoptosis;VEGFR;Raf;Autophagy, Biological_Activity: RAF265 is a potent RAF/VEGFR2 inhibitor.
IC50 & Target: RAF[1] 
VEGFR2[1]
In Vitro: The MTT assay reveals that in HT29 and MDAMB231 cells, RAF265 alone shows significant activity with IC20 values of 1 to 3 μM and IC50 values of 5 to 10 μM. In A549 and HCT116 cells, IC20 values are 1 μM for both, but RAF265 concentrations up to 10 μM do not reach IC50 values. However, in the presence of 1 nM RAD001, the IC50 for RAF265 is 5 μM in A549 cells and 10 μM in HCT116 cells[1].
In Vivo: In single-compound efficacy studies, optimal dosing of RAD001 and RAF265 is 5 to 12 mg/kg daily and 30 mg/kg every two days, respectively. However, combination tolerability studies in nontumor-bearing mice defin dose-limiting toxicity as a 10% weight loss with the combination of RAD001 at a dose of 12 mg/kg daily and RAF265 at a dose of 20 mg/kg every two days. Therefore, the combination of RAF265 at a dose of 12 mg/kg qd and RAD001 at a dose of 12 mg/kg qd seems to be the maximal tolerated dose. RAD001 and RAF265 are both given at a dose of 12 mg/kg qd, alone or concurrently, over 6 days. After a 2-day stop, the compounds are given for another 6 days, and the treatment is then stopped. To confirm the potential of the combination of RAF265 and RAD001, the antitumor effect of the combination is tested in HCT116 xenografts (KRAS mut, PIK3CA mut). In HCT116 xenografts, RAD001 or RAF265 given alone shows 60% to 65% and 71% to 72% TVI%, respectively[1].

Name: SB-743921, CAS: 940929-33-9, stock 10.3g, assay 98.2%, MWt: 553.52, Formula: C31H34Cl2N2O3, Solubility: DMSO : ≥ 100 mg/mL (180.66 mM), Clinical_Informat: Phase 2, Pathway: Cytoskeleton;Cell Cycle/DNA Damage, Target: Kinesin;Kinesin, Biological_Activity: SB-743921 is a potent inhibitor of the mitotic kinesin KSP (Eg5), with a Ki of 0.1 nM.
IC50 & Target: Ki: 0.1 nM (Eg5)[1]
In Vitro: SB-743921 is a potent inhibitor of Eg5, with a Ki of 0.1 nM[1]. SB-743921 (1 nM) potently inhibits colony forming cell (CFC) formation of chronic myeloid leukemia (CML) primary cells, but exhibits slight inhibitory activities on the colony-forming ability of normal bone marrow progenitors. SB-743921 (1, 3 nM) induces apoptosis of CML primary CD34 + cells, and shows slight effect on normal CD34 + cells. SB-743921 (2 nM) in combination with imatinib displays additive anti-proliferative effect in KCL22 and CML CD34 + cells. Furthermore, SB-743921 overcomes imatinib resistance in CML cells. SB-743921 (0.5 nM, 1 nM, 3 nM) inhibits MEK/ERK and AKT signaling in CML cells[2].
In Vivo: SB-743921 has good oral bioavailability and pharmacokinetics and induces complete tumor regression in nude mice bearing lung cancer patient xenografts[3].

Name: BAY 61-3606 (dihydrochloride), CAS: 648903-57-5, stock 30.8g, assay 98.8%, MWt: 463.32, Formula: C20H20Cl2N6O3, Solubility: DMSO : 7.14 mg/mL (15.41 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK, Target: Apoptosis;Syk, Biological_Activity: BAY 61-3606 dihydrochloride is an orally available, ATP-competitive, reversible and highly selective Syk inhibitor with a Ki of 7.5 nM an IC50 of 10 nM[1]. BAY 61-3606 dihydrochloride reduces ERK1/2 and Akt phosphorylation in neuroblastoma cell[2]. BAY 61-3606 dihydrochloride induces a large decrease of Syk phosphorylation in K-rn cell lysates[3]. Bay 61-3606 dihydrochloride sensitizes TRAIL-induced apoptosis by downregulating Mcl-1 in breast cancer cells[4].
IC50 & Target: Ki: 7.5 nM (Syk)[1] 
IC50: 10 nM (Syk)[1]
In Vitro: BAY 61-3606 (0.01-10 μM ; 48 hours) significantly reduces the cell viability of SYK-positive SH-SY5Y and SYK-negative SK-N-BE cells in a dose-dependent matter. SH-SY5Y cells expressing high SYK levels are significantly more sensitive to BAY 61-3606 in comparison to SK-N-BEcells expressing very low or no SYK[2]. 
BAY 61-3606 (0.4 and 0.8 μM; 4 or 24 hours) inhibits SYK activity by reducing ERK1/2 and Akt phosphorylation in neuroblastoma cell SH-SY5Y[2]. 
BAY 61-3606 (2 μM; 2 hours) induces a large decrease of Syk phosphorylation in K-rn cell lysates[3].
In Vivo: Bay 61-3606 (50 mg/kg; administered twice a week for two weeks by intraperitoneal injection) alone leads to more efficacious reductions than that of TNF-related apoptosis-inducing ligand (TRAIL; 10 mg/kg) alone in MCF-7 tumor xenograft-bearing BALB/c nude mice. Bay 61-3606 administered in TRAIL combination significantly reduces the volume of the xenografted tumor[4].

Name: Torin 2, CAS: 1223001-51-1, stock 35.2g, assay 98.6%, MWt: 432.40, Formula: C24H15F3N4O, Solubility: DMSO : 25 mg/mL (57.82 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage;Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: DNA-PK;DNA-PK;Apoptosis;mTOR;Autophagy, Biological_Activity: Torin 2 is an mTOR inhibitor with EC50 of 0.25 nM for inhibiting cellular mTOR activity, and exhibits 800-fold selectivity over PI3K (EC50: 200 nM). Torin 2 also inhibits DNA-PK with an IC50 of 0.5 nM in the cell free assay. Torin 2 can suppress both mTORC1 and mTORC2.
IC50 & Target: EC50: 0.25 nM (cellular mTOR), 200 nM (cellular PI3K)[1] 
IC50: 2.81 nM (mTOR), 0.5 nM (DNA-pK), 5.67 nM (p110γ), 8.58 nM (hVPS34), 18.3 nM (PI4Kβ), 24.5 nM (PI3K-C2β), 28.1 nM (PI3K-C2α)[1] 
mTORC1, mTORC2[4]
In Vitro: Torin 2 is subject to further profiling against a panel of lipid kinases with IC50s of 2.81 nM, 0.5 nM, 5.67 nM, 8.58 nM, 18.3 nM, 24.5 nM and 28.1 nM for mTOR, DNA-pK, p110γ, hVPS34, PI4Kβ, PI3K-C2β and PI3K-C2α, respectively. Torin 2 (Torin2) possesses a 250 pM EC50 for inhibiting mTOR in cells while maintaining 800-fold cellular selectivity relative to inhibition of PI3K and most other protein kinases[1]. Torin 2 (Torin2) exhibits potent biochemical and cellular activity against PIKK family kinases including ATM (EC50 28 nM), ATR (EC50 35 nM) and DNA-PK (EC50 118 nM). Torin 2 potently inhibits T308 of Akt, a direct substrate of PDK1 and an indirect substrate of PI3Ks, with an EC50 of less than 10 nM[2]. Torin-2 can suppress both
mTORC1 and mTORC2[4].
In Vivo: Torin 2 (Torin2) exhibits good bioavailability and exposure and can maintain strong inhibition of mTOR activity in lung and liver to at least six hours after a single dose of 20 mg/kg. Torin 2 is easier to produce on scale and exhibits improved pharmacokinetic properties which should enable it use in vivo experiments[1]. Torin 2 (Torin2) strongly suppresses pS6K(T389) and p4EBP1(T37/46) and partly suppresses pAkt(T308). Treatment of mice with AZD6244 at 25 mg/kg results in a profound inhibition of pERK. Combined administration of Torin 2 (40 mg/kg) and AZD6244 (25 mg/kg) demonstrates strong inhibition of all pharmacodynamics markers[2]. Treatment with Torin 2 (Torin2) and Rapamycin induces IL-6 secretion by astrocytes and may contribute to the reduction of mechanical hypersensitivity after SCI. Torin1 and Torin 2 treatment increases IL-6 mRNA, suggesting that the PI3K-mTOR pathway is a negative regulator of IL-6 expression in astrocytes. Importantly, Torin 2 treatment does not show any cell toxicity, as no signs of cell death are observed by TUNEL assay or by detection of cleaved-caspase 3 by western blotting[3].

Name: Torin 1, CAS: 1222998-36-8, stock 5.1g, assay 98.1%, MWt: 607.62, Formula: C35H28F3N5O2, Solubility: DMSO : 2 mg/mL (3.29 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Autophagy, Target: mTOR;Autophagy, Biological_Activity: Torin 1 is a potent inhibitor of mTOR with an IC50 of 3 nM. Torin 1 inhibits both mTORC1/2 complexes with IC50 values between 2 and 10 nM. Torin 1 is an effective inducer of autophagy.
IC50 & Target: IC50: 2-10 nM (mTORC1), 2-10 nM (mTORC2), 3 nM (mTOR), 0.6 μM (ATM), 1 μM (DNA-PK), 1.8 μM (PI3K-α), 3 μM (hVPS34)[2]
In Vitro: Torin1 (250 nM) completely inhibits proliferation and causes a G1/S cell cycle arrest, and decreases cell size to a greater degree than 50 nM rapamycin in wild-type MEFs[1]. Torin1 has more than 800-fold selectivity between mTOR and PI3Kis, and is very selective relative to other PIKK family kinases with the exception of DNA-PK[2].
In Vivo: Torin1 (20 mg/kg, i.p.) is efficacious in a U87MG xenograft model, and demonstrates good pharmacodynamic inhibition of downstream effectors of mTOR in tumor and peripheral tissues[2].

Name: VE-821, CAS: 1232410-49-9, stock 9.6g, assay 98.8%, MWt: 368.41, Formula: C18H16N4O3S, Solubility: DMSO : 50 mg/mL (135.72 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;PI3K/Akt/mTOR, Target: ATM/ATR;ATM/ATR, Biological_Activity: VE-821 is a potent ATP-competitive inhibitor of ATR with Ki/IC50 of 13 nM/26 nM.
IC50 & Target: Ki: 13 nM (ATR)[1] 
IC50: 26 nM (ATR)[2]
In Vitro: VE-821 shows excellent selectivity for ATR with minimal cross-reactivity against the related PIKKs ATM, DNA-PK, mTOR and PI3Kγ (Kis of 16 μM, 2.2 μM, >1 μM and 3.9 μM, respectively) and against a large panel of unrelated protein kinases[1]. VE-821 (compound 27) also inhibits ATM and DNA-PK wirh IC50 of >8 μM, and 4.4 μM, respectively[2]. VE-821 significantly enhances the sensitivity of PSN-1, MiaPaCa-2 and primary PancM pancreatic cancer cells to radiation and Gemcitabine under both normoxic and hypoxic conditions. ATR inhibition by VE-821 leads to inhibition of radiation-induced G2/M arrest in cancer cells. In both PSN-1 and MiaPaCa-2 cells, 1 µM VE-821 inhibits phosphorylation of Chk1 (Ser 345) after treatment with Gemcitabine (100 nM), radiation (6 Gy) or both, at 2 h post-irradiation[3].

Name: CDK-IN-2 CDK inhibitor II, CAS: 1269815-17-9, stock 3.3g, assay 98.1%, MWt: 363.81, Formula: C18H19ClFN3O2, Solubility: DMSO : ≥ 100 mg/mL (274.87 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CDK-IN-2 is a potent and specific CDK9 inhibitor with IC50 of <8 nM, extracted from reference 1, example 4.
IC50 Value: <8 nM [1]
Target: CDK9
In vitro:
In vivo:

Name: SU14813, CAS: 627908-92-3, stock 23.1g, assay 98.3%, MWt: 442.48, Formula: C23H27FN4O4, Solubility: DMSO : 44 mg/mL (99.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;c-Kit, Biological_Activity: SU14813 is a multi-targeted receptor tyrosine kinases inhibitor with IC50s of 50, 2, 4, 15 nM for VEGFR2, VEGFR1, PDGFRβ and KIT.
IC50 & Target: IC50: 50 nM (VEGFR2), 2 nM (VEGFR1), 4 nM (PDGFRβ), 15 nM (KIT)[1]
In Vitro: SU14813 inhibits ligand-dependent and ligand-independent proliferation, migration, and survival of endothelial cells and/or tumor cells expressing these targets. SU14813 inhibits cellular ligand-dependent phosphorylation of VEGFR-2 (transfected NIH 3T3 cells), PDGFR-β (transfected NIH 3T3 cells), KIT (Mo7e cells), and FLT3-internal tandem duplication (FLT3-ITD; MV4;11 cells) as well as FMS/CSF1R (transfected NIH 3T3 cells). SU14813 inhibits VEGFR-2, PDGFR-β, and KIT phosphorylation in porcine aorta endothelial cells overexpressing these targets, with cellular IC50 values of 5.2, 9.9, and 11.2 nM, respectively. SU14813 inhibits the growth of U-118MG with an IC50 of 50 to 100 nM[1].
In Vivo: SU14813 inhibits VEGFR-2, PDGFR-β, and FLT3 phosphorylation in xenograft tumors in a dose- and time-dependent fashion. The plasma concentration required for in vivo target inhibition is estimated to be 100 to 200 ng/mL. Used as monotherapy, SU14813 exhibits broad and potent antitumor activity resulting in regression, growth arrest, or substantially reduces growth of various established xenografts derived from human or rat tumor cell lines. Treatment in combination with docetaxel significantly enhances both the inhibition of primary tumor growth and the survival of the tumor-bearing mice compared with administration of either agent alone[1].

Name: Toceranib SU11654;PHA 291639E, CAS: 356068-94-5, stock 24.3g, assay 98.5%, MWt: 396.46, Formula: C22H25FN4O2, Solubility: DMSO : 2.5 mg/mL (6.31 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;c-Kit, Biological_Activity: Toceranib phosphate (SU11654 phosphate) is an orally active receptor tyrosine kinase (RTK) inhibitor, and it potently inhibits PDGFR, VEGFR, and Kit with Kis of 5 and 6 nM for PDGFRβ and Flk-1/KDR, respectively. Toceranib phosphate (SU11654 phosphate) has antitumor and antiangiogenic activity, and used in the treatment of canine mast cell tumors[1][2].
IC50 & Target: Ki: 6 nM (Flk-1/KDR), 5 nM (PDGFRβ)[1]
In Vitro: Toceranib (SU11654) is a selective inhibitor of the tyrosine kinase activity of several members of the split kinase RTK family, including PDGFR and Flk-1/KDR, with Kis of 5 and 6 nM, respectively[1]. 
To explore mechanisms of acquired Toceranib (TOC) resistance in canine MCT, three resistant sublines are generated from the Toceranib-sensitive exon 11 ITD c-kit mutant C2 cell line designated TR1, TR2, and TR3. Growth of the parental C2 cells is inhibited by Toceranib in a dose-dependent manner with an IC50 of <10 nM. In contrast, TR1, TR2, and TR3 sublines are resistant to inhibition by Toceranib (IC50> 1,000 nM). Sensitivity to three other KIT RTK inhibitors is similar to the observed resistance to Toceranib. The parental line as well as all three sublines retains sensitivity to the cytotoxic agents vinblastine (VBL) and CCNU. Following 72 hr culture in the presence of increasing concentrations of Toceranib, treatment naïve, parental C2 cells detach from the culture flask and become rounded, shrunken, and clumped with increased exposure to Toceranib. In contrast, Toceranib-induced morphologic differences are not identified in the resistant sublines[2].
In Vivo: Administration of Toceranib significantly decreases the number and percentage of Treg in the peripheral blood of dogs with cancer. Dogs receiving Toceranib and cyclophosphamide (CYC) demonstrate a significant increase in serum concentrations of IFN-γ, which is inversely correlated with Treg numbers after 6 weeks of combination treatment[3].

Name: Linsitinib OSI-906, CAS: 867160-71-2, stock 39.9g, assay 98.1%, MWt: 421.49, Formula: C26H23N5O, Solubility: DMSO : 62.5 mg/mL (148.28 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: IGF-1R;Insulin Receptor, Biological_Activity: Linsitinib (OSI-906) is a dual inhibitor of the IGF-1 receptor and IR with IC50s of 35 and 75 nM, respectively.
IC50 & Target: IC50: 35 nM (IGF-1R), 75 nM (InsR)
In Vitro: Linsitinib inhibits IGF-1R autophosphorylation and activation of the downstream signaling proteins Akt, ERK1/2 and S6 kinase with IC50 of 0.028 to 0.13 μM. Linsitinib enables an intermediate conformation of the target protein through interactions with the C-helix. Linsitinib displays favorable metabolic stability in liver microsomes. Linsitinib fully inhibits both IR and IGF-1R phosphorylation at a concentration of 1 μM. Linsitinib inhibits proliferation of several tumor cell lines including non-small-cell lung cancer and colorectal cancer (CRC) tumor cell line with EC50 of 0.021 to 0.810 μM[1].
In Vivo: Linsitinib inhibits tumor growth in an IGF-1R-driven xenograft mouse model, with 100% TGI and 55% regression at a dose of 75 mg/kg and 60% TGI and no regression at a dose of 25 mg/kg. Linsitinib administration induces different elimination half-lives of itself in dog, rat and mice, the elimination half-lives are 1.18 hours, 2.64 hours and 2.14 hours, respectively. Linsitinib administration at different single dose once-daily in femal Sprague-Dawley rat and femal CD-1 mouse reveal that the Vmax is not dose-proportional to Linsitinib dose. Linsitinib elevates the blood glucose levels at a dose of 25 mg/kg after 12 days administration. Linsitinib administration at a single dose of 75 mg/kg in IGF-1R-driven full-length human IGF-1R (LISN) xenograft mouse model achieve maximal inhibition of IGF-1R phosphorylation (80%) between 4 and 24 hours with plasma drug concentrations of 26.6-4.77 μM[1]. Linsitinib administered as a single dose of at 60 mg/kg in NCI-H292 xenografts mice inhibits uptake of glucose at 2, 4, and 24 hours post-treatment in vivo. Linsitinib inhibits the growth of tumors in NCI-H292 xenograft mouse model[2].

Name: TAK-901, CAS: 934541-31-8, stock 28.5g, assay 98.1%, MWt: 504.64, Formula: C28H32N4O3S, Solubility: DMSO : 2 mg/mL (3.96 mM; Need ultrasonic and warming), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: TAK-901 is a multi-targeted aurora inhibitor with IC50s of 21 and 15 nM for aurora A and B, respectively.
IC50 & Target: IC50: 21 nM (aurora A), 15 nM (aurora B), 1.2 nM (JAK3), 1.3 nM (Src), 2 nM (FGR), 5 nM (FLT3)[1]
In Vitro: TAK-901 exhibits time-dependent, tight-binding inhibition of Aurora B, but not Aurora A. Consistent with Aurora B inhibition, TAK-901 suppresses cellular histone H3 phosphorylation and induces polyploidy. In various human cancer cell lines, TAK-901inhibits cell proliferation with effective concentration values from 40 to 500 nM. Examination of a broad panel of kinases in biochemical assays reveals inhibition of multiple kinases. However, TAK-901 potently inhibits only a few kinases other than Aurora B in intact cells, including FLT3 and FGFR2[1].
In Vivo: In rodent xenografts, TAK-901 exhibits potent activity against multiple human solid tumor types, and complete regression is observed in the ovarian cancer A2780 model. TAK-901 also displayed potent activity against several leukemia models. TAK-901 induces pharmacodynamic responses consistent with Aurora B inhibition and correlating with retention of TAK-901 in tumor tissue[1].

Name: BMS-690514, CAS: 859853-30-8, stock 33.7g, assay 98.7%, MWt: 368.43, Formula: C19H24N6O2, Solubility: DMSO : ≥ 25 mg/mL (67.86 mM), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: VEGFR;EGFR;EGFR, Biological_Activity: BMS-690514 is a potent and orally active inhibitor of EGFR and VEGFR; has IC50s of 5, 20 and 60 nM for EGFR, HER 2 and HER 4, respectively.
IC50 & Target: IC50: 5 nM (EGFR), 20 nM (HER2), 60 nM (HER4)[1]
In Vitro: BMS-690514 targets several critical signaling pathways: human epidermal growth factor receptor (HER)/ErbB, angiogenesis signaling through VEGFR2, lymphangiogenesis through VEGFR3, and also shows activity against VEGFR1, Flt-3, and Lck. Permeability of BMS-690514 in Caco-2 cells is in the intermediate range with a moderate potential to be a P-gp substrate[2]. BMS-690514 inhibits members of the VEGFR family with IC50 values in the range of 25 to 50 nM. Non–small cell lung tumor cells with exon 19 deletion (HCC4006, HCC827, and PC9) are highly sensitive to BMS-690514, which inhibits their proliferation with IC50 values of 2 to 35 nM. Tumor cell lines with EGFR gene amplification (DiFi, NCI-H2073, A431) are also highly sensitive to inhibition by BMS-690514. Tumor cell lines that are dependent on HER2 signaling are also found to be highly sensitive to BMS-690514. Breast and gastric tumor cell lines that have HER2 gene amplification (N87, SNU-216, AU565, BT474, KPL4, and HCC202) are inhibited with IC50 values of 20 to 60 nM[1].
In Vivo: BMS-690514 has been shown to be efficacious in a broad spectrum of tumor xenografts. At doses that are efficacious and well tolerated in the animal models, BMS-690514 inhibits tumor cell proliferation and tumor blood flow[1]. The oral bioavailability of BMS-690514 is 78% in mice, 100% in rats, 8% in monkeys, and 29% in dogs. BMS-690514 is able to cross the blood–brain barrier with a brain-to-plasma ratio of 1. The preclinical ADME properties of BMS-690514 suggest good oral bioavailability in humans and metabolism by multiple pathways including oxidation and glucuronidation[2].

Name: XMD8-92, CAS: 1234480-50-2, stock 7.4g, assay 98%, MWt: 474.55, Formula: C26H30N6O3, Solubility: DMSO : 50 mg/mL (105.36 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway, Target: ERK;ERK, Biological_Activity: XMD8-92 is a highly selective ERK5/BMK1 inhibitor with dissociation constant (Kd) value of 80 nM.
IC50 & Target: Kd: 80 nM (ERK5/BMK1)[1]
In Vitro: XMD8-92 exhibits the greatest affinity towards BMK1 with a measured dissociation constant (Kd) of 80 nM, while DCAMKL2, TNK1 and PLK4 exhibit Kd’s of 190, 890 and 600 nM, respectively. XMD8-92 is profiled against all detectable kinases in HeLa cell lysates using the KiNativ method and is found to be about 10-fold more selective for BMK1 with a IC50 of 1.5 μM than the most potent off-targets, TNK1 (IC50=10 μM) and ACK1 (aka TNK2, IC50=18 μM). Other weak off-targets include the kinase domain 2 of RSK1 and RSK2, PIK4A and PIK4B, and FAK. Notably, MEK5 is not significantly inhibited by XMD8-92 at up to 50 μM[1]. XMD8-92 shows high selectivity to BMK1 in an in vitro ATP-site competition binding assay against 402 kinases as well as in the KiNativ method against all detectable kinases in HeLa cell lysates. XMD8-92 blocks EGF-induced activation of BMK1 with IC50 of 240 nM and, with concentration as high as 5 μM, XMD8-92 has no inhibitory effect on ERK1/2 activation by EGF[2].
In Vivo: XMD8-92 significantly inhibits tumor growth in vivo by 95%. The pharmacokinetics of XMD8-92 is evaluated in Sprague-Dawley rats given a single intravenous or oral dose. XMD8-92 is found to have a 2.0 hr half life clearance of 26 mL/min/kg. XMD8-92 has moderate tissue distribution with a calculated volume of distribution of 3.4 L/kg. XMD8-92 has high oral bioavailability with 69% of the dose absorbed. After a single oral dose of 2 mg/kg, maximal plasma concentrations of approximately 500 nM are observed by 30 minutes, with 34 nM remaining 8 hr post dose. In tolerability experiments, high plasma concentrations of drug (approximately 10 μM following IP dosing of 50 mg/kg) are maintained throughout the 14 days. XMD8-92 appeares to be well tolerated and the mice appeared healthy with no sign of distress. No vasculature instability is observed in the XMD8-92-treated mice[1]. XMD8-92 treatment in both immunocompetent and immunodeficient mice blocked the growth of lung and cervical xenograft tumors, respectively, by 95%. This remarkable anti-tumor effect of XMD8-92 in lung and cervical xenograft tumor models is due to XMD8-92’s capacity to inhibit tumor cell proliferation through the PML suppression-inducted p21 checkpoint protein, and by blocking of BMK1’s contribution in tumor-associated angiogenesis. Besides, BMK1 knockout (KO) in mice leads to complete and irreversible removal of the BMK1 protein, while XMD8-92 treatment in mice only suppresses the activity of BMK1, which is reversible. Second, the vasculature instability observed in BMK1 KO mice may be due to lack of the C-terminal non-kinase domain of BMK1, which is still present during XMD8-92 treatment of animals[2].

Name: LRRK2-IN-1, CAS: 1234480-84-2, stock 22.3g, assay 98.2%, MWt: 570.69, Formula: C31H38N8O3, Solubility: DMSO : ≥ 50 mg/mL (87.61 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;LRRK2, Biological_Activity: LRRK2-IN-1 is a potent and selective LRRK2 inhibitor with IC50 of 6 nM and 13 nM for LRRK2 (G2019S) and LRRK2 (WT), respectively.
IC50 & Target: IC50: 13 nM (WT), 6 nM (G2019S)
In Vitro: Wild-type and G2019S transduction results in 2.5 fold higher TR-FRET signal which can be inhibited by LRRK2-IN-1 in a dose-dependent manner with IC50 values of 0.08 µM and 0.03 µM, respectively[1]. LRRK2-IN-1 possessed an IC50 of 45 nM for inhibition of DCLK2 and exhibits an IC50 of greater than 1 µM when evaluated in biochemical assays for AURKB, CHEK2, MKNK2, MYLK, NUAK1, and PLK1. LRRK2-IN-1 is confirmed to inhibit MAPK7 with an EC50 of 160 nM. LRRK2-IN-1 induces a dose dependent inhibition of Ser910 and Ser935 phosphorylation accompanied by loss of 14-3-3 binding to both wild type LRRK2 and LRRK2[G2019S] stably transfected into HEK293 cells[2]. LRRK2-IN-1 is moderately cytotoxic with IC50 of 49.3 µM in HepG2 cells. LRRK2-IN-1 exhibits genotoxicity in the presence and absence of S9 at 15.6 and 3.9 µM, respectively[3]. LRRK2-IN-1 inhibits proliferation, migration, and induces cell death with hallmarks of apoptosis of HCT116 and AsPC-1 cells[4].
In Vivo: LRRK2-IN-1 (100 mg/kg, i.p.) induces dephosphorylation of LRRK2 in the kidney of the mice[2]. Peritumoral injection of LRRK2-IN-1 (100 mg/kg) results in a significant decrease in tumor volume and weight of AsPC-1 tumor xenografts[4].

Name: Torkinib PP 242, CAS: 1092351-67-1, stock 35.9g, assay 99%, MWt: 308.34, Formula: C16H16N6O, Solubility: DMSO : 50 mg/mL (162.16 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR;Autophagy;Autophagy, Target: Apoptosis;mTOR;Autophagy;Mitophagy, Biological_Activity: Torkinib (PP 242) is a selective and ATP-competitive mTOR inhibitor with an IC50 of 8 nM. PP242 inhibits both mTORC1 and mTORC2 with IC50s of 30 nM and 58 nM, respectively.
IC50 & Target: IC50: 8 nM (mTOR), 100 nM (p110δ), 410 nM (DNA-PK), 410 nM (PDGFR)[1] 
IC50: 30 nM (mTORC1), 58 nM (mTORC2)[2]
In Vitro: Torkinib (PP 242) potently inhibits mTOR (IC50=8 nM) but is much less active against other PI3K family members. Testing of Torkinib (PP 242) against 219 protein kinases reveals remarkable selectivity relative to the protein kinome: at a concentration 100-fold above its IC50 for mTOR, Torkinib (PP 242) inhibits only one kinase by more than 90% (Ret) and only three by more than 75% (PKCα, PKCβII and JAK2V617F)[1]. Torkinib (PP 242) has a dose-dependent effect on proliferation and at higher doses is much more effective than Rapamycin at blocking cell proliferation. The ability of Torkinib (PP 242) to block cell proliferation more efficiently than Rapamycin could be a result of its ability to inhibit mTORC1 and mTORC2, because Rapamycin can only inhibit mTORC1. In SIN1-/- mouse embryonic fibroblasts (MEFs), Rapamycin is also less effective at blocking cell proliferation than Torkinib. That Torkinib (PP 242) and Rapamycin exhibit very different anti-proliferative effects in SIN1-/- MEFs suggests that the two compounds differentially affect mTORC1[2].
In Vivo: In fat and liver, Torkinib (PP 242) is able to completely inhibit the phosphorylation of Akt at S473 and T308, consistent with its effect on these phosphorylation sites observed in cell culture. Surprisingly, Torkinib (PP 242) is only partially able to inhibit the phosphorylation of Akt in skeletal muscle and is more effective at inhibiting the phosphorylation of T308 than S473, despite it's ability to fully inhibit the phosphorylation of 4EBP1 and S6. These results will be confirmed by in vivo dose-response experiments, but, consistent with the partial effect of Torkinib (PP 242) on pAkt in skeletal muscle, a muscle-specific knockout of the integral mTORC2 component rictor resulted in only a partial loss of Akt phosphorylation at S473. These results suggest that a kinase other than mTOR, such as DNA-PK, may contribute to phosphorylation of Akt in muscle[2].

Name: Tirbanibulin KX2-391;KX-01, CAS: 897016-82-9, stock 17.7g, assay 98%, MWt: 431.53, Formula: C26H29N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage;Cytoskeleton, Target: Src;Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Tirbanibulin (KX2-391) is an inhibitor of Src that targets the peptide substrate site of Src, with GI50 of 9-60 nM in cancer cell lines.
IC50 & Target: GI50: 9 nM (Src, in HuH7 cells), 13 nM (Src, in PLC/PRF/5 cells), 26 nM (Src, in Hep3B cells), 60 nM (Src, in HepG2 cells)[1]
In Vitro: Tirbanibulin (KX2-391) is a Src inhibitor that is directed to the Src substrate pocket. Tirbanibulin (KX2-391) shows steep dose-response curves against Huh7 (GI50=9 nM), PLC/PRF/5 (GI50=13 nM), Hep3B (GI50=26 nM), and HepG2 (GI50=60 nM), four hepatic cell cancer (HCC) cell lines[1]. Tirbanibulin (KX2-391) is found to inhibit certain leukemia cells that are resistant to current commercially available drugs, such as those derived from chronic leukemia cells with the T3151 mutation. Tirbanibulin (KX2-391) is evaluated in engineered Src driven cell growth assays inNIH3T3/c-Src527F and SYF/c-Src527F cells and exhibits GI50 with 23 nM and 39 nM, respectively[2].
In Vivo: Orally administered Tirbanibulin (KX2-391) is shown to inhibit primary tumor growth and to suppress metastasis, in pre-clinical animal models of cancer[2].

Name: MRT67307, CAS: 1190378-57-4, stock 9.2g, assay 98.5%, MWt: 464.60, Formula: C26H36N6O2, Solubility: DMSO : ≥ 100 mg/mL (215.24 mM), Clinical_Informat: No Development Reported, Pathway: Autophagy;Autophagy;NF-κB, Target: ULK;Autophagy;IKK, Biological_Activity: MRT67307 is a dual inhibitor of the IKKε and TBK-1 with IC50s of 160 and 19 nM, respectively. MRT67307 also inhibits ULK1 and ULK2 with IC50s of 45 and 38 nM, respectively.
IC50 & Target: IC50: 160 nM (IKKε, ATP), 19 nM (TBK-1, ATP), 45 nM (ULK1), 38 nM (ULK2)
In Vitro: MRT67307 actually enhances phosphorylation in IKKα−/− MEFs, the IL-1-stimulated phosphorylation of p105 at Ser933 and RelA at both Ser468 and Ser536. MRT67307 also enhances IL-1-stimulated activation of NF-κB-dependent gene transcription in wild-type MEFs. Treatment of macrophages with MRT67307 leads to an increase in the poly(I:C)- and LPS-stimulated phosphorylation of p105 and RelA and enhanced NF-κB transcriptional activity[1]. MRT67307 (10 μM) is sufficient to reduce phospho-ATG13 to control levels, and in line with the in vitro IC50 values, 10-fold less MRT68921 (1 μM) results in a similar reduction. MRT67307 and MRT68921 inhibit ULK and block autophagy in cells[2]. MRT67307 increases IL-10 production and suppresses proinflammatory cytokine production in macrophages. MRT67307 increases CREB-dependent gene transcription by promoting the dephosphorylation of CRTC3. MRT67307 does not inhibit the brain-specific kinases (BRSKs) and only inhibits the maternal embryonic leucine zipper kinase (MELK) and AMPK itself more weakly[3].

Name: DPH, CAS: 484049-04-9, stock 18.9g, assay 99%, MWt: 336.32, Formula: C18H13FN4O2, Solubility: DMSO : 100 mg/mL (297.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Bcr-Abl, Biological_Activity: DPH is a potent cell permeable c-Abl activator, which displays potent enzymatic and cellular activity in stimulating c-Abl activation.
In Vitro: DPH binds to the myristoyl binding site and prevents the formation of the bent conformation of the αI helix through steric hindrance, a mode of action distinct from the previously identified allosteric c-Abl inhibitor, GNF-2, that also binds to the myristoyl binding site. DPH represents the first cell-permeable, small-molecule tool compound for c-Abl activation[1].

Name: CGI-1746, CAS: 910232-84-7, stock 12.9g, assay 98.6%, MWt: 579.69, Formula: C34H37N5O4, Solubility: DMSO : ≥ 50 mg/mL (86.25 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Autophagy, Target: Btk;Autophagy, Biological_Activity: CGI-1746 is a potent and highly selective inhibitor of the Btk with IC50 of 1.9 nM.
IC50 & Target: IC50: 1.9 nM (Btk)
In Vitro: CGI1746 is specific for Btk, with appr 1,000-fold selectivity over Tec and Src family kinases. In an ATP-free competition binding assay, the dissociation constant for Btk is 1.5 nM. CGI1746 inhibits Btk activity in a new binding mode that stabilizes an inactive nonphosphorylated enzyme conformation. CGI1746 inhibits both auto- and transphosphorylation steps necessary for enzyme activation. CGI1746 completely inhibits anti-IgM-induced murine and human B cell proliferation, with IC50s of 134 nM and 42 nM, respectively, but has no effect on anti-CD3- and anti-CD28-induced T cell proliferation. CGI1746 potently inhibits the proliferation of CD27+IgG+ B cells isolated from the tonsils of four human donors with an average IC50 of 112 nM. In macrophages, CGI1746 abolishes FcγRIII-induced TNFα, IL-1β and IL-6 production. CGI1746 potently inhibits TNFα, IL-1β and, to a lesser extent, IL-6 (three- to eight-fold higher IC50) production in human monocytes stimulated with immobilized or soluble immune complexes[1]. CGI-1746 does not kill cells as well as the irreversible BTK inhibitors at the same drug concentration. CGI-1746 significantly reduces phosphorylation of both the BTK-A and BTK-C proteins, indicating the auto-phosphorylation of the BTK-C isoform is inhibited in a manner similar to BTK-A. CGI-1746 does not kill LNCaP or DU145 prostate cancer cells at the same concentrations as Ibrutinib or AVL-292, but it demonstrates similar inhibition of BTK phosphorylation at tyrosine 233 in the SH3 domain[2].
In Vivo: CGI1746 abrogates B cell-dependent arthritis. CGI1746 treatment (100 mg/kg, s.c, twice-daily dosing) results in significant inhibition (97%) of overall clinical arthritis scores. CGI1746 treatment substantially reduces TNFα, IL-1β and IL-6, as well as MCP1 and MIP-1α on both the mRNA and protein level in the passive anti-collagen II antibody-induced arthritis (CAIA) model. CGI1746 shows comparable efficacy to TNFα blockade and significantly reduces clinical scores, as well as joint inflammation, in mice or rats with established arthritis[1].

Name: MK-0752, CAS: 471905-41-6, stock 19.3g, assay 98.6%, MWt: 442.90, Formula: C21H21ClF2O4S, Solubility: Ethanol : 10 mg/mL (22.58 mM; Need ultrasonic); DMSO : ≥ 100 mg/mL (225.78 mM), Clinical_Informat: Phase 1, Pathway: Stem Cell/Wnt;Neuronal Signaling, Target: γ-secretase;γ-secretase, Biological_Activity: MK-0752 is a moderately potent γ-secretase inhibitor, which reduces Aβ40 production with IC50 of 5 nM.
IC50 value: 5 nM (reduces Aβ40 production) [1]
Target: γ-secretase
in vitro: MK-0752 is identified as a moderately potent γ-secretase inhibitor, which reduces Aβ40 in a dose-dependent manner with an IC50 of 5 nM in human SH-SY5Y cells [1]. In vitro, MK-0752 blocks Notch-intracellular domain (ICD) cleavage and its subsequent nuclear translocation [2].
in vivo: MK-0752 (240 mg/kg) reduces the generation of newly produced Aβ with 90% decrease of AUV in the brain of rhesus monkeys. In addition, MK-0752 treatment increases levels of Aβ 1-14, Aβ 1-15, and Aβ 1-16 , while decreases levels of Aβ 1-17 [1]. In guinea-pigs, oral administration of MK-0752 (10 mg/kg -30 mg/kg) results in the dose-dependent reduction of Aβ40 in plasma, brain and cerebrospinal fluid (CSF) with IC50 of 440 nM in brain [2].

Name: GW788388, CAS: 452342-67-5, stock 15.6g, assay 98.3%, MWt: 425.48, Formula: C25H23N5O2, Solubility: DMSO : ≥ 48 mg/mL (112.81 mM), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: GW788388 is a potent and selective inhibitor of ALK5 with IC50 of 18 nM, and also inhibits TGF-β type II receptor and activin type II receptor activities, without inhibiting BMP type II receptor.
IC50 & Target: IC50: 18 nM (ALK5)
In Vivo: GW788388 given orally for 5 weeks significantly reduces renal fibrosis and decreased the mRNA levels of key mediators of extracellular matrix deposition in kidneys in db/db mice[1]. GW788388 (50 mg/kg/day, p.o.) significantly attenuates systolic dysfunction in the MI animals, together with the attenuation of the activated (phosphorylated) Smad2 (P < 0.01), α-smooth muscle actin (P < 0.001), and collagen I (P < 0.05) in the noninfarct zone of MI rats[2]. GW788388 reduces the expression of collagen IA1 by 80% at a dose of 1 mg/kg twice a day (b.i.d.). GW788388 significantly reduces the expression of collagen IA1 mRNA when administered orally at 10 mg/kg once a day (u.i.d.) in a model of puromycin aminonucleoside-induced renal fibrosis[3].

Name: Vismodegib GDC-0449, CAS: 879085-55-9, stock 19.4g, assay 98.7%, MWt: 421.30, Formula: C19H14Cl2N2O3S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 50 mg/mL (118.68 mM); Ethanol : 2.86 mg/mL (6.79 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Stem Cell/Wnt;Autophagy, Target: Hedgehog;Autophagy, Biological_Activity: Vismodegib (GDC-0449) is an orally active hedgehog pathway inhibitor with an IC50 of 3 nM. It also inhibits P-gp, ABCG2 with IC50 values of 3.0 μM and 1.4 μM, respectively.
IC50 & Target: IC50: 3 nM (hedgehog), 3.0 μM (P-gp), 1.4 μM (ABCG2)
In Vitro: Vismodegib (HhAntag691) is an ABCG2 inhibitor and can increase the effective intracellular concentration of NSC 279836, another ABCG2 substrate, through blocking its export in HEK293 cells. Vismodegib (HhAntag691, 10 µM), resensitizes MDCKII/Pgp cells and MDCKII/MRP1 cells to NSC757 treatment[2]. Vismodegib (25 μM or 50 μM) concentration dependently inhibits HCC and H1339 cells[3].
In Vivo: Vismodegib is a novel small molecule HPI, often used for clinical trials[1]. Vismodegib (0.3 to 75 mg/kg, p.o.) is highly efficacious in medulloblastoma allograft tumors. Vismodegib (> 46 mg/kg, p.o.) causes growth delay in patient-derived colorectal xenografts[4].

Name: Idelalisib CAL-101; GS-1101, CAS: 870281-82-6, stock 33.3g, assay 98.2%, MWt: 415.42, Formula: C22H18FN7O, Solubility: DMSO : ≥ 59.7 mg/mL (143.71 mM), Clinical_Informat: Launched, Pathway: PI3K/Akt/mTOR;Autophagy, Target: PI3K;Autophagy, Biological_Activity: Idelalisib (CAL-101; GS-1101) is a highly selective and orally bioavailable p110δ inhibitor with an IC50 of 2.5 nM, showing 40- to 300-fold selectivity for p110δ over other PI3K class I enzymes.
IC50 & Target: IC50: 2.5 nM (p110δ), 89 nM (p110γ), 565 nM (p110β), 820 nM (p110α)[1]
In Vitro: Idelalisib (CAL-101; GS-1101) is a highly selective and potent p110δ inhibitor (EC50=8 nM). Greater selectivity (400- to 4000-fold) is seen against related kinases C2β, hVPS34, DNA-PK, and mTOR, whereas no activity is observed against a panel of 402 diverse kinases at 10 μM. CAL-101 reduces PDGF-induced pAkt by only 25% at 10 μM. Idelalisib (CAL-101) inhibits LPA-induced pAkt with an EC50 of 1.9 μM. Idelalisib (CAL-101) blocks FcϵRI p110δ-mediated CD63 expression with an EC50 of 8 nM, whereas formyl-methionyl-leucyl-phenylalanine activation of p110γ is inhibited with an EC50 of 3 μM. Thus, in cell-based assays, CAL-101 has 240- to 2500-fold selectivity for p110δ over the other class I PI3K isoforms[1]. CAL-101Idelalisib (CAL-101)-induced apoptosis of chronic lymphocytic leukemia (CLL) cells is significant compare with vehicle treatment alone (P<0.001). Idelalisib (CAL-101) induces selective cytotoxicity in CLL cells independent of IgVH mutational status or interphase cytogenetics[2].
In Vivo: A significant reduction is observed in the CD11b+Ly6G+ neutrophils from brain homogenates of bothp110δD910A/D910A mice and Idelalisib (CAL-101) (40 mg/kg, i.v.) post-treated mice[3].

Name: OSI-027, CAS: 936890-98-1, stock 32.5g, assay 98.3%, MWt: 406.44, Formula: C21H22N6O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 83.33 mg/mL (205.02 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR;Autophagy, Target: mTOR;Autophagy, Biological_Activity: OSI-027 is an ATP-competitive mTOR kinase activity inhibitor with an IC50 of 4 nM. OSI-027 targets both mTORC1 and mTORC2 with IC50s of 22 nM and 65 nM, respectively.
IC50 & Target: IC50: 4 nM (mTOR kinase), 22 nM (mTORC1), 65 nM (mTORC2), 0.42 μM (PI3K-γ), 1.3 μM (PI3K-α), 1.0 μM (DNA-PK)[1]
In Vitro: OSI-027 is an ATP-competitive inhibitor, which targets both mTORC1 and mTORC2 with IC50s of 22 nM and 65 nM. OSI-027 also inhibits PI3K-α, PI3K-γ and DNA-PK with IC50s of 1.3 μM, 0.42 μM and 1.0 μM. OSI-027 inhibits mTOR signaling of phospho-4E-BP1 with an IC50 of 1 μM[1].
In Vivo: Effects on GEO colorectal xenograft growth treated with Rapamycin or OSI-027 for 12 days are consistent with our in vitro experiments. Treatment with Rapamycin (20 mg/kg) inhibits phospho-S6 and phospho-4E-BP1, while Akt phosphorylation is increased by 29%. In contrast, OSI-027 (65 mg/kg) inhibits both mTORC1 and mTORC2 effectors. After 2 hours, decreased 4E-BP1, Akt, and S6 phosphorylation is observed and inhibition of S6 and Akt is sustained for 24 hours. The plasma drug concentration of OSI-027 inversely correlated with these effects on mTORC1 and mTORC2 signaling. The median plasma drug concentration with OSI-027 is 21.3 μM at 2 hours and 14.9 μM at 8 hours. The in vivo efficacy of OSI-027 plus Sunitinib is tested in H292 human lung and Ovcar-5 human ovarian xenograft tumors. H292 tumors, treated with OSI-027 (50 mg/kg) for 21 days have 61% median tumor growth inhibition for the duration of treatment (TGI). Sunitinib (40 mg/kg) for 21 days had 47% median TGI. Combining OSI-027 with Sunitinib, however, has a median TGI of 100% with 59% maximal tumor regression, a statistically significant improvement over either agent alone. Ovcar-5 xenograft tumors treated with OSI-027 or Sunitinib have a 55% and 68% median TGI, respectively. OSI-027 administered with Sunitinib has a significantly better median TGI of 100% with 38% maximal tumor regression[1].In the Rapamycin (RAPA) group, three rats exhibit symptoms typical of LTx-aGVHD and die 27 to 35 days after liver transplantation (LT); the remaining five rats do not develop LTx-aGVHD symptoms and survive for more than 100 days. In contrast, seven rats in the OSI-027 group survive for more than 100 days without symptoms of LTx-aGVHD, and only one rat exhibits LTx-aGVHD symptoms and dies on day 33 after LT[2].

Name: Palomid 529 P529, CAS: 914913-88-5, stock 35.1g, assay 98.8%, MWt: 406.43, Formula: C24H22O6, Solubility: DMSO : 20.5 mg/mL (50.44 mM; Need ultrasonic and warming), Clinical_Informat: Phase 1, Pathway: Apoptosis;PI3K/Akt/mTOR, Target: Apoptosis;mTOR, Biological_Activity: Palomid 529 is a potent inhibitor of mTORC1 and mTORC2 complexes.
IC50 & Target: TORC1/TORC2[1]
In Vitro: Palomid 529 (P529) inhibits both VEGF-driven (IC50, 20 nM) and bFGF-driven (IC50, 30 nM) endothelial cell proliferation and retained the ability to induce endothelial cell apoptosis[1]. Palomid 529 (RES-529) is a PI3K/AKT/mTOR pathway inhibitor that interferes with the pathway through both mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) dissociation. Palomid 529 inhibits mTORC1/mTORC2 activity in various cancer cell lines, as noted by decreased phosphorylation of substrates including ribosomal protein S6, 4E-BP1, and AKT, leading to cell growth inhibition and death, with activity generally in the range of 5-15 μM. At 10 μM concentrations, Palomid 529 reduces the binding of 0.5 nM [3H]estradiol to estrogen receptor (ER)α and ERβ by 3% or less. Palomid 529 inhibits both VEGF-stimulated and β fibroblast growth factor-stimulated HUVEC cell proliferation with IC50 of ~10 and 30 nM, respectively. Treatment of HUVEC cells with Palomid 529 also results in a four-fold induction of apoptosis on the basis of DNA fragmentation. Growth inhibition is observed with Palomid 529 treatment in various cancer cell lines from the National Cancer Institute-60 (NCI-60) tumor panel, with IC50 ranges of 5-15 μM for central nervous system cancer cells and 5-30 μM for prostate cancer cells[2]. Palomid 529 (P529) results in a dose- and time-dependent decrease in Akt activity in PC3, LnCaP, and 22rv1 cells as evidenced by a reduced phosphorylation of Akt (Ser473). Similar results are observed in all PCa cells with similar enzymatic IC50s of about 0.2 μM. Palomid 529 inhibits the cell proliferation of neoplastic cells at different extent (IC50s ranged from 5 to 28 μM), whereas very few effects are observed in non-neoplastic BPH1 and EPN cells. Treatment with Palomid 529 results in a concentration-dependent reduction in viable/proliferating tumor cells compared with non-neoplastic BPH1 and EPN cells. IC50s range from 5 to 28 μM[3].
In Vivo: Palomid 529 (200 mg/kg/2d) inhibits C6V10 glioma tumor growth in nude mice following i.p. dosing. Analysis of signaling within the tumor lysates reveals that Palomid 529 (P529) also reduces AktS473 but not AktT308 signaling[1]. Palomid 529 (RES-529) has shown antitumor activity in a variety of mouse models, including those for glioblastoma, and prostate and breast cancer. In a C6V10 glioblastoma subcutaneous xenograft model, mice pretreated with Palomid 529 (200 mg/kg/2 days, intraperitoneal) 1 week before and for 3 weeks after a tumor cell injection showed an ~70% decrease in tumor volume compared with the control. In another glioblastoma tumor model using human U87 cells, mice treated with micronized Palomid 529 3 days after a tumor cell injection showed a reduction in tumor growth by ~78 and 29% with 50 and 25 mg/kg/2 days, intraperitoneal, Palomid 529, respectively, after 24 days compared with the control[2]. Palomid 529 (P529) is able to reduce tumor growth in a dose-dependent manner both in PC3 and 22rv1 xenografts. A 10, 47.6, and 59.3% reduction of tumor mass is demonstrated in mice bearing PC3 xenografts receiving 50, 100, and 200 mg/kg Palomid 529 respectively and a 9, 38.7, and 51.5% reduction of tumor mass in mice bearing 22rv1 xenografts receiving 50, 100, and 200 mg/kg Palomid 529 respectively[3].

Name: BX795, CAS: 702675-74-9, stock 16.1g, assay 98.1%, MWt: 591.47, Formula: C23H26IN7O2S, Solubility: DMSO : 50 mg/mL (84.54 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;NF-κB, Target: PDK-1;IKK, Biological_Activity: BX795 is a potent and selective inhibitor of PDK1, with an IC50 of 6 nM. BX795 is also a potent and relatively specific inhibitor of TBK1 and IKKɛ, with an IC50 of 6 and 41 nM, respectively. BX795 blocks phosphorylation of S6K1, Akt, PKCδ, and GSK3β, and has lower selectivity over PKA, PKC, c-Kit, GSK3β etc.
IC50 & Target: IC50: 6 nM (PDK1)[1], 6 nM (TBK1), 41 nM (IKKɛ)[2]
In Vitro: BX795 effectively blocks PDK1 activity in PC-3 cells, as shown by their ability to block phosphorylation of S6K1, Akt, PKCδ, and GSK3β. BX795 potently inhibits tumor cell growth on plastic with IC50 of 1.6, 1.4, and 1.9 μM for MDA-468, HCT-116 and MiaPaca cells, respectively. In soft agar, BX795 displays higher growth inhibition with IC50 of 0.72, and 0.25 μM for MDA-468, and PC-3 cells, respectively[1]. In addition, BX795, as an inhibitor of the TBK1/IKKε, blocks TBK1- and IKKε-mediated activation of IRF3 and production of IFN-β[2]. In platelet physiological responses, BX795 produces inhibitory effect on 2-MeSADP-induced or collagen-induced aggregation, ATP secretion and thromboxane generation[3].

Name: Ki20227, CAS: 623142-96-1, stock 35.2g, assay 98.3%, MWt: 480.54, Formula: C24H24N4O5S, Solubility: DMSO : 62.5 mg/mL (130.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;c-Fms;c-Kit, Biological_Activity: Ki20227 is an orally active and highly selective c-Fms tyrosine kinase (CSF1R) inhibitor with IC50s of 2 nM, 12 nM, 451 and 217 nM for CSF1R, VEGFR2 (vascular endothelial growth factor receptor-2), c-Kit (stem cell factor receptor) and PDGFRβ (platelet-derived growth factor receptor β). Ki20227 suppresses osteoclast differentiation and osteolytic bone destruction[1].
IC50 & Target: IC50: 2 nM (CSF1R), 12 nM (VEGFR2), 451 nM (c-Kit) and 217 nM (PDGFRβ)[1]
In Vitro: Ki20227 (0.1-1000 nM; 72 hours) with 100 and 1,000 nM almost suppresses M-NFS-60 cell growth and HUVEC cell growth, respectively[1]. 
Ki20227 (0.1-1000 nM; 1 hour) suppresses M-CSF-dependent c-Fms phosphorylation in a dose-dependent manner[1]. 
In Vivo: Ki20227 (orally;10-50 mg/kg/d for 20 days) of 50 mg/kg/d of Ki20227 for 20 days markedly decreases the osteolytic lesion areas[1]. 
ki20227 during global ischemia led to a significant deficit in microglial density in the CNS in mice, and CSF1R-inhibition led to a significant reduction in the neuronal density of mice[2].

Name: CC-401 (hydrochloride) CC401 HCl, CAS: 1438391-30-0, stock 33g, assay 98.7%, MWt: 424.93, Formula: C22H25ClN6O, Solubility: DMSO : 100 mg/mL (235.33 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: MAPK/ERK Pathway, Target: JNK, Biological_Activity: CC-401 hydrochloride is a potent inhibitor of all three forms of JNK with Ki of 25 to 50 nM.
IC50 & Target: Ki: 25 to 50 nM (JNK)[1]
In Vitro: CC-401 has at least 40-fold selectivity for JNK compared with other related kinases, including p38, extracellular signal-regulated kinase (ERK), inhibitor of κB kinase (IKK2), protein kinase C, Lck, zeta-associated protein of 70 kDa (ZAP70). In cell-based assays, 1 to 5 μM CC-401 provides specific JNK inhibition. CC-401, a small molecule that is a specific inhibitor of all three JNK isoforms. CC-401 competitively binds the ATP binding site in JNK, resulting in inhibition of the phosphorylation of the N-terminal activation domain of the transcription factor c-Jun. The specificity of this inhibitor is tested in vitro using osmotic stress of the HK-2 human tubular epithelial cell line. CC-401 inhibits sorbitol-induced phosphorylation of c-Jun in a dosage-dependent manner. However, CC-401 does not prevent sorbitol-induced phosphorylation of JNK, p38, or ERK[1].
In Vivo: The staining of p-JNK is moderately induced in bevazicumab and Oxaliplatin treatments as compared to control, and in the CC-401-treated samples p-cJun content is significantly lower, consistent with effective JNK inhibition. DNA damage is modestly elevated in combined treatments with CC-401[2]. CC-401 treatment from days 7 to 24 slows the progression of proteinuria, which is significantly reduced compared to the no-treatment and vehicle groups at days 14 and 21. However, there is still an increase in the degree of proteinuria at day 21 in CC-401-treated rats compared to proteinuria at day 5. The vehicle and no-treatment groups developed renal impairment at day 24 as shown by an increase in serum creatinine. This is prevented by CC-401 treatment[3].

Name: CP-724714, CAS: 383432-38-0, stock 6.9g, assay 98.2%, MWt: 469.54, Formula: C27H27N5O3, Solubility: DMSO : ≥ 50 mg/mL (106.49 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: Apoptosis;EGFR;EGFR, Biological_Activity: CP-724714 is a potent, selective inhibitor of HER2/ErbB2 with IC50 of 10 nM, >640-fold selectivity against EGFR, InsR, IRG-1R, PDGFR, VEGFR2, Abl, Src, c-Met etc. Phase 2.
IC50 value: 10 nM [1]
Target: HER2/ErbB2
in vitro: CP-724714 is marked selectively against EGFR with IC50 of 6.4 μM. CP-724714 is >1,000-fold less potent for IR, IGF-1R, PDGFRβ, VGFR2, abl. Src, c-Met c-jun NH2-terminal kinase (JNK)-2, JNK-3, ZAP-70, cyclin-dependent kinase (CDK)-2, and CDK-5. CP-724714 potently reduces the EGF-induced autophosphorylation of the chimera containing the erbB2 kinase domain with IC50 of 32 nM, but is markedly less potent against EGFR in transfected NIH3T3 cells. CP-724714 sensitively inhibits the proliferation of erbB2-amplified cells including BT-474 and SKBR3, with IC50 of 0.25 and 0.95 μM. CP-724714 induces the accumulation of cells in G1 phase and a marked reduction in S-phase in BT-474 cells at 1 μM [1]. CP-724714 likely exerts its hepatotoxicity via both hepatocellular injury and hepatobiliary cholestatic mechanisms. CP-724714 displays inhibition of cholyl-lysyl fluorescein and taurocholate (TC) efflux into canaliculi in cryopreserved and fresh cultured human hepatocytes, respectively. CP-724714 inhibits TC transport in membrane vesicles expressing human bile salt export pump with IC50 of 16 μM and inhibits the major efflux transporter in bile canaliculi, MDR1, with IC50 of ~28 μM [2].
in vivo: CP-724714 (25 mg/kg) is rapidly absorbed after p.o. administration and causes reduction of tumor erbB2 receptor phosphorylation after dosing in FRE-erbB2 or BT-474 xenografts. CP-724714 induces apoptosis in FRE-erbB2 xenograft–bearing (s.c.) mice and shows 50% tumor growth inhibition at 50 mg/kg, without weight loss or mortality. CP-724714 also has great antitumor activity in MDA-MB-453, MDA-MB-231, LoVo (colon), and Colo-205 (colon) xenografts. Furthermore, CP-724714 (30 or 100 mg/kg) reduces the extracellular signal–regulated kinase and Akt phosphorylation in BT-474 xenografts [1].

Name: Canertinib (dihydrochloride) CI-1033 dihydrochloride;PD-183805 dihydrochloride, CAS: 289499-45-2, stock 33.9g, assay 98.8%, MWt: 558.86, Formula: C24H27Cl3FN5O3, Solubility: DMSO : ≥ 155 mg/mL (277.35 mM), Clinical_Informat: Phase 2, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Canertinib dihydrochloride (CI-1033 dihydrochloride) is a potent and irreversible EGFR inhibitor; inhibits cellular EGFR and ErbB2 autophosphorylation with IC50s of 7.4 and 9 nM.
IC50 & Target: IC50: 7.4 nM (EGFR), 9 nM (ErbB2)[1]
In Vitro: Canertinib dihydrochloride (CI-1033 dihydrochloride) significantly inhibits growth of cultured melanoma cells, RaH3 and RaH5, in a dose-dependent manner. IC50 is approximately 0.8 μM and by 5μM both cell lines are completely growth-arrested within 72 h of treatment. Incubation of exponentially growing RaH3 and RaH5 with 1 μM canertinib accumulated the cells in the G1-phase of the cell cycle within 24 h of treatment without induction of apoptosis. 1 μM canertinib inhibits ErbB1-3 receptor phosphorylation with a concomitant decrease of Akt-, Erk1/2- and Stat3 activity in both cell lines[2].
In Vivo: Canertinib dihydrochloride (CI-1033 dihydrochloride) shows superior in vivo antitumor activity, giving growth delays in A431 xenografts exceeding 50 days following oral administration[1]. The growth of human malignant melanoma xenografts, RaH3 and RaH5, in nude mice is significantly inhibited by i.p. injections of 40 mg/kg/day canertinib (Fig. 4). The anti-proliferative effect on melanoma xenografts is visible already within 4 days of treatment and further increased throughout the treatment period as observed through the differences in tumor volumes, reaching statistical significance within 18 days of treatment[2].

Name: DAPT GSI-IX, CAS: 208255-80-5, stock 24g, assay 98.9%, MWt: 432.46, Formula: C23H26F2N2O4, Solubility: DMSO : ≥ 100 mg/mL (231.24 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Neuronal Signaling;Apoptosis;Autophagy, Target: γ-secretase;γ-secretase;Apoptosis;Autophagy, Biological_Activity: DAPT is a γ-secretase inhibitor with IC50s of 115 and 200 nM for total Aβ and Aβ42, respectively.
IC50 & Target: IC50: 115 nM (Aβ), 200 nM (Aβ42)[5]
In Vitro: DAPT inhibits Aβ production over 90%, effects only a modest reduction in APPβ in the culture media. Although APPβ is reduced by about 30% by DAPT treatment, this effect is not concentration-dependent and is reversed by the removal of DAPT[1]. CNE-2 cells are treated with increasing concentrations of DAPT (0, 25, 50 and 75 μM), and the γ-secretase-generated Notch 1 fragment Val1744-NICD is decreased after 48 h in a dose-dependent manner (P<0.01). The activation of γ-secretase is almost completely inhibited by DAPT at the concentration of 50 μM[2].
In Vivo: DAPT is administered to PDAPP mice (100 mg/kg s.c.) and the levels of DAPT and Aβ are examined in the brain cortex. Peak DAPT levels of 490 ng/g are achieved in the brain 3 h after treatment, and levels greater than 100 ng/g (~200 nM) are sustained throughout the first 18 h. These brain concentrations of DAPT are in excess of its IC50 for lowering Aβ in neuronal cultures (115 nM), and results in a robust and sustains pharmacodynamic effect[1]. DAPT protects brain against cerebral ischemia by down-regulating the expression of Notch 1 and Nuclear factor kappa B in rats. Western blot analyses also show a significant decrease of Notch 1 and NF-κB expression in DAPT (0.03 mg/kg) group (P<0.05 vs. MCAO group)[3].

Name: SRT3190, CAS: 1204707-73-2, stock 14.1g, assay 98.8%, MWt: 475.53, Formula: C18H23F2N5O4S2, Solubility: DMSO : ≥ 100 mg/mL (210.29 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: SRT3190 is an antagonist of CXCR2, used in the research of chemokine mediated diseases.
IC50 & Target: CXCR2[1]
In Vitro: SRT3190 (Reference Example 2) is an antagonist of CXCR2, used in the research of chemokine mediated diseases[1].

Name: URB-597 KDS-4103, CAS: 546141-08-6, stock 2.4g, assay 98.6%, MWt: 338.40, Formula: C20H22N2O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (295.51 mM), Clinical_Informat: Phase 1, Pathway: Neuronal Signaling;Metabolic Enzyme/Protease;Autophagy;Autophagy, Target: FAAH;FAAH;Autophagy;Mitophagy, Biological_Activity: URB597 is a potent, orally bioavailable FAAH inhibitor with IC50 of 4.6 nM, with no activity on other cannabinoid-related targets.
IC50 value: 4.6 nM [1]
Target: FAAH
in vitro: URB597 binds in the hydrophobic pocket and catalytic core of FAAH that connects the active site residues to the membrane surface of FAAH [1]. URB597 reduces the expression of the LPS-induced enzymes cyclo-oxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS; NOS2) in primary rat microglial cell, with a concomitant reduction in the release of the inflammatory mediators prostaglandin E2 (PGE2) and (NO) nitric oxide [2].
in vivo: URB597 inhibits [3H]anandamide hydrolysis in rat brain membranes with a parallel increase in brain anandamide, OEA, and PEA content by inhibition of FAAH. URB597 enhances the hypothermia effect induced by ethanolamide by inhibiting FAAH [3]. When delivered intraperitonealy (0.3 mg/kg) URB597 reduces allodynia and hyperalgesia through cannabinoid CB1 and CB2 receptor-mediated analgesia in rats with inflammatory pain [4].

Name: Panobinostat LBH589;NVP-LBH589, CAS: 404950-80-7, stock 15.2g, assay 98.6%, MWt: 349.43, Formula: C21H23N3O2, Solubility: DMSO : ≥ 57 mg/mL (163.12 mM), Clinical_Informat: Launched, Pathway: Apoptosis;Autophagy;Epigenetics;Cell Cycle/DNA Damage;Anti-infection, Target: Apoptosis;Autophagy;HDAC;HDAC;HIV, Biological_Activity: Panobinostat is an orally bioavailable non-selective histone deacetylase (HDAC) inhibitor.
In Vitro: Panobinosta (LBH589) induces apoptosis of both MOLT-4 and Reh cells in a time- and dose-dependent manner. Panobinosta treatment results in histone (H3K9 and H4K8) hyperacetylation and regulation of cell-cycle control genes in Reh cells[1]. Panobinostat exhibites potent antiproliferative activity in human NSCLC cell lines with the IC50 ranging from 5 to 100 nM[2].
In Vivo: Panobinosta (10, 20 mg/kg, i.p.) significantly slows tumor growth derived from Meso and NSCLC cells in vivo models. Panobinosta markedly increases acetylation of histone H3 and H4 of H69 human SCLC cells harvest from SCID mice[2]. Panobinostat (5, 10 and 20 mg/kg i.p.) demonstrates a clear benefit of decreased tumor burden, significantly improves TTE and reduces bone density loss in a disseminated multiple myeloma mouse model[3].

Name: VX-222 VCH-222, CAS: 1026785-59-0, stock 13.6g, assay 98.8%, MWt: 445.61, Formula: C25H35NO4S, Solubility: DMSO : ≥ 32 mg/mL (71.81 mM), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: HCV, Biological_Activity: VX-222 (VCH-222) is a novel, potent and selective inhibitor of HCV polymerase with IC50 of 0.94-1.2 μM, 15.3-fold less effective for mutant M423T, and 108-fold less effective for mutant I482L.
IC50 Value: 0.94 μM (HCV NS5B 1a); 1.2 μM (HCV NS5B 1b)
Target: HCV
VX-222 is a small molecule non-nucleoside inhibitor of HCV NS5B polymerase that is being investigated for the treatment of hepatitis C virus infection. VX-222 exhibits non-competitive and selective inhibition in HCV NS5B of genotype 1a and 1b, with IC50 of 0.94 and 1.2 μM, respectively. VX-222 selectively inhibits the replication of subgenomic HCV genotype 1a and 1b with an EC50 of 22.3 and 11.2 nM, respectively. [1] Similarly, a recent study shows that VX-222 inhibits the 1b/Con1 HCV subgenomic replicon, with an EC50 of 5 nM. In rats and dogs, VCH-222 displays fine pharmacokinetic pro le, including low total body clearance and excellent oral bioavailability (greater than 30%) and good ADME properties. VCH-222 is biotransformed by several enzymes (CYP1A1, 2A6, 2B6, 2C8, CYP 3A4, UGT1A3) and is predicted to be actively transported in liver and excreted mainly intact in bile or as glucuronide adducts.

Name: Pazopanib GW786034, CAS: 444731-52-6, stock 9.5g, assay 98.5%, MWt: 437.52, Formula: C21H23N7O2S, Solubility: DMSO : ≥ 43 mg/mL (98.28 mM), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;Autophagy;FGFR;c-Kit, Biological_Activity: Pazopanib is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFRβ, c-Kit, FGFR1, and c-Fms with IC50 of 10, 30, 47, 84, 74, 140 and 146 nM, respectively.

IC50 & Target: IC50: 10 nM (VEGFR1), 30 nM (VEGFR2), 47 nM (VEGFR3), 74 nM (c-Kit), 84 nM (PDGFRβ), 140 nM (FGFR1), 146 nM (c-Fms)[1]
In Vitro: Pazopanib shows good potency against all the human VEGFR receptors with an IC50 of 10, 30, and 47 nM for VEGFR-1, -2, and -3, respectively. Significant activity is also seen against the closely related tyrosine receptor kinases PDGFRβ, c-Kit, FGF-R1, and c-fms with IC50s of 84, 74, 140, and 146 nM, respectively. In cellular assays, in addition to inhibiting the VEGF-induced proliferation of HUVECs, Pazopanib potently inhibits VEGF-induced phosphorylation of VEGFR-2 in HUVEC cells with an IC50 of ~8 nM. Pazopanib possesses good pharmacokinetics in rat, dog, and monkey with low clearances (1.4-1.7 mL/min/kg) and good oral bioavailabilities (72, 47, 65%) dosed at 10, 1, and 5 mg/kg, respectively. The cytochrome P450 profile is also improved with inhibition >10 μM against the isozymes tested, with the exception of 2C9 (7.9 μM)[1].
In Vivo: Treatment of mice with 100 mg/kg of Pazopanib twice daily for five days results in significant inhibition in the degree of vascularization. The antiangiogenic activity of Pazopanib is examined in mice bearing established human xenografts (200−250 mm3) using HT29 (colon carcinoma), A375P (melanoma), and HN5 (head and neck carcinoma) tumors following a standard three-week course of therapy. The HN5 and HT29 xenografts responded better at all doses compared to the A375P model, which is historically more resistant to VEGFR-2 inhibitors. As support that the observed inhibition of xenograft growth is working through an antiangiogenic rather than antitumor mechanism, no antiproliferative activity is observed below 10 μM for Pazopanib against these human tumor lines (HT29, HN5, A375P) growing in serum-containing media. No significant effect on the body weight of mice is observed, and the animals appeared healthy and active throughout the study duration[1]. The quantity of adherent leukocytes in the Pazopanib eye drops group is less than untreated diabetic animals and more than the healthy animals. Average leukocytes adhered to the retinal vasculature in healthy animals is 37.2±7.8, whereas diabetic animals have an average value of 102±15.6, approximately 3-fold higher than healthy animals. Animals treated with 0.5 % w/v Pazopanib suspension demonstrate 69.5±9.5 leukocytes adhered in their retinal vasculature, which is found to be significantly lower than diabetic animals[2].

Name: Daclatasvir (dihydrochloride) BMS-790052 dihydrochloride, CAS: 1009119-65-6, stock 21.1g, assay 98.6%, MWt: 811.80, Formula: C40H52Cl2N8O6, Solubility: DMSO : ≥ 56 mg/mL (68.98 mM); H2O : 50 mg/mL (61.59 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: HCV, Biological_Activity: Daclatasvir dihydrochloride (BMS-790052 dihydrochloride) is a highly selective inhibitor of HCV NS5A with EC50 of 9-50 pM, for a broad range of HCV replicon genotypes and the JFH-1 genotype 2a infectious virus in cell culture.
IC50 Value: 9-50 pM
Target: HCV NS5A
Daclatasvir has broad genotype coverage and exhibits picomolar in vitro potency against genotypes 1a (EC50 50pm) and 1b (EC50 9pm). Daclatasvir produces a robust decline in HCV RNA (-3.6 logs after 48 hours from a single 100 mg) dosefollowing a single dose in patients chronically infected with HCV genotype 1.

Name: A-867744, CAS: 1000279-69-5, stock 33.6g, assay 98.3%, MWt: 402.89, Formula: C20H19ClN2O3S, Solubility: DMSO : ≥ 100 mg/mL (248.21 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: A-867744 is a highly potent and selective type II positive allosteric modulator (PAM) of the alpha7 nicotinic acetylcholine receptors (nAChR) with an EC50 of 1.0 μM[1].
IC50 & Target: EC50: 1.0 μM (alpha7 nAChR)[1]

Name: ICG-001, CAS: 780757-88-2, stock 39.5g, assay 98.6%, MWt: 548.63, Formula: C33H32N4O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 50 mg/mL (91.14 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Stem Cell/Wnt, Target: Apoptosis;β-catenin, Biological_Activity: ICG-001 is an inhibitor of β-catenin/TCF mediated transcription. ICG-001 works by specifically binding to cyclic AMP response element-binding protein with an IC50 of 3 μM. ICG-001 selectively blocks the β-catenin/CBP interaction without interfering with the β-catenin/p300 interaction.
IC50 & Target: IC50: 3 μM (CBP)
In Vitro: ICG-001 (5μM) inhibits leptin-induced EMT, invasion and tumorsphere formation in MCF7 cells[1]. ICG-001 can phenotypically rescue normal nerve growth factor (NGF)-induced neuronal differentiation and neurite outgrowth in the presenilin-1 mutant cells, emphasizing the importance of the TCF/β-catenin signaling pathway on neurite outgrowth and neuronal differentiation[2]. ICG-001 (25μM) treatment reduces the steady-state levels of Survivin and Cyclin D1 RNA and protein in SW480 cells, both of which can be up-regulated by β-catenin. ICG-001 selectively induces apoptosis in transformed cells but not in normal colon cells, and reduces in vitro growth of colon carcinoma cells[3].
In Vivo: ICG-001 (5 mg/kg per day) significantly inhibits beta-catenin signaling in mice, while concurrently preserving the epithelium[2]. Administration of a water-soluble analog of ICG-001 for 9 weeks reduces the formation of colon and small intestinal polyps by 42% as effectively as the nonsteroidal antiinflammatory agent MK-231, which has consistently demonstrated efficacy in this model. ICG-001 (150 mg/kg, i.v.) demonstrates a dramatic reduction in tumor volume over the 19-day course of treatment, with no mortality or weight loss in the SW620 nude mouse xenograft model of tumor regression[3].

Name: Volasertib BI 6727, CAS: 755038-65-4, stock 16.4g, assay 98.9%, MWt: 618.81, Formula: C34H50N8O3, Solubility: DMSO : 50 mg/mL (80.80 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;Polo-like Kinase (PLK), Biological_Activity: Volasertib is a highly potent Polo-like kinase 1 (PLK1) inhibitor with an IC50 of 0.87 nM, as well as the two closely related kinases PLK2 and PLK3 with IC50s of 5 and 56 nM, respectively.
IC50 & Target: IC50: 0.87 nM (PLK1), 5 nM (PLK2), 56 nM (PLK3)[3]
In Vitro: Volasertib is potent against HeLa and Caski cells with IC50 values of 0.02 μM and 2.02 μM, respectively. Volasertib (0.03 μM) induces cell cycle arrest at G2/M Phase in cervical cancer cells. Volasertib (0.003-0.03 μM) induces apoptosis in HeLa cells, and Volasertib (0.3-3 μM) results in Caski cell apoptosis. Volasertib (1, 3 μM or 0.01,0.03 μM) augments the fluorescent intensity of DHE in Caski and HeLa cells in a dose-dependent manner[1]. Volasertib shows inhibitory activities against the proliferation of all 40 cell lines tested, with a mean half-maximal growth inhibitory concentration of 313 nM (range: 4-5000 nM)[2]. Volasertib inhibits proliferation of multiple cell lines derived from various cancer tissues, including carcinomas of the colon (HCT 116, EC50=23 nM) and lung (NCI-H460, EC50=21 nM), melanoma (BRO, EC50=11 nM), and hematopoietic cancers (GRANTA-519, EC50=15 nM; HL-60, EC50=32 nM; THP-1, EC50=36 nM and Raji, EC50=37 nM) with EC50 values of 11 to 37 nM. Volasertib (100 nM) causes G2-M arrest and induces apoptosis in NCI-H460 cells[3].
In Vivo: Volasertib (15 mg/kg, i.p.) inhibit xenograft tumor growth of cervical cancer cells in nude mice[1]. Volasertib (70 mg/kg, p.o. once a week or 10 mg/kg, p.o. daily) significantly delays tumor growth in a non-small cell lung carcinoma xenograft model. In addition, Volasertib (15 mg/kg, i.v.) markedly suppresses tumor growth and is well tolerated[3].

Name: Zosuquidar (trihydrochloride) RS 33295-198 trihydrochloride;LY-335979 trihydrochloride, CAS: 167465-36-3, stock 32.4g, assay 98.3%, MWt: 636.99, Formula: C32H34Cl3F2N3O2, Solubility: H2O : 5 mg/mL (7.85 mM; Need ultrasonic); DMSO : 1 mg/mL (1.57 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Membrane Transporter/Ion Channel, Target: P-glycoprotein, Biological_Activity: Zosuquidar trihydrochloride is an inhibitor of P-glycoprotein with a Ki value of 59 nM.
IC50 & Target: Ki: 59nM (P-glycoprotein)[1].
In Vitro: Zosuquidar completely or partially restores drug sensitivity in all P-gp-expressing leukemia cell lines and enhances the cytotoxicity of anthracyclines (daunorubicin, idarubicin, mitoxantrone) and gemtuzumab ozogamicin (Mylotarg) in primary AmL blasts with active P-gp. In addition, P-gp inhibition by zosuquidar is found to be more potent than cyclosporine A in cells with highly active P-gp[2].
In Vivo: Zosuquidar trihydrochloride is only moderately active as an inhibitor of P-gp at the blood-brain. An oral dose of 25 mg/kg of zosuquidar trihydrochloride increases the brain concentrations by about 2.5-fold at 1 h and 5-fold at 24 h after paclitaxel administrationbarrier[3]. Zosuquidar enhances the brain uptake of nelfinavir in a dose-dependent manner. Brain tissue/plasma nelfinavir concentration ratios increase from 0.06±0.03 in the absence of zosuquidar administration and 0.09±0.02 between 2 and 6 h after a 2 mg/kg intravenous dose of zosuquidar to 0.85±0.19 after 6h and 1.58±0.67 after 20 mg/kg zosuquidar[4].

Name: Odanacatib MK-0822, CAS: 603139-19-1, stock 13.8g, assay 98.8%, MWt: 525.56, Formula: C25H27F4N3O3S, Solubility: DMSO : ≥ 25 mg/mL (47.57 mM), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Cathepsin, Biological_Activity: Odanacatib (MK-0822) is a potent and selective inhibitor of cathepsin K, with an IC50 of 0.2 nM for human cathepsin K.
IC50 & Target: IC50: 0.2 nM (Human Cathepsin K), 1 nM (Rabbit Cathepsin K)
In Vitro: Odanacatib is a weak inhibitor of antigen presentation, measured in a mouse B cell line (IC50=1.5±0.4 μM), compared to the Cat S inhibitor LHVS (IC50=0.001 μM) in the same assay. Odanacatib also shows weak inhibition of the processing of the MHC II invariant chain protein Iip10 in mouse splenocytes compared to LHVS (minimum inhibitory concentration 1-10 μM versus 0.01 μM, respectively)[1]. Odanacatib reduces resorption activity as measured by CTx release (IC50=9.4 nM) or resorption area (IC50=6.5 nM), but has no impact on OC activation. Odanacatib dose-dependently reduces CTx release with an IC50=9.4±1.0 nM. Odanacatib treated OC accumulates labeled degraded bone matrix proteins in CatK containing vesicles[2].
In Vivo: Odanacatib (30 mg/kg, orally, once daily) persistently suppresses bone resorption markers and serum bone formation markers versus vehicle-treated OVX monkeys. Odanacatib displays compartment-specific effects on trabecular versus cortical bone formation, with treatment resulting in marked increases in periosteal bone formation and cortical thickness in ovariectomized monkeys whereas trabecular bone formation is reduced[3]. The bone volume/total volume (BV/TV) and bone mineral density (BMD) of the OVX + ODN-h group is significantly higher than that of the OVX + Veh group (p < 0.05). The expressions of Runx2, Collagen-1, BSP, Osterix, OPN and SPP1 are significantly lower in the OVX + ODN-h group than in the OVX + Veh group (p < 0.01). Compared with the OVX + Veh group, the expressions of Collagen-I, BSP, Osterix, OPN and ALP reduce in the OVX + ODN-l group, but are upregulated in the OVX + ODN-h group[4].

Name: Cabozantinib XL184;BMS-907351, CAS: 849217-68-1, stock 30.2g, assay 98%, MWt: 501.51, Formula: C28H24FN3O5, Solubility: DMSO : ≥ 30 mg/mL (59.82 mM), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;Apoptosis;VEGFR;FLT3;TAM Receptor;c-Kit, Biological_Activity: Cabozantinib is a potent multiple receptor tyrosine kinases (RTKs) inhibitor that inhibits VEGFR2, c-Met, Kit, Axl and Flt3 with IC50s of 0.035, 1.3, 4.6, 7 and 11.3 nM, respectively.
IC50 & Target: IC50: 0.035 nM (VEGFR2), 1.3 nM (c-Met), 4.6 nM (Kit), 7 nM (Axl), 11.3 nM (Flt3)[1]
In Vitro: Cabozantinib is a potent inhibitor of MET and VEGFR2 with IC50 values of 1.3 and 0.035 nM, respectively. MET-activating kinase domain mutations Y1248H, D1246N, or K1262R are also inhibited by Cabozantinib (IC50=3.8, 11.8, and 14.6 nM, respectively). Cabozantinib displays strong inhibition of several kinases that have also been implicated in tumor pathobiology, including KIT, RET, AXL, TIE2, and FLT3 (IC50=4.6, 5.2, 7, 14.3, and 11.3 nM, respectively). In cellular assays, Cabozantinib inhibits phosphorylation of MET and VEGFR2, as well as KIT, FLT3, and AXL with IC50 values of 7.8, 1.9, 5.0, 7.5, and 42 μM, respectively. The effect of Cabozantinib on proliferation is evaluated in a number of human tumor cell lines. SNU-5 and Hs746T cells harboring amplified MET are the most sensitive to Cabozantinib (IC50=19 and 9.9 nM, respectively); however, SNU-1 and SNU-16 cells lacking MET amplification are more resistant (IC50=5,223 and 1,149 nM, respectively). MDA-MB-231 and U87MG cells exhibit comparable levels of sensitivity to Cabozantinib (IC50=6,421 and 1,851 nM, respectively), whereas H441, H69, and PC3 cell lines are the least sensitive to Cabozantinib with IC50 values of 21,700, 20,200, and 10,800 nM, respectively. In addition, BaF3 cells expressing human FLT3-ITD, an activating mutation in acute myelogenous leukemia, are sensitive to Cabozantinib (IC50=15 nM) when compared with wild-type BaF3 cells (IC50=9,641 nM)[2].
In Vivo: Tumor vascularity decreases after Cabozantinib (XL184), with reductions ranging from 67% at 3 mg/kg to 83% at 30 mg/kg for 7 days[1]. In mouse models, Cabozantinib dramatically alters tumor pathology, resulting in decreased tumor and endothelial cell proliferation coupled with increased apoptosis and dose-dependent inhibition of tumor growth in breast, lung, and glioma tumor models. Importantly, treatment with Cabozantinib does not increase lung tumor burden in an experimental model of metastasis, which has been observed with inhibitors of VEGF signaling that do not target MET. On a body weight dosage basis, Cabozantinib plasma exposures range from 6- to 10-fold higher in rats than in mice, which accounts for lower doses inducing tumor growth inhibition/regression in rats than in mice. Subchronic administration of Cabozantinib is well tolerated in mice and rats with no signs of toxicity, as determined by stable and/or increasing body weights during the treatment period[2].

Name: Bay 60-7550 BAY 607550, CAS: 439083-90-6, stock 34g, assay 98.4%, MWt: 476.57, Formula: C27H32N4O4, Solubility: DMSO : ≥ 33.3 mg/mL (69.87 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Bay 60-7550 is a potent and selective PDE2 inhibitor with a Ki of 3.8 nM.
IC50 & Target: Ki: 3.8±0.2 nM (PDE2)[1]
In Vitro: Bay 60-7550 (1 μM) increases cGMP in the neuronal cultures compared with control [F(6,14)=12.97, p<0.05 for Bay 60-7550]. Bay 60-7550 in the presence of NMDA (30 μM) results in further increases in cGMP compared with NMDA alone. The NMDA receptor antagonist MK-801 (10 μM) blocks both Bay 60-7550+NMDA-induced elevation in cGMP in neuronal cultures[1]. Compared with untreated control cells, proliferation of PASMCs from IPAH patients is significantly reduced by BAY 60-7550 (1 μM)[2].
In Vivo: The PDE2 inhibitors Bay 60-7550 (1 mg/kg) reverses restraint stress-induced alterations in behavior, resulting in increased percentages of open-arm entries and open-arm time compared with the vehicle + restraint stress condition. In nonstressed mice, Bay 60-7550 produces a dose-dependent increase in percentages of open-arm entries and open-arm time compared with the vehicle-treated group; significant increases are observed at a dose of 3 mg/kg. In nonstressed mice, Bay 60-7550 increases, in a dose-dependent manner, the number of head-dips and time spent head-dipping, compared with vehicle-treated mice; significant increases are observed at doses of 1 and 3 mg/kg[1].

Name: GW-1100, CAS: 306974-70-9, stock 29.3g, assay 99%, MWt: 520.58, Formula: C27H25FN4O4S, Solubility: DMSO : 50 mg/mL (96.05 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPR40, Biological_Activity: GW-1100 is a selective GPR40 antagonist with a pIC50 of 6.9. GW1100 acts as a GPR40 inverse agonist.
IC50 & Target: pIC50: 6.9 (GPR40)[1]
In Vitro: GW-1100 (GW1100) dose dependently inhibits GPR40-mediated Ca2+ elevations stimulated by GW9508 and linoleic acid (pIC50 values of 5.99±0.03 and 5.99±0.06, respectively). GW-1100 at a concentration of 1 μM produces a significant rightward shift in the concentration-response curve to GW9508 (pEC50=7.17±0.08 in the absence and pEC50=6.79±0.09 in the presence of 1 μM GW-1100; P<0.05; n=3). At concentrations of GW-1100 of 3 μM and higher a significant decrease in the maximal response is observed with a continuing rightward shift in the pEC50 response[2]. GW-1100 (GW1100) reduces FFAR1 ligand-induced intracellular calcium in CHO-K1/bFFAR1 cells and neutrophils. CHO-K1/bFFAR1 cells are incubated for 15 min with 10 μM GW1100 or vehicle (0.1% DMSO) and then stimulated with vehicle, oleic acid, linoleic acid or GW9508. GW-1100 significantly reduces the increase in intracellular calcium induced by 300 μM oleic acid (AUC(60-150 s), p<0.05), 100 μM linoleic acid (AUC(60-150 s), p<0.05) and 10 μM GW9508 (AUC(60-150 s), p<0.05)[3].
In Vivo: The intracerebroventricular injection of DHA (50 µg) and GW9508 (1.0 µg), a GPR40-selective agonist, significantly reduces mechanical allodynia and thermal hyperalgesia at day 7, but not at day 1, after CFA injection. These effects are inhibited by intracerebroventricular pretreatment with GW-1100 (10 µg), a GPR40 antagonist[4].

Name: CTS-1027 Ro 1130830;RS 130830, CAS: 193022-04-7, stock 36.5g, assay 98.8%, MWt: 425.88, Formula: C19H20ClNO6S, Solubility: DMSO : ≥ 100 mg/mL (234.81 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: CTS-1027 is a potent small molecule inhibitor of MMPs, with IC50s of 0.3 nM, 0.5 nM for MMP2, MMP13, respectively, and has > 1,000 fold selectivity over MMP1.
IC50 & Target: IC50: 0.2 nM (MMP2), 0.5 nM (MMP13), 0.7 nM (MMP12), 0.9 nM (MMP8), 9.5 nM (MMP3), 15 nM (MMP14)
In Vivo: CTS-1027 significantly reduces the hepatocyte apoptosis, features of cholestatic liver injury, amd markers of hepatic fibrogenesis in the BDL mouse. CTS-1027 improves overall animal survival following 14 days of BDL in mice[1]. In male animals treated for 8 weeks the terminal plasma concentration of RS-130830 is 311±45 nM. Treatment of male mice with RS-130830 for 8 weeks causes an 89% increase in plasma triglyceride concentration, but there is no corresponding effect in female mice treated for 12 weeks. The plaque lipid content of animals receiving RS-130830 is increased by 81% at 12 weeks, and increased by 41% at 16 weeks[2].

Name: Fasiglifam TAK-875, CAS: 1000413-72-8, stock 21.2g, assay 98.9%, MWt: 524.63, Formula: C29H32O7S, Solubility: DMSO : ≥ 128 mg/mL (243.98 mM), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein, Target: GPR40, Biological_Activity: Fasiglifam (TAK-875) is a potent, selective and orally bioavailable GPR40 agonist with EC50 of 72 nM.
IC50 & Target: EC50: 72 nM (GPR40)
In Vitro: Fasiglifam (TAK-875) (0.01-10 μM) produces a concentration-dependent increase in intracellular IP production in CHO-hGPR40, with EC50 of 0.072 μM. Fasiglifam (TAK-875) (0.1-10 μM) dose-dependently augments intracellular IP production in CHO cells[1]. Fasiglifam (TAK-875) (3-30 μM) concentration-dependently augments [Ca2+]i. In the presence of 10 mM glucose, TAK-875 (0.001-10 μM) dose-dependently stimulats insulin secretion from INS-1 833/15 cells[2].
In Vivo: Fasiglifam (TAK-875) (10 mg/kg, p.o.) increases plasma insulin levels in ZDF rats. Fasiglifam (TAK-875) (30 mg/kg, p.o.) improves fasting hyperglycemia without affecting fasting normoglycemia. Fasiglifam (TAK-875) at 30 mg/kg, which is a 3- to 10-fold higher dose compared with the dose that improved glucose tolerance in diabetic rats, does not alter fasting glucose levels in SD rats with normal glucose homeostasis. Likewise, Fasiglifam (TAK-875) does not significantly alter insulin secretion in SD rats with normal fasting glucose levels [1].

Name: ACHP (Hydrochloride) IKK-2 Inhibitor VIII, CAS: 406209-26-5, stock 35g, assay 98.9%, MWt: 400.90, Formula: C21H25ClN4O2, Solubility: DMSO : 50 mg/mL (124.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: IKK, Biological_Activity: ACHP Hydrochloride (IKK-2 Inhibitor VIII) is a highly potent and selective IKK-β inhibitor with an IC50 of 8.5 nM.
IC50 & Target: IC50: 8.5 nM (IKK-β), 250 nM (IKK-α), >20000 nM (IKK3, Syk and MKK4)[1]
In Vitro: ACHP Hydrochloride (Compound 4j) exhibits potent IKK-β inhibitory (IC50: 8.5 nM) and cellular activities (IC50=40 nM, in A549 cells). ACHP moderately inhibits IKK-α with an IC50 of 250 nM but exhibits good selectivity towards other kinases, such as IKK3, Syk and MKK4 (IC50>20,000 nM). Moreover, ACHP demonstrates quite potent activity in various cellular assays. ACHP inhibits NF-κB-dependent reporter gene activation in TNFα-activated HEK293 cells and PMA/calcium ionophore-activated Jurkat T cells. ACHP fails to inhibit PMA-induced AP-1 activation in MRC-5 cells and PMA/calcium ionophore induced NF-κB dependent reporter gene transcription in Jurkat cells even at concentrations exceeding 10 μM. ACHP selectively interferes with the NF-κB signaling cascade by inhibition of IKK-β in living cells[1]. ACHP inhibits the growth of these cells in a dose-dependent manner. Tax-active cell lines are more susceptible to ACHP than Tax-inactive cell lines and Jurkat (IC50 values in Tax-active cell lines, Tax-inactive cell lines or Jurkat are 3.1±1.3 μM, 10.7±1.7 μM and 23.6 μM, respectively), suggesting that the growth of Tax-active cells depends on NF-κB more than Tax-inactive cells[2].
In Vivo: ACHP (Compound 4j) is orally bioavailable in mice and rats and demonstrates significant in vivo activity in anti-inflammatory models (arachidonic acid-induced mouse ear edema model). ACHP has reasonable aqueous solubility (0.12 mg/mL in pH 7.4 isotonic buffer) and excellent Caco-2 permeability (Papp 62.3×10-7 cm/s), and demonstrates orally bioavailability in mice (BA: 16%) and rats (BA: 60%). The favourable bioavailability of ACHP in rats is likely due to its low clearance (0.33 L/h/kg). In an acute inflammation model, ACHP exhibits oral efficacy at 1 mg/kg in a dose-dependent manner[1].

Name: Silodosin KAD 3213;KMD 3213, CAS: 160970-54-7, stock 36.9g, assay 98.4%, MWt: 495.53, Formula: C25H32F3N3O4, Solubility: DMSO : ≥ 50 mg/mL (100.90 mM), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Silodosin (Rapaflo; KMD-3213) is an α1-adrenoceptor antagonist with high uroselectivity; In treatment of dysuria.
IC50 Value:
Target: Adrenergic Receptor
in vitro: Silodosin potently inhibited 2-[2-(4-hydroxy-3-[125I]iodophenyl)ethylaminomethyl]-alpha-tetralone binding to the cloned human alpha 1a-AR, with a Ki value of 0.036 nM, but had 583- and 56-fold lower potency at the alpha 1b- and alpha 1d-ARs, respectively. Silodosin inhibited norepinephrine-induced increases in intracellular Ca2+ concentrations in alpha 1a-AR-expressing Chinese hamster ovary cells with an IC50 of 0.32 nM but had a much weaker inhibitory effect on the alpha 1b- and alpha 1d-ARs.
in vivo: Using pharmacologically well characterized native rat tissues [submaxillary gland (alpha 1A-AR-expressing tissue), liver (alpha 1B-AR-expressing tissue), and heart (mixed alpha 1A- and alpha 1B-AR-expressing tissue)], binding studies showed that inhibition curves for Silodosin in submaxillary gland and liver best fit a one-site model (with Ki values of 0.15 and 16 nM, respectively), whereas Silodosin had high and low affinity sites in heart membranes. Chloroethylclonidine treatment of rat heart membranes completely eliminated the low affinity sites for Silodosin. Furthermore, in human liver and prostate Silodosin could identify high and low affinity sites, the Ki values of which corresponded well to those for the cloned human alpha 1a- and alpha 1b-ARs, respectively. Moreover, the affinity of Silodosin was found to be approximately 10-fold higher at the cloned human alpha 1a-AR than at the cloned rat alpha 1a-AR.v

Name: Telaprevir VX-950, CAS: 402957-28-2, stock 28.7g, assay 98.8%, MWt: 679.85, Formula: C36H53N7O6, Solubility: DMSO : ≥ 50 mg/mL (73.55 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: HCV Protease;HCV, Biological_Activity: Telaprevir is a highly selective, reversible, and potent peptidomimetic inhibitor of the HCV NS3-4A protease, the steady-state inhibitory constant (Ki) of Telaprevir is 7 nM against a genotype 1 (H strain) NS3 protease domain plus a NS4A cofactor peptide.
IC50 & Target: Ki: 7 nM (genotype 1 HCV NS3-4A protease)[1]
In Vitro: Telaprevir (VX-950) is a covalent, reversible inhibitor of the NS3-4A protease with a slow-binding and slow-dissociation mechanism. Telaprevir exhibits significantly different kinetics in enzyme inhibition, which is most clearly exemplified by a very long half-life (58 min) of the bound enzyme-inhibitor complex. Telaprevir is additive to moderately synergistic with IFN-α in inhibiting HCV replication and in suppressing the emergence of resistance in replicon cells. Telaprevir reduces HCV RNA levels in a time- and dose-dependent manner. The IC50s following a 24, 48, 72, and 120 h incubation with Telaprevir are determined to be 0.574, 0.488, 0.21, and 0.139 μM, respectively, indicating an increase in inhibitory effects with time. Following three independent experiments using the 48 h incubation in the presence of 2% FBS, the average IC50 of Telaprevir is determined to be 0.354 ± 0.035 μM, and the average IC90 is 0.830 ± 0.190 μM[1]. Telaprevir (VX-950) is a potent, selective, peptidomimetic inhibitor of the hepatitis C virus (HCV) NS3-4A serine protease, and Telaprevir demonstrates excellent antiviral activity both in genotype 1b HCV replicon cells (IC50=354 nM) and in human fetal hepatocytes infected with genotype 1a HCV-positive patient sera (IC50=280 nM)[2].
In Vivo: There is an ~5-fold reduction of serum SEAP activity in mice dosed with Telaprevir (VX-950) at either 10 or 25 mg/kg, which has an average value (±SEM) of 18.7±8.3% or 18.4±5.4%, respectively, compare to those administered vehicle (100±28%). These data demonstrates that Telaprevir is able to inhibit the HCV NS3-4A serine protease activity in mouse liver and block cleavage and subsequent secretion of SEAP into blood circulation in these mice[2].

Name: Triptolide PG490, CAS: 38748-32-2, stock 3.2g, assay 98.2%, MWt: 360.40, Formula: C20H24O6, Solubility: DMSO : ≥ 33 mg/mL (91.56 mM), Clinical_Informat: Phase 3, Pathway: Apoptosis;NF-κB, Target: Apoptosis;NF-κB, Biological_Activity: Triptolide is a diterpenoid triepoxide extracted from the root of Tripterygium wilfordii with immunosuppressive, anti-inflammatory and antiproliferative effects. Triptolide is a NF-κB activation inhibitor.
IC50 & Target: heat shock factor (HSF1)[1] 
IC50: 47 to 73 nM (MDM2, in ALL cell lines)[2]
In Vitro: Triptolide induces apoptosis in cultured and primary Chronic Lymphocytic Leukemia (CLL) B-cells. Treatment of CD19+ B cells with Triptolide, induces a dose-dependent increase in apoptosis in cultured and primary CLL cells. Triptolide is selectively toxic to both high risk (n=5) and low risk CLL (n=12) B cells (10 to 50 nM range) while largely sparing normal B-cells (n=5). Consistent with the inhibition of heat-shock induced HSP transcription, treatment with Triptolide attenuates heat-shock induced expression of HSPs[1]. Triptolide is a natural product derived from the Chinese plant Tripterygium wilfordii, is reported to exhibit antitumor effects in a broad range of cancers. Triptolide inhibits MDM2 expression in a dose-dependent manner, even at low concentrations spanning 20-100 nM in acute lymphoblastic leukemia (ALL) cells. Triptolide exhibits strongly cytotoxic activity in all 8 cell lines having native MDM2 overexpression, with IC50 values range from 47 to 73 nM. Triptolide exhibits much less cytotoxic effect on EU-4 cells that express very low level of MDM2, while it effectively kill these cells when MDM2 is stably transfected (IC50 values: 725 nM vs. 88 nM)[2]. Differentiated PC12 cells are incubated with different concentrations of Triptolide (0.01, 0.1, and 1 nM) in the presence of 10 μM Aβ25-35 for 24 hours and MTT assay is used to detect the effect of Triptolide. The results show that Aβ25-35 can decrease the cell viability and when treated with Triptolide the viability of differentiated PC12 cells is significantly increased. The results indicate that Triptolide can alleviate cellular damage caused by Aβ25-35, which means that Triptolide has a neuroprotective effect[3].
In Vivo: The Triptolide (TP) plasma concentrations are declined rapidly in mice after receive an intravenous dose. After 2h of injection, the Triptolide concentrations are dropped below the lower limit of quantification for all three groups. A comparison of the parameters is made between the control and the treated groups to assess the effect of P-gp inhibition on the Triptolide exposure and elimination. Treatment with the mdr1a-siRNA can significantly enhance the Triptolide plasma exposure, with the Cmax increases from 413±74 to 510±94 ng/mL (P<0.05) and the AUC from 103.5±9.6 to 154.3±30.2 ng•h/mL (P<0.05). In the concomitant group with Tariquidar, the significantly increased AUC is also noted, from 103.5±9.6 of the control to 145.9±24.6 ng•h/mL of the Triptolide+Tariquidar group (P<0.05). Accordingly, the total body clearance of Triptolide in mice is remarkably decreased, from 9564±1024.2 mL/min/kg of the control to 6576.4±1438.5 (P<0.05) and 5755.4±1200.1 mL/min/kg (P<0.05) for Triptolide+Tariquidar and Triptolide+mdr1a-siRNA groups, respectively[4].

Name: Cinacalcet AMG 073, CAS: 226256-56-0, stock 30.7g, assay 98.1%, MWt: 357.41, Formula: C22H22F3N, Solubility: DMSO : ≥ 100 mg/mL (279.79 mM), Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: CaSR, Biological_Activity: Cinacalcet (AMG 073) is an orally active, allosteric agonist of Ca receptor (CaR), used for cardiovascular disease treatment.
In Vivo: Cinacalcet HCl (5 and 10 mg/kg) results in a significant reduction in parathyroid gland weight in 5/6 nephrectomy animals. In sham animals, Cinacalcet HCl has no effect on parathyroid gland cell proliferation or parathyroid weight compared with vehicle treatment. There are no differences in serum phosphorus levels in Cinacalcet HCl (10, 5, or 1 mg/kg) treated 5/6 nephrectomized animals compared with vehicle-treated 5/6 nephrectomized animals. Cinacalcet HCl treatment significantly reduces blood ionized calcium levels in sham animals[1]. Cinacalcet (30 mg/kg/24 h) leads to a marked reduction in circulating parathyroid hormone and a modest reduction in serum Ca. Cinacalcet does not alter UCa when the GHS rats are fed the normal Ca diet but lowers UCa when they are fed the low Ca diet. Cinacalcet does not alter U supersaturation with respect to either CaOx or CaHPO4 on either diet[2].

Name: Cinacalcet (hydrochloride) AMG-073 (hydrochloride), CAS: 364782-34-3, stock 19.5g, assay 98.1%, MWt: 393.87, Formula: C22H23ClF3N, Solubility: DMSO : ≥ 50 mg/mL (126.95 mM), Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: CaSR, Biological_Activity: Cinacalcet hydrochloride (AMG-073 hydrochloride) is an orally active, allosteric agonist of Ca receptor (CaR), used for cardiovascular disease treatment.
In Vivo: Cinacalcet (5 and 10 mg/kg) results in a significant reduction in parathyroid gland weight in 5/6 nephrectomy animals. In sham animals, Cinacalcet has no effect on parathyroid gland cell proliferation or parathyroid weight compared with vehicle treatment. There are no differences in serum phosphorus levels in Cinacalcet (10, 5, or 1 mg/kg) treated 5/6 nephrectomized animals compared with vehicle-treated 5/6 nephrectomized animals. Cinacalcet treatment significantly reduces blood ionized calcium levels in sham animals[1]. Cinacalcet (30 mg/kg/24 h) leads to a marked reduction in circulating parathyroid hormone and a modest reduction in serum Ca. Cinacalcet does not alter UCa when the GHS rats are fed the normal Ca diet but lowers UCa when they are fed the low Ca diet. Cinacalcet does not alter U supersaturation with respect to either CaOx or CaHPO4 on either diet[2].

Name: Taranabant MK-0364, CAS: 701977-09-5, stock 33.9g, assay 98.1%, MWt: 515.95, Formula: C27H25ClF3N3O2, Solubility: DMSO : ≥ 42 mg/mL (81.40 mM), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cannabinoid Receptor;Cannabinoid Receptor, Biological_Activity: Taranabant is a highly potent and selective cannabinoid 1 (CB1) receptor inverse agonist that inhibits the binding and functional activity of various agonists, with a binding Ki of 0.13 nM for the human CB1R in vitro.

IC50 & Target: IC50: 0.3 nM (hCB1R), 0.4 nM (rCB1R)[1] Ki: 0.13 nM (hCB1R), 0.27 nM (rCB1R)[1]
In Vitro: Taranabant (MK-0364) binds to human or rat CB1R with an IC50 of 0.3 and 0.4 nM, respectively, corresponding to a Ki value of 0.13 and 0.27 nM, respectively. Taranabant binds to the human or rat CB2R with an IC50 value of 290 and 470 nM, respectively, corresponding to a Ki value of 170 and 310 nM, respectively. The selectivity ratio of CB1R over CB2R is approximately 1000-fold[1]. Taranabant (MK-0364) is a novel, acyclic cannabinoid-1 receptor inverse agonist for the treatment of obesity. IC50s of Taranabant for CB1R and CB2R by substituted amides is 0.3±0.1 nM, and 290±60 nM, respectively. Taranabant is a CB1R inverse agonist with minimal potential for covalent protein binding. Taranabant is an exceptionally potent and selective (900-fold over CB2) CB1R inverse agonist with >500-fold improvement in affinity over the original lead. In a functional assay of cyclic-AMP production, Taranabant is determined to be an inverse agonist (EC50=2.4±1.4 nM)[2].
In Vivo: Taranabant (MK-0364) dose-dependently inhibits 2 h and overnight food intake as well as overnight gains in body weight in C57BL/6N mice. At the 1- and 3-mg/kg doses (p.o.), Taranabant significantly inhibits 2-h food intake (36 and 69% reductions, respectively; P<0.05 and P<0.00001, respectively) and overnight food intake (13 and 40% reductions, respectively; P<0.05 and P<0.00001, respectively) as well as overnight gains in body weight (48 and 165% reductions, respectively; P<0.01 and P<0.00001, respectively). Taranabant dose-dependently inhibits food intake and weight gain, with an acute minimum effective dose of 1 mg/kg in diet-induced obese (DIO) rats[1]. Taranabant (MK-0364) has a good pharmacokinetic profile in three species (rat, 1 mg/kg iv, 2 mg/kg po, F=74%, t1/2=2.7 h; dog, 0.2 mg/kg iv, 0.4 mg/kg po, F=31%; t1/2=14 h; rhesus monkey, 0.2 mg/kg iv, 0.4 mg/kg po, F=31%, t1/2=3.6 h) and good brain exposure (1 mg/kg iv, brain and plasma concentrations of 0.11 and 0.18 μM at 1 h, respectively)[2].

Name: Toll-like receptor modulator, CAS: 926927-42-6, stock 18.2g, assay 98.3%, MWt: 348.27, Formula: C15H13F5N2O2, Solubility: DMSO : ≥ 100 mg/mL (287.13 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: Toll-like receptor modulator is a modulator of TLR7/8, which modulates immune function.
IC50 & Target: TLR7/8[1]
In Vitro: Toll-like receptor modulator (Compound 7) is a modulator of TLR7/8, which modulates immune function[1].

Name: Telcagepant MK-0974, CAS: 781649-09-0, stock 8.9g, assay 98.4%, MWt: 566.52, Formula: C26H27F5N6O3, Solubility: DMSO : ≥ 50 mg/mL (88.26 mM), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;Neuronal Signaling, Target: CGRP Receptor;CGRP Receptor, Biological_Activity: Telcagepant (MK-0974) is a calcitonin gene-related peptide (CGRP) receptor antagonist with Kis of 0.77 nM and 1.2 nM for human and rhesus CGRP receptors, respectively.
IC50 & Target: Ki: 0.77 nM (human CGRP), 1.2 nM (rhesus CGRP)
In Vitro: Telcagepant (MK-0974) displays affinity (Ki) for the canine and rat receptors, with values of 1204 nM and 1192 nM (n=10), respectively. Telcagepant (MK-0974) potently blocks human α-CGRP-stimulated cAMP responses in human CGRP receptor expressing HEK293 cells with an IC50 of 2.2 nM[1]. Telcagepant (MK-0974) displays saturable binding to SK-N-MC membranes with a KD of 1.9 nM and Bmax of 479 fmol/mg protein. Telcagepant (MK-0974) also displays saturable binding to rhesus cerebellum homogenate with a KD of 1.3 nM and Bmax of 20 fmol/mg[2].
In Vivo: Telcagepant (MK-0974) (i.v. bolus, 1 mg/kg) demonstrates that the efficacy of this antagonist is time-dependent and correlated with plasma levels[1]. The pharmacokinetics of Telcagepant (MK-0974) remains linear across 0.5-10 mg/kg intravenous dose in monkeys, but the oral area under the plasma concentration-time curve (AUC) increase (5-30 mg/kg) is 15-fold over dose-proportional[3].

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