EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2353

EOS Med Chem is TOP 100 of China CRO & CMO company, mainly in custom synthesis.
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Name: MA-0204, CAS: 2095128-17-7, stock 5.3g, assay 98.4%, MWt: 476.49, Formula: C25H27F3N2O4, Solubility: DMSO : 43.33 mg/mL (90.94 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: MA-0204 is a potent, highly selective and orally available peroxisome proliferator activated receptor δ (PPARδ) modulator with EC50s of 0.4 nM, 7.9 nM and 10 nM for human, mouse and rat PPARδ, respectively. Potential treatment for Duchene Muscular Dystrophy (DMD)[1].
IC50 & Target: EC50: 0.4 nM (human PPARδ), 7.9 nM (mouse PPARδ) and 10 nM (rat PPARδ)[1]
In Vitro: MA-0204 is >10,000-fold selective for activation of PPARδ over PPARα and PPARγ receptors. MA-0204 exhibits high protein binding to mouse plasma, good permeability and low potential for efflux. C[1].
MA-0204 (1.2-12 nM) improves fatty acid oxidation in DMD patient muscle myoblasts mice[1].
MA-0204 (0.04-40 nM) engages target gene expression in DMD patient muscle myoblasts[1].
In Vivo: PPARδ (30, 100 mg/kg) increases target gene transcription in the muscle[1].

Name: Pyridoxal isonicotinoyl hydrazone PIH, CAS: 737-86-0, stock 35.3g, assay 98.6%, MWt: 286.29, Formula: C14H14N4O3, Solubility: DMSO : 14.71 mg/mL (51.38 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Pyridoxal isonicotinoyl hydrazone (PIH) is a lipophilic, tridentate Fe-chelating agent that shows high Fe chelation efficacy[1].

Name: RCGD423, CAS: 108237-91-8, stock 31.5g, assay 98.7%, MWt: 331.23, Formula: C15H11BrN2S, Solubility: DMSO : ≥ 160 mg/mL (483.05 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Interleukin Related, Biological_Activity: RCGD423 is a gp130 modulator, which prevents articular cartilage degeneration and promotes repair.
IC50 & Target: gp130[1]
In Vitro: RCGD423 is a gp130 modulator, which prevents articular cartilage degeneration and promotes repair[1].
In Vivo: RCGD423 greatly reduces chondrocyte hypertrophy, loss and degeneration while increasing chondrocyte proliferation beyond that observed in response to injury in a rat partial meniscectomy model. Moreover, RCGD 423 improves cartilage healing in a rat full-thickness osteochondral defect model, increasing proliferation of mesenchymal cells in the defect and also inhibiting breakdown of cartilage matrix in de novo generated cartilage[1].

Name: BIBB 515, CAS: 156635-05-1, stock 7.7g, assay 98.6%, MWt: 380.87, Formula: C22H21ClN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BIBB 515 is a potent, selective and orally active 2,3-oxidosqualene cyclase (OSC) inhibitor with ED50 values of 0.2-0.5 mg/kg and 0.36-33.3 mg/kg in rats and mice (1-5 hours), respectively. BIBB 515 exerts lipid-lowering effect mainly by inhibiting the production of low-density lipoprotein (LDL)[1].
IC50 & Target: 2,3-oxidosqualene cyclase (OSC)[1]
In Vitro: Sterol synthesis, 2,3-oxidosqualene cyclase activity, HMGCoA reductase activity, and the specificity of BIBB 51 5 versus 2,3-oxidosqualene cyclase are measured in intact HepG2 cells or cell homogenates.Concentration-dependent inhibition of cholesterol biosynthesis by BIBB 515 as monitored by [14C]-acetate incorporation into digitonin precipitable sterols could be demonstrated in HepG2 cells (ED50 = 4.11 nM). A similar inhibition of OSC activity (ED50= 8.69 nM) is seen in HepC2 cell homogenates. No inhibition of HMGCoA reductasc could be measured in HepG2 cell homogenates at concentrations of BIBB 515 up to 1 and 10 μM[1].
In Vivo: BIBB 515 (16.0-148.2 mg/ kg; oral administration; daily; for 40 days; male golden Syrian hyperlipemic hamsters) treatment shows dose-dependent lipid-lowering activity in normolipemic hamsters (-19% for total cholesterol and -32% for VLDL + LDL cholesterol) and in hyperlipemic hamsters (-25% for total cholesterol and -59% for LDL-cholesterol)[1].

Name: 2-NBDG, CAS: 186689-07-6, stock 30.5g, assay 98.6%, MWt: 342.26, Formula: C12H14N4O8, Solubility: H2O : 5 mg/mL (14.61 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2-NBDG is a fluorescent indicator for direct glucose uptake measurement and also is an indicator of cell viability.

Name: ONO-8590580, CAS: 1802661-73-9, stock 36.1g, assay 98.3%, MWt: 376.43, Formula: C21H21FN6, Solubility: DMSO : 62.5 mg/mL (166.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: ONO-8590580 is a GABAA α5 negative allosteric modulator.
IC50 & Target: GABAA α5[1].
In Vivo: The effect of ONO-8590580 on the MK-801/scopolamine-induced cognitive deficit in the 8-arm radial maze test is investigated. Doses of MK-801 and scopolamine for this test are 0.075 mg/kg (i.p.) and 0.2 mg/kg (i.p.) respectively. ONO-8590580 (20 mg/kg, p.o.) significantly decreases the number of errors and total latency compared to the control. The present study in which ONO-8590580 but not donepezil significantly decreases the number of errors may suggest that ONO-8590580 could be more potent for the treatment of AD patients. The data showing that ONO-8590580 has not anxiogenic-like or proconvulsant effects are in agreement with the behavioral phenotype of α5-/- mice[1].

Name: (+)-JQ1 PA, CAS: 2115701-93-2, stock 10.8g, assay 98.4%, MWt: 437.95, Formula: C22H20ClN5OS, Solubility: Ethanol : 50 mg/mL (114.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: (+)-JQ1 PA is a derivative of the Bromodomain and extra-terminal (BET) inhibitor JQ1, with an IC50 of 10.4 nM.
IC50 & Target: 10.4 nM (BET)[1].
In Vitro: (+)-JQ1 PA is a derivative of JQ1, which is the inhibitor of BET. The IC50 of (+)-JQ1 PA for BET is 10.4 nM, and the IC50 of JQ1 is 14.3 nM in MV4;11 cells[1].

Name: BT2, CAS: 34576-94-8, stock 34.5g, assay 98.1%, MWt: 247.10, Formula: C9H4Cl2O2S, Solubility: DMSO : 83.33 mg/mL (337.23 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: BT2 is a BCKDC kinase (BDK) inhibitor with an IC50 of 3.19 μM. BT2 binding to BDK triggers helix movements in the N-terminal domain, resulting in the dissociation of BDK from the branched-chain α-ketoacid dehydrogenase complex (BCKDC)[1]. BT2 (compound 4) is also a potent and selective Mcl-1 inhibitor with a Ki value of 59 μM[2].
IC50 & Target: IC50: 3.19 μM (BCKDC kinase)[1]; Ki: 59 μM (Mcl-1)[2]
In Vivo: BT2 (20 mg/kg/day; intraperitoneal injection; daily; for 7 days; C57BL/6J male mice) treatment robustly enhances BCKDC activity in the heart (12.3-fold) compared with the vehicle-treated animals. Less activation is obtained in muscle and kidney at 3.6- and 3.8-fold, respectively. The -fold activation of BCKDC activity in the above tissues correlates with decreased phosphorylation in heart, muscle, and kidney after the long term BT2 treatment. BT2 treatment reduces the protein levels of BDK in kidneys and heart[1].

Name: NCT-502, CAS: 1542213-00-2, stock 24.1g, assay 98.7%, MWt: 395.45, Formula: C18H20F3N5S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 130 mg/mL (328.74 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NCT-502 is a human phosphoglycerate dehydrogenase (PHGDH) inhibitor, cytotoxic to PHGDH-dependent cancer cells, and reduces glucose-derived serine production, with an IC50 of 3.7 μM against PHGDH[1].
IC50 & Target: IC50: 3.7 μM (PHGDH)[1]
In Vitro: NCT-502 is cytotoxic to MDA-MB-468, with an EC50 of 15.2 µM[1].

Name: AZD7507, CAS: 1041852-85-0, stock 16.6g, assay 98.4%, MWt: 454.50, Formula: C23H27FN6O3, Solubility: DMSO : 130 mg/mL (286.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Fms, Biological_Activity: AZD7507 is a potent and orally active CSF-1R inhibitor, with antitumor activity.
IC50 & Target: CSF-1R[1]
In Vitro: AZD7507 (Compound 31) inhibits the proliferation of 3T3 cells engineered to express CSF-1R and stimulated with CSF-1 (IC50, 32 nM), shows inhibitory activity against hERG and NaV1.5, with IC50s of >30 and 26 μM[1].
In Vivo: AZD7507 has good rat oral PK, with in vivo clearance of 7 mL/min/kg and 42% bioavailability. In the canine L-type Ca channel assay, the IC50 is >20 μM[1]. AZD7507 significantly decreases the number of CD68+ macrophages in mice, and also reduces the volume and mass in mice bearing CC-LP-1 and SNU-1079 cells, but not WITT-1 cells[2].

Name: Filipin complex, CAS: 11078-21-0, stock 34.4g, assay 98.1%, MWt: 654.80, Formula: C35H58O11 (for Filipin III), Solubility: DMSO : ≥ 100 mg/mL (152.72 mM); Ethanol : 25 mg/mL (38.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Filipin, produced as a mixture of related compounds known as the filipin complex (filipins I-IV) in nature[1], is a 28-membered ring pentaene macrolide antifungal antibiotic produced by S. filipinensis, S. avermitilis and S. miharaensis. Filipin interacts with membrane sterols causing the alteration of membrane structure. Filipin III is the major component of Filipin[2].

Name: KT185, CAS: 1472640-86-0, stock 14.2g, assay 99%, MWt: 519.64, Formula: C32H33N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: KT185 is an orally-bioavailable, brain-penetrant and selective ABHD6 inhibitor, with an IC50 0.21 nM in Neuro2A cells[1].
IC50 & Target: IC50: ABHD6 (0.21 nM in Neuro2A cells)[1].

Name: PH-002, CAS: 1311174-68-1, stock 32.2g, assay 98.2%, MWt: 491.58, Formula: C27H33N5O4, Solubility: DMSO : ≥ 75 mg/mL (152.57 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PH-002 is an inhibitor of apolipoprotein (apo) E4 intramolecular domain interaction in neuronal cells that could rescue impairments of mitochondrial motility and neurite outgrowth.
IC50 & Target: 116 nM (Apo E4 in FRET)[1].
In Vitro: PH-002 is an inhibitor of apolipoprotein (apo) E4 intramolecular domain interaction in neuronal cells, with an IC50 of 116 nM in FRET[1].
In Vivo: PH-002 is also shown to increase COX1 levels in primary neurons from NSE-apoE4 transgenic mouse cortex and hippocampus. After 4 days of treatment with PH-002 (200 nM), COX1 levels are increased by ~60%. PH-002 (100 nM) increases dendritic spine development in primary neurons from NSE-apoE4 transgenic mice to levels comparable with those in NSE-apoE3 primary neurons (apoE3-expressing primary neurons treated with PH-002 gave results identical to untreated primary neurons)[2].

Name: Cyclo(Phe-Pro) Cyclo(phenylalanylprolyl);A-64863, CAS: 14705-60-3, stock 31.6g, assay 98.8%, MWt: 244.29, Formula: C14H16N2O2, Solubility: DMSO : 125 mg/mL (511.69 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cyclo(Phe-Pro) (Cyclo(phenylalanylprolyl)), a Vibrio vulnificus quorum-sensing molecule, inhibits retinoic acid-inducible gene-I (RIG-I) polyubiquitination, through its specific interaction with RIG-I, to blunt IRF-3 activation and type-I IFN production. Cyclo(Phe-Pro) (Cyclo(phenylalanylprolyl)) enhances susceptibility to hepatitis C virus (HCV), as well as Sendai and influenza viruses[1].

Name: Dichlorophenyl-ABA, CAS: 18201-65-5, stock 15.1g, assay 98.1%, MWt: 282.12, Formula: C13H9Cl2NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dichlorophenyl-ABA is an inhibitor of transthyretin (TTR) amyloid fibril formation, inhibiting aggregate formation in more than 80% in TTR L55P-expressing cells[1].
IC50 & Target: Transthyretin (TTR) amyloid fibril formation
In Vitro: Dichlorophenyl-ABA (DCPA) is able to prevent L55P aggregate formation in the conditioned medium. With regard to the ultrastructural analysis, Dichlorophenyl-ABA does not show an inhibitory effect as high as DFPB and benzoxazole, indicating that the Y78F mutant may not be as sensitive to this drug as TTR L55P and V30M are[1]. 
Dichlorophenyl-ABA is the best stabilizers of V30M tetramers in plasma from carriers of this mutant, and clearly inhibit aggregation in the cellular system. Therefore Dichlorophenyl-ABA is promising for the treatment of valine at position 30 (V30M)-associated familial amyloidotic polyneuropathy (FAP) but need to undergo further stages of drug development to overcome their toxicity[1].

Name: Prolyl Endopeptidase Inhibitor 1 Boc-Pro-prolinal;(Boc)-Prolyl-prolinal;BPP, CAS: 86925-97-5, stock 34.6g, assay 98.1%, MWt: 296.36, Formula: C15H24N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Prolyl Endopeptidase Inhibitor 1 (Boc-Pro-prolinal) is a potent prolyl endopeptidase (PEP; PE) inhibitor, with a Ki value of 15 nM. Prolyl Endopeptidase Inhibitor 1 has anti-amnesic effect[1].
IC50 & Target: Ki: 15 nM (prolyl endopeptidase)[1]
In Vitro: Prolyl Endopeptidase Inhibitor 1 (Boc-Pro-prolinal) strongly inhibits the mammalian prolyl endopeptidase with a Ki value of nM order, while the Ki value for the microbial enzyme is only of microM order (Ki=3.2 μM for Flavobacterium)[1].

Name: Actinonin (-)-Actinonin, CAS: 13434-13-4, stock 14.4g, assay 98.3%, MWt: 385.50, Formula: C19H35N3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease;Anti-infection;Metabolic Enzyme/Protease, Target: Apoptosis;MMP;Bacterial;Aminopeptidase, Biological_Activity: Actinonin ((-)-Actinonin) is a naturally occurring antibacterial agent produced by Actinomyces. Actinonin inhibits aminopeptidase M, aminopeptidase N and leucine aminopeptidase. Actinonin is a potent reversible peptide deformylase (PDF) inhibitor with a Ki of 0.28 nM. Actinonin also inhibits MMP-1, MMP-3, MMP-8, MMP-9, and hmeprin α with Ki values of 300 nM, 1,700 nM, 190 nM, 330 nM, and 20 nM, respectively. Actinonin is an apoptosis inducer. Actinonin has antiproliferative and antitumor activities[1][2][3][4][5].
IC50 & Target: Ki: 0.28 nM (Peptide deformylase (PDF))[2], 300 nM (MMP-1), 1,700 nM (MMP-3), 190 nM (MMP-8), 330 nM (MMP-9)[3], and 20 nM (hmeprin α)[5] 
Apoptosis[1] 
Aminopeptidase M, Aminopeptidase N and Leucine aminopeptidase[1]
In Vitro: Actinonin inhibits cell growth in various human tumor cell lines. The IC50 of 4, 6.9, 12.8, 16.6, 27.4, 15.7 and 49.3 μM for Raji cells, MDA-MB-468 cells,PC3 cells, SK-LC-19 cells, Hela cells, HT-1080 cells and AL67 cells, respectively[1]. 
HsPDF is a critical target of actinonin and that the inhibition of this protein in the mitochondria leads to cell death in tumor cells. Actinonin treatment of cells led to a tumor-specific mitochondrial membrane depolarization and ATP depletion in a time- and dose-dependent manner[1]. 
Actinonin is a potent inhibitor of all three forms (Zn-, Ni-, and Fe-) of peptide deformylases from both S. aureus and E. coli bacteria. Under the assay conditions, the IC50 values for Actinonin are 90, 3, 0.8, and 11 nM for Zn-PDF (E. coli), Ni-PDF (E. coli), Fe-PDF (E. coli), and Ni-PDF (S. aureus), respectively[2]. 
Actinonin is active against Gram-positive bacteria, including S. aureus (MIC value of 8-16 µg/mL), Streptococcus pyogenes (MIC value of 8 µg/mL) and Streptococcus epidermidis (MIC value of 2-4 µg/mL). Actinonin is also active against fastidious Gramne-gative bacteria, such as H. influenzae (MIC value of 1-2 µg/mL), Moraxella catarrhalis (MIC value of 0.5 µg/mL), and Neisseria gonorrheae (MIC value of 1-4 µg/mL). Actinonin is very active against the H. influenzae acr (MIC value of 0.13 µg/mL) and E. coli acr (MIC value of 0.25 µg/mL) efflux pump mutants[2].
In Vivo: Actinonin has been safely administered to mice as an antibiotic at doses up to 400 mg/kg. Actinonin does not appear to have significant toxicity to normal tissues, despite its antitumor activity in vitro. Remarkably, Actinonin exhibits significant antitumor activity when given i.p. or orally in a CWR22 human prostate tumor xenograft model in nude mice. During treatment, the animals show no signs of toxicity[1].

Name: Z-Asp-CH2-DCB, CAS: 153088-73-4, stock 8.3g, assay 98.4%, MWt: 454.26, Formula: C20H17Cl2NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Caspase, Biological_Activity: Z-Asp-CH2-DCB is an irreversible broad spectrum caspase inhibitor. Z-Asp-CH2-DCB also inhibits proteases with caspase-like activity. Z-D-CH2-DCB blocks the production of IL-1β, TNF-α, IL-6, and IFN-γ in staphylococcal enterotoxin B (SEB)-stimulated peripheral blood mononuclear cells (PBMC), and reduces SEB-1-stimulated T-cell proliferation in a dose-dependent manner. Z-Asp-CH2-DCB prevents SU5416-induced septal cell apoptosis and emphysema development[1][2][3].
In Vitro: Z-Asp-CH2-DCB (10-100 μM) blocks the production of IL-1β, TNF-α, IL-6, and IFN-γ in SEB-stimulated (200 ng; 16 hours) PBMC in a dose-dependent manner. The production of the chemokines MCP-1, MIP-1α, and MIP-1β was also suppresses. The inhibitory effect of Z-Asp-CH2-DCB on TSST-1-activated PBMC is similar, reducing IL-1β, IL-6, TNF-α, IFN-γ, MCP-1, MIP-1α, and MIP-1β to 10, 36, 25, 10, 11, 25, and 30%, respectively, of levels in untreated cells[1]. 
Z-Asp-CH2-DCB (10-100 μM; 48 hours) inhibits T-cell proliferation in PBMC stimulated with 200 ng of SEB/ml [1].
In Vivo: Z-Asp-CH2-DCB (1 mg; i.p.; every day for 3 weeks) prevents SU5416-induced septal cell apoptosis[1].

Name: HA155, CAS: 1312201-00-5, stock 6.1g, assay 98.7%, MWt: 463.29, Formula: C24H19BFNO5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: HA-155 is a potent and selective autotaxin (ATX) inhibitor with an IC50 of 5.7 nM[1][2][3].
IC50 & Target: IC50: 5.7 nM (ATX)[1]
In Vitro: HA-155 inhibits ATX by binding to the ATX active site[1]. 
HA155 completely attenuates the thrombin-mediated increase in platelet-derived LPA in a dose-dependent manner[3].

Name: ERRα antagonist-1, CAS: 1072145-33-5, stock 10.6g, assay 98.5%, MWt: 377.53, Formula: C21H19N3S2, Solubility: DMSO : 7.14 mg/mL (18.91 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: ERRα antagonist-1 (Compound A) is a selective and high affinity estrogen-related receptor α (ERRα) antagonist. ERRα antagonist-1 inhibits interaction of ERRα with Proliferator-activated Receptor γ Coactivator-1α (PGC-1α) and PGC-1β, the IC50 values are 170 nM and 180 nM, respectively. ERRα antagonist-1 does not inhibit the interaction of either ERRβ or ERRγ with PGC-1α and PGC-1β coactivator, and also does not inhibit interaction of ERα or ERβ with PGC-1α or SRC-1[1].

Name: 7α,25-Dihydroxycholesterol 7α,25-OHC, CAS: 64907-22-8, stock 35.8g, assay 98.2%, MWt: 418.65, Formula: C27H46O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease, Target: EBI2/GPR183;Endogenous Metabolite, Biological_Activity: 7α, 25-dihydroxycholesterol (7α,25-OHC) is a potent and selective agonist and endogenous ligand of the orphan GPCR receptor EBI2 (GPR183). 7α, 25-dihydroxycholesterol is highly potent at activating EBI2 (EC50=140 pM; Kd=450 pM). 7α, 25-dihydroxycholesterol can serve as a chemokine directing migration of B cells, T cells and dendritic cells[1][2].
In Vitro: In vitro, 7α, 25-dihydroxycholesterol (7α,25-OHC) stimulates the migration of EBI2-expressing mouse B and T cells with half-maximum effective concentration values around 500 pM, but had no effect on EBI2-deficient cells[1].
In Vivo: EBI2-deficient B cells or normal B cells desensitized by 7α,25-Dihydroxycholesterol (1 μM; 1.5 hours) pre-treatment shows reduced homing to follicular areas of the spleen[1].

Name: Methyl mycophenolate, CAS: 31858-66-9, stock 24.7g, assay 98.2%, MWt: 334.36, Formula: C18H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Methyl mycophenolate is a methyl ester of mycophenolic acid and is also found in marine-derived fungus Phaeosphaeria spartinae[1][2].

Name: LPA2 antagonist 2, CAS: 36840-10-5, stock 24.5g, assay 98.2%, MWt: 380.35, Formula: C20H16N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: LPA2 antagonist 2 (H2L 5226501) is a selective LPA2 antagonist with an IC50 of 28.3 nM, which is ＞480-fold more selective than LPA3 (IC50 of 13.85 μM)[1].
IC50 & Target: IC50: 28.3 nM (LPA2); 13.85 μM (LPA3)[1]

Name: trans-AUCB t-AUCB, CAS: 885012-33-9, stock 9.5g, assay 98.6%, MWt: 412.52, Formula: C24H32N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: trans-AUCB (t-AUCB) is a potent, orally active and selective soluble epoxide hydrolase (sEH) inhibitor with IC50s of 1.3 nM, 8 nM, 8 nM for hsEH, mouse sEH and rat sEH, respectively. trans-AUCB has anti-glioma activity[1][2].
IC50 & Target: IC50: 1.3 nM (hsEH), 8 nM (mouse sEH) and 8 nM (rat sEH)[2]
In Vitro: trans-AUCB (t-AUCB; 25-300 μM; 48 hours) suppresses U251 and U87 cell growth in a dose-dependent manner[1]. 
trans-AUCB (200 μM; 48 or 96 hours) induces cell-cycle G0/G1 phase arrest in U251 and U87 cells[1]. 
trans-AUCB (200 μM; 10 min-4 hours) can increase the phosphorylation levels of p65 after 10 min, reaching to peak after 30 min and lasting for at least 2 hours[1]. 
trans-AUCB (200 μM; 48 hours) suppresses U251 and U87 cell growth by activating NF-jB-p65[1]. 
trans-AUCB (10 μM; 30 min) efficiently inhibits sEH activities in human glioblastoma cell lines (U251, U87) and human hepatocellular carcinoma cell line (HepG2 cells)[1]. 
In Vivo: trans-AUCB (t-AUCB; p.o.; 0.1, 0.5, 1 mg/kg) ameliorates the LPS-induced hypotension in a dose-dependent manner[2]. 
trans-AUCB (p.o.; 0.1, 0.5, 1 mg/kg) has t1/2 values of 20, 30, 15 min and Cmax values of 30, 100, 150 nmol/L for p.o. of 0.1, 0.5, 1 mg/kg[2]. 
trans-AUCB (s.c.; 1, 3, 10 mg/kg) has t1/2 values of 60, 85, 75 min and Cmax values of 245, 2700, 3600 nmol/L for s.c. of 1, 3, 10 mg/kg[2]. 
trans-AUCB (i.v.; 0.1 mg/kg) has t1/2 values of 70 min and 10 hours for distribution (α) and elimination (β) phases. trans-AUCB has a CL of 0.7 L/h•kg and a Vdss was 17 L/kg[2].

Name: AZ304, CAS: 942507-42-8, stock 3g, assay 98.2%, MWt: 451.52, Formula: C27H25N5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (276.84 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: Raf;Autophagy, Biological_Activity: AZ304 is an ATP-competitive dual BRAF kinase inhibitor, potently inhibits wild type BRAF, V600E mutant BRAF and wild type CRAF, with IC50s of 79 nM, 38 nM and 68 nM, respectively. AZ304 also has significant effect on other kinases, such as p38 (IC50, 6 nM), CSF1R (IC50, 35 nM). Anti-tumor activity[1].
IC50 & Target: IC50: 79 nM (BRAFWT), 38 nM (BRAFV600E), 68 nM (CRAFWT), 6 nM (p38), 35 nM (CSF1R), 6400 nM (MAP3K7), 7050 nM (CSK)[1]
In Vitro: AZ304 (1 nM-100 μM) potently reduces ERK phosphorylation (p-ERK), with a mean EC50 of 65 nM in the V600E mutant BRAF containing melanoma cell line A375, and EC50s of 52 nM, 60 nM in the wild type BRAF melanoma cell line SK-MEL-31 with and without EGF[1].
AZ304 also potently inhibits p-p38 in both BRAF genetic statuses cell lines[1]. 
AZ304 (0, 0.1, 1, 10, 100 μM, 48 and 72 hours) dose-dependently inhibits the growth of RKO, HT-29, DiFi, and Caco-2, with GI50s of 4.539 μM, 3.896 μM, 4.987 μM, 1.763 μM (48 hours) and 0.5032 μM, 0.3887 μM, 0.6354 μM, 0.3772 μM (72 hours), respectively[1]. 
AZ304 (2 μM, 36 and 48 hours) decreases BRAF, p-ERK, p-AKT and p-mTOR levels, increases p-EGFR in both BRAF V600E mutant and BRAF wild type cells. AZ304 down-regulates p-EGFR, inhibits p-ERK, more potently suppresses BRAF, ERK, AKT and mTOR signalling pathways in combination with C225[1].

Name: (S)-Metolachor, CAS: 87392-12-9, stock 10.2g, assay 98.1%, MWt: 283.79, Formula: C15H22ClNO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (S)-Metolachor, a derivative of aniline, is a major pesticide in use.

Name: H4 Receptor antagonist 1, CAS: 848217-00-5, stock 21.1g, assay 98.6%, MWt: 316.79, Formula: C16H17ClN4O, Solubility: DMSO : 10 mg/mL (31.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: H4 Receptor antagonist 1 is a potent and selective histamine H4 receptor inverse agonist, with an IC50 of 19 nM.
IC50 & Target: IC50: 19 nM (H4R)[1].
In Vitro: H4 Receptor antagonist 1 is a potent and selective histamine H4 receptor inverse agonist, with an IC50 of 19 nM[1].
In Vivo: H4 Receptor antagonist 1 indicates that metabolic stability in rat microsomes is very low with only 1% parent compound remaining after 10 min incubation[1].

Name: JG-98, CAS: 1456551-16-8, stock 36.6g, assay 98.2%, MWt: 534.54, Formula: C24H21Cl2N3OS3, Solubility: DMSO : 5 mg/mL (9.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: Apoptosis;HSP;HSP, Biological_Activity: JG-98, an allosteric heat shock protein 70 (Hsp70) inhibitor, which binds tightly to a conserved site on Hsp70 and disrupts the Hsp70-Bag3 interaction. JG-98 shows anti-cancer activities affecting both cancer cells and tumor-associated macrophages[1][2][3].
IC50 & Target: Heat shock protein 70[1]
In Vitro: JG-98 (30 nM-30 μM; 72 hours) has antiproliferative activity across a range of cell lines with the EC50s between ~0.3 and 4 μM[2]. 
JG-98 (10 μM; 48 hours) activates apoptotic mediators (cleavage of caspase-3 and PARP) in MDA-MB-231 cells[1]. 
JG-98 destabilizes FoxM1 and relieves suppression of downstream effectors, including p21 and p27[2].
In Vivo: JG-98 (3 mg/kg; i.p.; on days 0, 2, and 4) suppresses tumor growth in xenograft models bearing MCF7 and HeLa cells[2].

Name: (S)-JQ-35 TEN-010, CAS: 1349719-98-7, stock 35.3g, assay 98.7%, MWt: 540.12, Formula: C27H34ClN7OS, Solubility: DMSO : ≥ 85 mg/mL (157.37 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: (S)-JQ-35 (TEN-010) is an inhibitor of the Bromodomain and Extra-Terminal (BET) family bromodomain-containing proteins with potential antineoplastic activity.

Name: PF-00356231 (hydrochloride), CAS: 820223-77-6, stock 28.8g, assay 98.8%, MWt: 464.96, Formula: C25H21ClN2O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: PF-00356231 hydrochloride is a specific, non-peptidic, non-zinc chelating ligand and inhibitor of matrix metalloproteinase MMP-12 (IC50=1.4 μM). PF-00356231 hydrochloride binds to MMP-12 and forms PF-00356231/MMP-12 complex. PF-00356231 hydrochloride shows potency against MMP-13, MMP-8, MMP-9, MMP-3 with IC50s of 0.00065, 1.7, 0.98, 0.39 μM, respectively[1].
In Vitro: PF-00356231 hydrochloride against MMP-12/13 can be affected significantly by the presence of acetohydroxamate (AH). PF-00356231 hydrochloride decreases the IC50 values of MMP-12 (0.014 μM) and MMP-13 (0.27 μM) in the presence AH[1].

Name: KU-0063794, CAS: 938440-64-3, stock 22.5g, assay 98.5%, MWt: 465.54, Formula: C25H31N5O4, Solubility: DMSO : 16.67 mg/mL (35.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: mTOR, Biological_Activity: KU-0063794 is a potent and highly specific dual-mTOR inhibitor, with IC50 of appr 10 nM for mTORC1 and mTORC2 in cell-free assays, but has no effect on PI3Ks.
IC50 & Target: IC50: 10 nM (mTORC1), 10 nM (mTORC2)[1]
In Vitro: Ku-0063794 is cell permeant, suppresses activation and hydrophobic motif phosphorylation of Akt, S6K and SGK, but not RSK (ribosomal S6 kinase), an AGC kinase not regulated by mTOR. Ku-0063794 also inhibits phosphorylation of the T-loop Thr308 residue of Akt phosphorylated by PDK1 (3-phosphoinositide-dependent protein kinase-1). Ku-0063794 induces a much greater dephosphorylation of the mTORC1 substrate 4E-BP1 (eukaryotic initiation factor 4E-binding protein 1) than rapamycin, even in mTORC2-deficient cells, suggesting a form of mTOR distinct from mTORC1, or mTORC2 phosphorylates 4E-BP1. Ku-0063794 also suppresses cell growth and induced a G1-cell-cycle arrest[1]. Ku0063794 does not alter nuclear phospho-Mst1-Thr-120 levels in LNCaP cell nuclei, whereas Ku0063794 or CCI-779 increases phospho-Mst1-Thr-120 levels in C4-2 cell nuclei[2]. The combination of GDC-0941 and KU0063794 inhibits the phosphorylation of 4EBP1 and S6 to a similar extent to that caused by single agent NVP-BEZ235 in HCT116, DLD1 and HT29 cell lines[3].

Name: BMS-986165, CAS: 1609392-27-9, stock 17.8g, assay 98.1%, MWt: 425.46, Formula: C20H19D3N8O3, Solubility: DMSO : 62.5 mg/mL (146.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: Interleukin Related;JAK;JAK;JAK, Biological_Activity: BMS-986165 is a highly selective, orally bioavailable allosteric TYK2 inhibitor for the treatment of autoimmune diseases, which selectively binds to TYK2 pseudokinase (JH2) domain (IC50=1.0 nM) and blocks receptor-mediated Tyk2 activation by stabilizing the regulatory JH2 domain. BMS-986165 inhibits IL-12/23 and type I IFN pathways[1][2].
IC50 & Target: Tyk2[1]
In Vitro: BMS-986165 is differentiated from previous JAK inhibitors due its unique ability to selectively bind to the pseudokinase (JH2) domain of TYK2 and inhibit its function through an allosteric mechanism[1]. 
BMS-986165 maintains excellent potency in human and mouse whole blood (IC50s=13 and 100 nM, respectively) and shows no significant hERG inhibition in the flux assay (IC50>80 μM)[1].

Name: S55746 BLC201, CAS: 1448584-12-0, stock 22g, assay 98.6%, MWt: 710.82, Formula: C43H42N4O6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (70.34 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: S55746 (BLC201) is a potent, orally active and selective BCL-2 inhibitor, with a Ki of 1.3 nM and a Kd of 3.9 nM. S55746 (BLC201) has antitumor activity with low toxicity[1].
IC50 & Target: Ki: 1.3 nM (BCL-2)[1].
In Vitro: S55746 (0-1 μM) potently and selectively induces cell death[1]. 
S55746 selectively induces apoptosis through BCL-2 inhibition in a BAX/BAK-dependent manner[1].
In Vivo: S55746 is a highly efficacious and well-tolerated (even at doses up to 300 mg/kg) orally active BCL-2 inhibitor [1]. 
S55746 (20-100 mg/kg, p.o.) inhibits xenograft growth in RS4;11 and Toledo models time- and dose-dependently[1].

Name: AKOS B018304, CAS: 6308-22-1, stock 0g, assay 98.7%, MWt: 266.30, Formula: C10H6N2O3S2, Solubility: DMSO : ≥ 77.5 mg/mL (291.03 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AKOS B018304 is an arylalkylidene derivative, with polar substitution at para-position.
In Vitro: AKOS B018304 (compound 6) is an arylalkylidene derivative, with polar substitution at para-position[1].

Name: Org-12962, CAS: 132834-56-1, stock 39.2g, assay 98.1%, MWt: 265.66, Formula: C10H11ClF3N3, 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: Org-12962 is a potent, selective and orally active 5-HT2C receptor agonist with a pEC50 value of 7.01. Org-12962 also exhibits high effacy for the 5-HT2A and 5-HT2B receptor with pEC50s of 6.38 and 6.28, respectively[1][3].Org-12962 displays antiaversive effects in a rat model of panic-like anxiety[2].
In Vivo: Org-12962 (intraperitoneal injection; 0.3-3.2 mg/kg) significantly increases the postinjection frequency thresholds for self-interruption (F3.71=11.40). Org-12962 is dissolved or microsuspended in 0.3% v/v Tween 80 in physiological saline (NaCl 0.9%)[1].

Name: all-trans-4-Oxoretinoic acid all-trans 4-Keto Retinoic Acid, CAS: 38030-57-8, stock 3.1g, assay 98.2%, MWt: 314.42, Formula: C20H26O3, Solubility: DMSO : 150 mg/mL (477.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: all-trans-4-Oxoretinoic acid, an active metabolite of vitamin A, induces gene transcription via binding to nuclear retinoic acid receptors (RARs).
In Vitro: all-trans-4-Oxoretinoic acid, an active metabolite of vitamin A, induces gene transcription via binding to nuclear retinoic acid receptors (RARs)[1]. all-trans-4-Oxoretinoic acid is a biologically active geometric isomer of retinoic acid (RA) [2].

Name: Pironetin, CAS: 151519-02-7, stock 5.7g, assay 98.8%, MWt: 324.45, Formula: C19H32O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Pironetin is an α/β unsaturated lactone isolated from Streptomyces species. Pironetin binds to α-tubulin and is a potent inhibitor of microtubule polymerization, and has cell cycle arrest and antitumor activity[1][2].
IC50 & Target: Microtubule[1]
In Vitro: Pironetin (20-100 ng/mL; 24 hours; 3Y1 cells) treatment arrests the cell cycle progression at G2/M in 3Y1 cells[1]. 
Pironetin (1-10000 ng/mL; 3 days; HeLa, A2780 and K-NRK cells) treatment inhibits the cell proliferation. IC50 values against these cell lines are almost 10 ng/mL[1].
In Vivo: Pironetin (0.78-6.25 mg/kg; intraperitoneal injection; daily; for 5 days; female CDF1-SLC mice) treatment shows a moderate antitumor effect, however, a severe weight loss is observed as a side effect[1].

Name: Metaflumizone BAS-320I, CAS: 139968-49-3, stock 11.4g, assay 98.4%, MWt: 506.40, Formula: C24H16F6N4O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 300 mg/mL (592.42 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Anti-infection, Target: Sodium Channel;Parasite, Biological_Activity: Metaflumizone is a semicarbazone insecticide, acts as a potent sodium channel blocker[1].
IC50 & Target: Sodium channel[1]
In Vitro: Metaflumizone (10 μM) completely inhibits the Para/TipE sodium currents in Xenopus oocytes[1].

Name: USP25/28 inhibitor AZ1 AZ1, CAS: 2165322-94-9, stock 23.2g, assay 98.8%, MWt: 422.21, Formula: C17H16BrF4NO2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 250 mg/mL (592.12 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: USP25/28 inhibitor AZ1 (AZ1) is a potent, selective, noncompetitive, dual ubiquitin specific protease (USP) 25/28 inhibitor with IC50s of 0.7 μM and 0.6 μM, respectively. USP25/28 inhibitor AZ1 reduces cell viability across a range of cancer cell lines[1].
IC50 & Target: IC50: 0.7 nM (USP25) and 0.6 nM (USP28)[1]

Name: E1R, CAS: 1301211-78-8, stock 7.2g, assay 98%, MWt: 232.28, Formula: C13H16N2O2, Solubility: DMSO : 60 mg/mL (258.31 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Sigma Receptor;Sigma Receptor, Biological_Activity: E1R is a positive allosteric modulator of sigma-1 receptors (Sig1R PAM) with cognition-enhancing activity[1].
In Vitro: The only target for E1R (inhibition or enhancement of radioligand binding exceeding 20%) is the sigma receptor. 10 μM E1R does not displace the radioligand, but instead increases the specific binding of a non-selective radioligand ([3H]1,3-di(2-tolyl)guanidine) for the sigma receptor by 38% in Jurkat cells[1].
In Vivo: E1R demonstrates efficacy against scopolamine-induced cholinergic dysfunction in mice. Treatment with E1R (0.1-10 mg/kg; administered i.p. 60 min before the training session) significantly improves cognitive function in a dose-related manner in mice[1].

Name: BTdCPU, CAS: 1257423-87-2, stock 29g, assay 98.2%, MWt: 339.20, Formula: C13H8Cl2N4OS, Solubility: DMSO : ≥ 250 mg/mL (737.03 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Phosphatase, Biological_Activity: BTdCPU is a potent heme-regulated eIF2α kinase (HRI) activator. BTdCPU promotes eIF2α phosphorylation and induced apoptosis in resistant cell[1].

Name: NGI-1 ML414, CAS: 790702-57-7, stock 15.9g, assay 98.8%, MWt: 394.51, Formula: C17H22N4O3S2, Solubility: DMSO : 160 mg/mL (405.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Virus Protease, Biological_Activity: NGI-1 (ML414) is a potent oligosaccharyltransferase (OST) inhibitor, directly targeting and blocking the function of the OST catalytic subunits STT3A and STT3B[1]. NGI-1 is a cell permeable inhibitor and can effectively reduce virus infectivity without affecting cell viability[2].
IC50 & Target: OST[1]
In Vitro: NGI-1 inhibits the glycosylation of LASV GP mediated by STT3A-OST (in STT3B- and MAGT1-TUSC3- cells) or STT3B-OST (in STT3A- cells) and impaires its proteolytic cleavage in a dose-dependent manner[1]. 
NGI-1 blocks EGFR N-linked glycosylation in lung adenocarcinoma cells as assessed. In controls EGFR is biotinylated, consistent with its plasma membrane expression, but in NGI-1 treated cells the EGFR is predominantly found in the non-biotinylated intracellular fraction suggesting a change in cellular localization[2].

Name: Vicagrel, CAS: 1314081-53-2, stock 1.4g, assay 99%, MWt: 379.86, Formula: C18H18ClNO4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: P2Y Receptor, Biological_Activity: Vicagrel, an acetate derivative of Clopidogrel, is a P2Y12 platelet inhibitor potentially for the treatment of thrombosis, the substrate of carboxylesterase 2 (CES2)[1]. Vicagrel demonstrates a favorable safety profile and excellent anti-platelet activity, which could be an anti-platelet drug and for the unmet medical needs of cardiovascular diseases[2].

Name: ML753286, CAS: 1699720-89-2, stock 6.8g, assay 98.1%, MWt: 355.43, Formula: C20H25N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: BCRP, Biological_Activity: ML753286 is an orally active and selective BCRP (Breast cancer resistance protein) inhibitor with an IC50 of 0.6 μM. ML753286 has high permeability and low to medium clearance in rodent and human liver S9 fractions, and is stable in plasma cross species[1].
IC50 & Target: IC50: 0.6 μM (BCRP)[1]
In Vitro: ML753286 has IC50 values of >30, 0.6, and 39.0 μM for the inhibition of P-gp-, BCRP-, and OATP mediated transport, respectively[1].
In Vivo: ML753286 (25- or 50-mg/kg (PO); 10 or 20 mg/kg (IV); 0.083-24 hours) appears to completely inhibit Bcrp functions in rats at 25 mg/kg PO or at 20 mg/kg IV. The tmax values in plasma were 1.4, 4.0, and 4.1 hours in Bcrp KO rats, WT rats pre-administered 25-mg/kg ML753286, and WT rats pre-administered 50-mg/kg ML753286, respectively[1].

Name: (S)-(−)-Perillyl alcohol, CAS: 18457-55-1, stock 18.4g, assay 98.8%, MWt: 152.23, Formula: C10H16O, Solubility: DMSO : ≥ 250 mg/mL (1642.25 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: (S)-(−)-Perillyl alcohol is a monoterpene found in lavender, inhibits farnesylation of Ras, upregulates the mannose-6-phosphate receptor and induces apoptosis. Anti-cancer activity[1].

Name: S130, CAS: 1160852-22-1, stock 7.9g, assay 98.6%, MWt: 387.47, Formula: C24H25N3O2, Solubility: DMSO : 125 mg/mL (322.61 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy;Metabolic Enzyme/Protease, Target: Apoptosis;Autophagy;Cathepsin, Biological_Activity: S130 is a high affinity, selective inhibitor of ATG4B (a major cysteine protease) with an IC50 of 3.24 µM. S130 suppresses autophagy flux[1].
IC50 & Target: IC50: 3.24 µM (ATG4B)[1]
In Vitro: S130 suppresses autophagy and activates apoptosis by inhibiting ATG4B, leads to enhanced cytotoxicity[1]. 
S130 (10 μM; 6 hours) suppresses autophagy at the early LC3 priming step or late autolysosome degradation stage[1]. 
S130 accumulates autolysosomes with more lipidated LC3[1]. 
S130 (0-25 μM; 48 hours) induces cell death through inhibiting the activity of ATG4B at a dose higher than 6.3 µM. And such cytotoxicity might not cause cell death through necroptosis[1]. 
Nutrient deprivation enhances S130-induced cytotoxicity[1]. 
S130 (0-10μM; 24 hours) suppresses approximately 79% of the cleavage of full-length LC3-GST at the 10 µM, while no substrates were processed in ATG4B KO cells. S130 displays obvious inhibitory effects on ATG4B[1]. 
In Vivo: S130 (20 mg/kg; i.p.; daily; 3 weeks) suppresses tumor growth, and shows an efficient in vivo antitumor effect with a sound safety on vital organs[1].

Name: AZD3229, CAS: 2248003-60-1, stock 13.3g, assay 98.5%, MWt: 479.51, Formula: C24H26FN7O3, Solubility: DMSO : ≥ 100 mg/mL (208.55 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Kit, Biological_Activity: AZD3229 is a potent pan-KIT mutant inhibitor for the treatment of gastrointestinal stromal tumors.
IC50 & Target: KIT[1].
In Vitro: AZD3229 is a potent, pan-KIT mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant KIT driven Ba/F3 cell lines (GI50=1-50 nM). AZD3229 demonstrates potent single digit nM growth inhibition across a broad cell panel, with good margin to KDR-driven effects. Selectivity over KDR can be rationalised predominantly by the interaction of water molecules with the protein and ligand in the active site and its kinome selectivity is similar to the best of the approved GIST agents[1].

Name: SGC-iMLLT, CAS: 2255338-25-9, stock 9.9g, assay 98.3%, MWt: 388.47, Formula: C22H24N6O, Solubility: DMSO : 83.33 mg/mL (214.51 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: SGC-iMLLT is a first-in-class chemical probe and a potent, selective inhibitor of MLLT1/3-histone interactions with an IC50 of 0.26 μM. SGC-iMLLT shows high binding activity towards MLLT1 YEATS domain (YD) and MLLT3 YD (AF9/YEATS3) with Kds of 0.129 and 0.077 μM, respectively[1].
IC50 & Target: IC50: 0.26 μM (MLLT1 YD)[1] 
Kd: 0.077 μM (MLLT3 YD), 0.129 μM (MLLT1 YD)[1]
In Vivo: SGC-iMLLT shows moderate metabolic resistance with t1/2 of 53 min and 48 % remaining after 60 min, and the primary process for metabolism is N demethylation[1].

Name: ALK2-IN-2, CAS: 2254409-25-9, stock 24g, assay 98.3%, MWt: 497.61, Formula: C28H27N5O2S, Solubility: DMSO : 125 mg/mL (251.20 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: ALK2-IN-2 is a potent and selective inhibitor of activin receptor-like kinase 2 (ALK2) with an IC50 of 9 nM, and over 700-fold selectivity against ALK3[1].
IC50 & Target: IC50: 9 nM (ALK2)[1]

Name: Chlorantraniliprole, CAS: 500008-45-7, stock 24.8g, assay 98.8%, MWt: 483.15, Formula: C18H14BrCl2N5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 62.5 mg/mL (129.36 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chlorantraniliprole is an insecticide that potently and selectively activates insect ryanodine receptor, with EC50s of 40 nM and 50 nM for Drosophila melanogaster and H. virescens ryanodine receptor, and ∼300-fold more potent than that in the mouse myoblast cell line, C2C12 (EC50, 14 μM).
IC50 & Target: EC50: 40 nM (Drosophila melanogaster Ryanodine receptor), 50 nM (H. virescens Ryanodine receptor), 14 μM (Ryanodine receptor, in C2C12 cells)
In Vitro: Chlorantraniliprole is an insecticide that potently and selectively activates insect ryanodine receptor. Chlorantraniliprole actions by release of intracellular Ca2+ stores mediated by the ryanodine receptor. Chlorantraniliprole is ∼300-fold less potent against ryanodine receptor (RyRs) in the mouse myoblast cell line, C2C12 (EC50, 14 μM), than in insect RyRs from Drosophila melanogaster and H. virescens (EC50, 40 nM, 50 nM), and shows little selectivity at the rat cell line RyR2 (EC50, >100 μM)[1].
In Vivo: Chlorantraniliprole has low acute mammalian toxicity with an acute oral LD50 of >5000 mg/kg in rats, and little to no toxicity in 90-day studies, at dosing as high as 1500 mg/kg/day[1].

Name: TUG-1375, CAS: 2247372-59-2, stock 39.1g, assay 98.7%, MWt: 442.92, Formula: C22H19ClN2O4S, Solubility: DMSO : 125 mg/mL (282.22 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TUG-1375 is an agonist of free fatty acid receptor 2 (FFA2/GPR43), with a pKi of 6.69. TUG-1375 is inactive on FFA3, FFA4, PPARα, PPARγ, PPARδ, LXRα or LXRβ[1].
IC50 & Target: pKi: 6.69 (FFA2)[1]
In Vitro: TUG-1375 exhibits pEC50 of 7.11 in the cAMP FFA2 assay, also active on murine FFA2 orthologue (pEC50, 6.44 ± 0.13 in the cAMP assay)[1].

Name: KAN0438757, CAS: 1451255-59-6, stock 32.3g, assay 98.5%, MWt: 447.43, Formula: C21H18FNO7S, Solubility: DMSO : 130 mg/mL (290.55 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KAN0438757 is a potent and selective inhibitor of the metabolic kinase PFKFB3 with an IC50 of 0.19 μM [1].
IC50 & Target: IC50: 0.19 μM (PFKFB3)[1]

Name: Homocarbonyltopsentin PK4C9, CAS: 172286-77-0, stock 20.1g, assay 98.3%, MWt: 370.36, Formula: C21H14N4O3, Solubility: DMSO : 125 mg/mL (337.51 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Homocarbonyltopsentin (PK4C9) is a small-molecule TSL2-binding compound, binds to pentaloop conformations of TSL2 and promotes a shift to triloop conformations that display enhanced SMN2 exon 7 (E7) splicing with EC50 value of 16 μM[1].
In Vitro: Homocarbonyltopsentin (PK4C9) (10-40 μM; 24 hours) shows an up to 5.2-fold decrease in the expression of E7-excluding SMN2 isoforms, and up to three-fold increase in E7-including isoforms in GM03813C cells[1].
Homocarbonyltopsentin (PK4C9) (40 μM; 24 hours) increased 1.5-fold SMN protein expression compared to GM03813C cells treated with DMSO[1].

Name: ALLO-2, CAS: 1357350-60-7, stock 13.9g, assay 98.3%, MWt: 371.32, Formula: C18H12F3N5O, Solubility: DMSO : 125 mg/mL (336.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: Smo, Biological_Activity: ALLO-2 is a potent drug-resistant Smoothened (Smo) mutant antagonist that inhibits Smo agonist Hh-Ag1.5-induced luciferase expression in TM3-Gli-Luc cells with IC50 of 6 nM[1].
IC50 & Target: IC50: Smo[1].

Name: Vipivotide tetraxetan PSMA-617, CAS: 1702967-37-0, stock 18.7g, assay 98.6%, MWt: 1042.14, Formula: C49H71N9O16, Solubility: DMSO : 125 mg/mL (119.95 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Vipivotide tetraxetan (PSMA-617) is a high potent prostate-specific membrane antigen (PSMA) inhibitor, with a Ki of 0.37 nM.
IC50 & Target: Ki: 0.37 nM (PSMA)[1].
In Vitro: Vipivotide tetraxetan (PSMA-617) demonstrates high radiolytic stability for at least 72 h. A high inhibition potency (equilibrium dissociation constant Ki=2.34±2.94 nM on LNCaP; Ki=0.37±0.21 nM enzymatically determined) and highly efficient internalization into LNCaP cells are demonstrated[1].
In Vivo: Organ distribution with 68Ga-labeled Vipivotide tetraxetan (PSMA-617) after 1 h (n=3) reveals a high specific uptake in LNCaP tumors and in the kidneys. The high uptake in the kidneys is nearly completely blocked by coinjection of 2 mg of 2-PMPA per kilogram. Other organs such as the liver, lung, and spleen show rather low uptake and no blocking effect, with the exception of the spleen. Tumor-to-background ratios are 7.8 (tumor to blood) and 17.1 (tumor to muscle) at 1 h after injection. As compared with the 68Ga-labeled version, the organ distribution with 177Lu-labeled Vipivotide tetraxetan (PSMA-617) (n=3) show a similar uptake in the LNCaP tumors and in the kidneys. The liver uptake is found to be statistically different. Tumor-to-background ratios determined 1 h after injection show slightly higher values (tumor to blood, 22.1; tumor to muscle, 25.6) than previous organ distribution with 68Ga-labeled Vipivotide tetraxetan (PSMA-617)[1].

Name: Lotilaner, CAS: 1369852-71-0, stock 25.9g, assay 98.9%, MWt: 596.76, Formula: C20H14Cl3F6N3O3S, Solubility: DMSO : ≥ 150 mg/mL (251.36 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel;Anti-infection, Target: GABA Receptor;GABA Receptor;Parasite, Biological_Activity: Lotilaner is a parasiticide, acts as a potent non-competitive antagonist of insects GABACl receptors, with an IC50 of 23.84 nM for Drosophila melanogaster GABA receptor. No effect on a dog GABAA receptor[1].
IC50 & Target: IC50: 23.84 nM (DmS-GABA), 38.25 nM (DmR2-GABA), 52.40 nM (Ls-GABA1), 36.79 nM (Rm-GABA)[1]
In Vitro: Lotilaner shows IC50s of 38.25 ± 3.75, 52.40 ± 4.54, 36.79 ± 4.39 nM for Drosophila melanogaster dieldrin/fipronil-resistant forms (DmR2), Lepeophtheirus salmonis (Ls) and Rhipicephalus microplus (Rm) GABACl receptors, respectively[1].

Name: CM-579, CAS: 1846570-40-8, stock 37.4g, assay 98.4%, MWt: 492.65, Formula: C29H40N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Histone Methyltransferase;DNA Methyltransferase, Biological_Activity: CM-579 is a first-in-class reversible, dual inhibitor of G9a and DNMT, with IC50 values of 16 nM, 32 nM for G9a and DNMT, respectively. Has potent in vitro cellular activity in a wide range of cancer cells[1].
IC50 & Target: IC50: 16 nM (G9a), 32 nM (DNMT)[1].
In Vitro: The Kd of CM-579 for DNMT1 is 1.5 nM, CM-579 also inhibits DNMT3A and DNMT3B, with IC50s of 92 nM and 1000 nM, respectively[1].

Name: 2-Methoxycinnamaldehyde o-Methoxycinnamaldehyde, CAS: 1504-74-1, stock 16.6g, assay 99%, MWt: 162.19, Formula: C10H10O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: 2-Methoxycinnamaldehyde (o-Methoxycinnamaldehyde) is a natural compound of Cinnamomum cassia, with antitumor activity[1][2][3]. 2-Methoxycinnamaldehyde inhibits proliferation and induces apoptosis by mitochondrial membrane potential (ΔΨm) loss, activation of both caspase-3 and caspase-9[2]. 2-Methoxycinnamaldehyde effectively inhibits platelet-derived growth factor (PDGF)-induced HASMC migration[3].

Name: WYE-132 WYE-125132, CAS: 1144068-46-1, stock 9.8g, assay 98.9%, MWt: 519.60, Formula: C27H33N7O4, Solubility: DMSO : 25 mg/mL (48.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR, Target: Apoptosis;mTOR, Biological_Activity: WYE-132 (WYE-125132) is a highly potent, ATP-competitive, and specific mTOR kinase inhibitor (IC50: 0.19±0.07 nM; >5,000-fold selective versus PI3Ks). WYE-132 (WYE-125132) inhibits mTORC1 and mTORC2.
IC50 & Target: IC50: 0.19±0.07 nM (mTOR), 1179 nM (PI3Kα), 2380 nM (PI3Kδ), 1250 nM (hSMG1)[1]
In Vitro: WYE-132 (WYE-125132) potently inhibits recombinant mTOR via an ATP-competitive mechanism. WYE-132 is a potent antiproliferative agent against a panel of cancer cell lines with IC50 values generally in the nanomolar range. In the typical 3-day dose-response studies, WYE-132 exhibits a more profound antiproliferative activity than CCI-779 in MDA361 and other cells, as shown by the sharper inhibition at doses up to 10 μM. Fluorescence-activated cell sorting (FACS) analysis of inhibitor-treated (1 μM, 24 hours) MDA468, PC3MM2, U87MG, A549, and HCT116 cells indicates that WYE-132 elicits a more profound increase in G1-phase and a reduction in S-phase cells than CCI-779. The WYE-132-induced cell death is evident at 10 and 30 nM (6.2% and 13%, respectively) and is dose dependent, reaching 47% at 1 μM and 59% at 3 μM[1].
In Vivo: A single i.v. administration of 50 mg/kg WYE-132 (WYE-125132) into tumor-bearing mice leads to suppression of P-S6K(T389) and P-AKT(S473) for at least 8 hours in PC3MM2, MDA361, HCT116, and HT29 tumors, whereas the steady-state level of P-AKT(T308) is not significantly reduced, indicating that the antitumor efficacy of WYE-132 under such dosing regimens reflects the suppression of mTOR rather than PI3K. Oral administration of WYE-132 causes dose-dependent tumor growth delay in the PI3K/mTOR- and HER2-hyperactive MDA361 tumors with significant antitumor activity at 5 mg/kg, which correlates with a suppression P-S6 and P-AKT(S473) but not P-AKT(T308). An optimal dose of 50 mg/kg WYE-132 induces a substantial regression of large MDA361 tumors. WYE-132 also causes a potent and substantial tumor growth delay in the PTEN-null U87MG glioma[1].

Name: MJN110, CAS: 1438416-21-7, stock 13.5g, assay 98.9%, MWt: 462.33, Formula: C22H21Cl2N3O4, Solubility: DMSO : 250 mg/mL (540.74 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: MJN110 is an orally active and selective monoacylglycerol lipase (MAGL) inhibitor with IC50s of 9.1 nM and 2.1 nM for hMAGL and 2-arachidonoylglycerol (2-AG), respectively[1]. MJN110 produces opioid-sparing effects and displays strong antihyperalgesic activity[2].
IC50 & Target: IC50: 9.1 nM (hMAGL) and 2.1 nM (2-AG)[1]
In Vitro: MJN110 (0.01-1000 nM; 4 hours) has the primary serine hydrolase target, hMAGL, with an IC50 of ~1 nM and 10- and 100-fold selectivity windows over ABHD6 and LYPLA1/2, respectively[2].
In Vivo: MJN110 (i.p.; 0.0818 mg/kg; twice daily for 5.5 days) reverses chronic constriction injury (CCI)-induced mechanical allodynia and thermal hyperalgesia in a dose-dependent manner. The respective ED50 value (95% confidence limits) is 0.430 (0.233-0.793) mg/kg[1].

Name: ON-013100, CAS: 865783-95-5, stock 25.3g, assay 98.3%, MWt: 394.44, Formula: C19H22O7S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: ON-013100, an antineoplastic drug, acts a mitotic inhibitor that could inhibit Cyclin D1 expression.
IC50 & Target: Cyclin D1[1].
In Vitro: ON-013100 induces apoptosis, and has activity against most human cancer cell lines in vitro<sup. ON013100 significantly alters the cell cycle profile, dramatically increasing the number of cells in G2/M phase. Treatment of the cells with even 0.1 μM of ON013100 results in an arrest of the G2/M phase of the cell cycle[2]. ON 013100 inhibits the proliferation of MCL (JEKO-1 and MINO), breast (MCF7 and MDA-MB-231), gastric (AGS), and esophageal (OE19, OE33, and FLO-1) cancer cell lines at a nanomolar concentration (ON 013100 GI50=6.7-11.2 nM) [3].

Name: CB1 antagonist 2, CAS: 614726-85-1, stock 4.1g, assay 98%, MWt: 380.66, Formula: C17H12Cl3N3O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (164.19 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cannabinoid Receptor;Cannabinoid Receptor, Biological_Activity: CB1 antagonist 2 is caimabinoid 1 (CB1) antagonist extracted from patent WO2016184310A1, compound 3, inhibits CB1 in vivo with an IC50 of 25.5 nM[1].

Name: JNJ-54175446, CAS: 1627902-21-9, stock 30.6g, assay 98%, MWt: 440.78, Formula: C18H13ClF4N6O, Solubility: DMSO : 62.5 mg/mL (141.79 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Membrane Transporter/Ion Channel, Target: P2X Receptor, Biological_Activity: JNJ-54175446 is a potent and selective brain penetrant P2X7 receptor antagonist, with pIC50s of 8.46 and 8.81 for hP2X7 receptor and rP2X7 receptor, respectively.
IC50 & Target: pIC50: 8.46 (hP2X7 receptor), 8.81 (rP2X7 receptor)[1]
In Vitro: JNJ-54175446 (Compound 14) is a potent and selective brain penetrant P2X7 antagonist, with pIC50s of 8.46 and 8.81 for hP2X7 and rP2X7, respectively. JNJ-54175446 shows less potent activity against mouse, dog and Macaque P2X7 (pIC50, 7.8, 7.9 and 8.1, respectively)[1].
In Vivo: JNJ-54175446 shows dose-dependent occupancy with the ED50 of 0.46 mg/kg, corresponding to plasma EC50 of 105 ng/mL[1].

Name: Tyrphostin AG30 AG30, CAS: 122520-79-0, stock 14.9g, assay 98%, MWt: 205.17, Formula: C10H7NO4, Solubility: DMSO : 125 mg/mL (609.25 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Tyrphostin AG30 (AG30) is a potent and selective EGFR tyrosine kinase inhibitor. Tyrphostin AG30 (AG30) selectively inhibits self renewal induction by c-ErbB, and is able to inhibit activation of STAT5 by c-ErbB in primary erythroblasts[1][2].

Name: PF-06700841 (P-Tosylate), CAS: 2140301-96-6, stock 38.3g, assay 98.8%, MWt: 561.60, Formula: C25H29F2N7O4S, Solubility: DMSO : 62.5 mg/mL (111.29 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: PF-06700841 P-Tosylate is a potent dual Janus kinase 1 (JAK1) and TYK2 inhibitor with IC50s of 17 nM and 23 nM, respectively. PF-06700841 P-Tosylate also inhibits JAK2 and JAK3 with IC50s of 77 nM and 6.49 μM, respectively[1].
IC50 & Target: IC50: 17 nM (JAK1), 23 nM (TYK2)[1]
In Vitro: PF-06700841 (Compound 23) potently inhibits TYK2/JAK2 mediated IL-12/pSTAT4 and IL-23/pSTAT3 (human whole blood (HWB) IC50s of 65 and 120 nM, respectively). PF-06700841 has good potency against IL6/pStat1 in the CD3+ cellular subset (IC50 of 81 nM), but lower inhibition of IL6/pSTAT3, again in the CD3+ cellular subset (IC50 of 641 nM). PF-06700841 also inhibits the JAK1/JAK3 driven γ-common chain cytokines, represented by IL-15/pStat5 and IL-21/pSTAT3 with reasonable potency (HWB IC50s of 238 and 204 nM, respectively). PF-06700841 inhibits EPO/pSTAT5 (JAK2 homodimer) in HWB spiked with CD34+ progenitor cells (IC50 of 577 nM). IL10/pSTAT3 (TYK2/JAK1) and IL27/pSTAT3 (JAK1/JAK2/TYK2) are also inhibited by PF-06700841 with IC50s of 305 nM and 86 nM, respectively[1].
In Vivo: PF-06700841 (Compound 23; 3-30 mg/kg; oral administration; for 7 consecutive days; female Lewis rats) treatment significantly reduces paw volume increase in a dose-dependent manner. The plasma concentrations in animals dosed with PF-06700841 at peak (30 min) and trough (24 h) time intervals post final dose respectively are as follows: 3 mg/kg, 3.54 μM, 0.0221 μM; 10 mg/kg, 10.95 μM, 0.06 μM; and 30 mg/kg, 23.89 μM, 0.06 μM[1].

Name: FASN-IN-2, CAS: 1399177-37-7, stock 38.5g, assay 98.7%, MWt: 439.55, Formula: C27H29N5O, Solubility: DMSO : ≥ 250 mg/mL (568.76 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Fatty Acid Synthase (FAS), Biological_Activity: FASN-IN-2 is a Fatty Acid Synthase (FASN) inhibitor extracted from patent WO2012122391A1, compound 152, has an IC50 of 0.052 μM and an EC50 of 0.072 μM[1].
IC50 & Target: IC50: 0.052 μM (FASN)[1]

Name: SR10067, CAS: 1380548-02-6, stock 2.1g, assay 98.8%, MWt: 465.58, Formula: C31H31NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SR10067 is a potent, selective and brain penetrant Rev-Erbα/β agonist, with IC50 values are 160 and 170 nM for Rev-Erbβ and Rev-Erbα, respectively. SR10067 has anxiolytic activity[1][2].
IC50 & Target: IC50: 160 nM (Rev-Erbβ), 170 nM (Rev-Erbα)[1].

Name: PIN1 inhibitor API-1, CAS: 680622-70-2, stock 9.9g, assay 98.4%, MWt: 366.30, Formula: C15H13F3N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PIN1 inhibitor API-1 is a specific Pin1 (peptidyl-prolyl cis-trans isomerase NIMA-interacting 1) inhibitor (API-1) with an IC50 of 72.3 nM. PIN1 inhibitor API-1 directly and specifically binds to the Pin1 peptidyl-prolyl isomerase (PPIase) domain and potently inhibits Pin1 cis-trans isomerizing activity. PIN1 inhibitor API-1 retains the active conformation of pXPO5 and restores the ability of pXPO5 to transport pre-miRNAs from nucleus to cytoplasm, thus up-regulating the anticancer miRNA biogenesis to suppress both in vitro and in vivo hepatocellular carcinoma development[1].
IC50 & Target: IC50: 72.3 nM (Pin1)[1]
In Vitro: PIN1 inhibitor API-1 obviously inhibits SK-Hep-1, SNU-423, and Hep3B cell proliferation with low IC50 values (IC50=0.683-4.16 μM)[1].
In Vivo: PIN1 inhibitor API-1 suppresses tumor growth in mice by up-regulating mature miRNA biogenesis[1].

Name: CDK2-IN-4, CAS: 2079895-42-2, stock 30.5g, assay 98.8%, MWt: 442.49, Formula: C23H18N6O2S, Solubility: DMSO : 20.83 mg/mL (47.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CDK2-IN-4 is a potent and selective CDK2 inhibitor with an IC50 of 44 nM for CDK2/cyclin A, shows 2,000-fold selectivity over CDK1/cyclin B (IC50=86 uM)[1].
IC50 & Target: IC50: 44 nM (CDK2/cyclin A), 86 μM (CDK1/cyclin B)[1]

Name: Glycyl-glutamine Glycyl-L-glutamine, CAS: 13115-71-4, stock 6.3g, assay 98.4%, MWt: 203.20, Formula: C7H13N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Glycyl-glutamine (Glycyl-L-glutamine), as a enzymatic cleavage product of β-endorphin, is apparently an endogenous antagonist of beta-endorphin(1-31) in several systems[1]. Glycyl-glutamine (Glycyl-L-glutamine) is an activate and stable glutamine-containing neuropeptide over glutamine (Gln)[2].
In Vitro: Glycyl-glutamine (Glycyl-L-glutamine) is an activate and stable glutamine-containing neuropeptide. Glycyl-glutamine (Glycyl-L-glutamine) has an advantage over free glutamine (Gln) as growth factors for cell culture during both autoclaving and storage[2].
In Vivo: Glycyl-glutamine (Glycyl-L-glutamine) (0.3, 0.6, 1.0 and 10.0 nM) can dose-dependently inhibit beta-End-(1-31)-induced hypotension in pentobarbital-anesthetized rats[1].

Name: Ibrolipim NO-1886, CAS: 133208-93-2, stock 29.7g, assay 98.2%, MWt: 451.25, Formula: C19H20BrN2O4P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ibrolipim (NO-1886) is an orally active lipoprotein lipase (LPL)-promoting agent. Ibrolipim decreases plasma triglycerides, increases high-density lipoprotein cholesterol levels. Ibrolipim has renoprotective and hypolipidemic effects[1][2][3].
IC50 & Target: Lipoprotein lipase (LPL)[1][2][3]
In Vitro: Ibrolipim (0.5-10 μM; 0-24 hours; THP-1 macrophage-derived foam cells) treatment increases ABCA1 and ABCG1 expression at translational levels in a dose-dependent and time-dependent manner [1]. 
Ibrolipim (0.5-10 μM; 0-24 hours; THP-1 macrophage-derived foam cells) treatment increases ABCA1 and ABCG1 expression at the transcriptional levels in a dose-dependent and time-dependent manner [1]. 
Ibrolipim 5 and 50 μmol/L significantly increases cholesterol efflux from THP-1 macrophage-derived foam cells to apoA-I or HDL. LXRα is also upregulated by the Ibrolipim treatment. LXRα small interfering RNA completely abolishes the promotion effect that is induced by Ibrolipim[1].
In Vivo: Ibrolipim (NO-1886; 100 mg/kg; oral administration; daily; for 8 weeks; female Sprague-Dawley rats) treatment decreases accumulation of visceral fat and suppresses the increase in body weight resulting from the ovariectomy. Ibrolipim decreases the respiratory quotient and increases expression of the fatty acid translocase messenger RNA (mRNA) in the liver, soleus muscle, and mesenteric fat. Ibrolipim also increases the expression of fatty acid-binding protein mRNA in the liver and soleus muscle and the expression of the uncoupling protein 3 (UCP3) mRNA in the heart, soleus muscle, and mesenteric fat, but not in the brown adipose tissue[2].

Name: BI-409306, CAS: 1189767-28-9, stock 19.5g, assay 98.8%, MWt: 311.34, Formula: C16H17N5O2, Solubility: DMSO : ≥ 75 mg/mL (240.89 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: BI-409306 is a potent and selective PDE9A inhibitor, with an IC50 of 52 nM, and shows weak activity against other PDEs, such as PDE1A (IC50, 1.4 µM), PDE1C (IC50, 1.0 µM), PDE2A, PDE3A, PDE4B, PDE5A, PDE6AB, PDE7A, and PDE10A (IC50 all > 10 μM); BI-409306 can be used in the research of memory enhancement in CNS disorders.
IC50 & Target: IC50: 52 nM (PDE9A), 1.4 µM (PDE1A), 1.0 µM (PDE1C)[1]
In Vitro: BI-409306 is a potent and selective PDE9A inhibitor, with an IC50 of 52 nM, and shows weak activity against other PDEs, such as PDE1A (IC50, 1.4 µM), PDE1C (IC50, 1.0 µM), PDE2A, PDE3A, PDE4B, PDE5A, PDE6AB, PDE7A, and PDE10A (IC50 all > 10 μM), and has no obvious effect on 95 non-PDE targets at 10 µM. BI-409306 enhances long-term potentiation (LTP) in rat hippocampal slices[1].

Name: GSK467, CAS: 1628332-52-4, stock 32g, assay 98.7%, MWt: 319.32, Formula: C17H13N5O2, Solubility: DMSO : 20.83 mg/mL (65.23 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: GSK467 is a cell penetrant and selective KDM5B (JARID1B or PLU1) inhibitor with a Ki of 10 nM, shows 180-fold selectivity for KDM4C and no measurable inhibitory effects toward KDM6 or other Jumonji family members[1].
IC50 & Target: Ki: 10 nM (KDM5B)[1]

Name: Lipofermata, CAS: 297180-15-5, stock 24.4g, assay 98.4%, MWt: 360.23, Formula: C15H10BrN3OS, Solubility: DMSO : 100 mg/mL (277.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Lipofermata is a fatty acid transport proteins (FATP) inhibitor that abrogates lipid transport into melanoma cells and reduces melanoma growth and invasion[1].

Name: BPN14770, CAS: 1606974-33-7, stock 3g, assay 98.6%, MWt: 405.80, Formula: C21H15ClF3NO2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: BPN14770 is a selective phosphodiesterase 4D (PDE4D) allosteric inhibitor with IC50s of 7.8 nM and 7.4 nM for PDE4D7 and PDE4D3, respectively[1].
IC50 & Target: IC50: 7.8 nM (PDE4D7), 7.4 nM (PDE4D3)[1]
In Vivo: BPN14770 increases brain cAMP, increases phosphorylation of CREB and increases production of brain-derived neurotrophic factor (BDNF) in hippocampus[1]. 
BPN14770 (0.1-30 mg/kg; p.o.; 24 hours) provides cognitive benefit in the mouse novel object recognition (NOR) at doses above 0.3 mg/kg[2].

Name: ML401, CAS: 1597489-14-9, stock 28.5g, assay 98.3%, MWt: 419.74, Formula: C20H20BrClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: EBI2/GPR183, Biological_Activity: ML401, a potent chemical probe, selectively antagonizes EBI2 (also known as GPR183) with an IC50 of 1.03 nM. ML401 displays activity in a chemotaxis assay (IC50=6.24 nM). ML401 shows good stability and no toxicity[1].
IC50 & Target: IC50: 1.03 nM (EBI2)[1]
In Vitro: ML401 shows no toxicity (>50 μM) towards immortalized Fa2-N4 human hepatocytes and non-cytotoxic in MTT in both LnCap and IMR-32 cells (>50 μM)[1].
In Vivo: ML401 shows very good stability in both human plasma and mouse plasma[1].

Name: RU-301, CAS: 1110873-99-8, stock 32.9g, assay 98.7%, MWt: 480.46, Formula: C21H19F3N4O4S, Solubility: , Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: TAM Receptor, Biological_Activity: RU-301 is a pan-TAM receptor inhibitor, exerts pan-TAM inhibitory activity by binding at the interface between Gas6 and the Ig1 domain of the respective TAMs with Kd and IC50 values of 12 μM and 10 μM, respectively[1].
IC50 & Target: IC50: 10 μM (TAM)[1]

Name: BRD0705, CAS: 2056261-41-5, stock 7.8g, assay 99%, MWt: 321.42, Formula: C20H23N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR, Target: GSK-3;GSK-3, Biological_Activity: BRD0705 is a potent, paralog selective and orally active GSK3α inhibitor with an IC50 of 66 nM and a Kd of 4.8 μM. BRD0705 displays increased selectivity for GSK3α (8-fold) versus GSK3β (IC50 of 515 nM). BRD0705 can be used to treat acute myeloid leukemia (AML)[1].
In Vitro: BRD0705 displays excellent selectivity in a penal of 311 kinases, the CDK family of kinases (CDK2, 3 and 5) are next most potently inhibits at values of 6.87 μM, 9.74 μM and 9.20 μM (87-fold, 123-fold and 116-fold selectivity relative to GSK3α)[1]. 
BRD0705 (10-40 μM; 2-24 hours; U937 cells) treatment impairs GSK3α Tyr279 phosphorylation in a time-and concentration-dependent manner without affecting GSK3β Tyr216 phosphorylation[1]. 
Using a β-catenin dependent TCF/LEF luciferase reporter assay, the absence of β-catenin induced target activation after treatment with BRD0705 in AML cell lines[1]. 
BRD0705 impairs AML colony formation in all six tested cell lines, MOLM13, TF-1, U937, MV4-11, HL-60 and NB4, in a concentration-dependent manner, as opposed to BRD3731 which impairs colony formation in TF-1 while increasing colony forming ability in the MV4-11 cell line[1].
In Vivo: BRD0705 (30 mg/kg; oral gavage; twice daily; NSG mice) treatment impairs leukemia initiation and prolongs survival in AML mouse models[1].

Name: PF-04634817, CAS: 1228111-63-4, stock 2.7g, assay 98.4%, MWt: 511.58, Formula: C25H36F3N5O3, Solubility: DMSO : 50 mg/mL (97.74 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: PF-0463481, an oral CCR2/5 dual antagonist, with a favorable ocular safety profile versus intravitreal therapies[1]. PF-0463481 is safe and well-tolerated and being developed for the treatment of diabetic nephropathy[2].

Name: ABX-1431, CAS: 1446817-84-0, stock 32g, assay 98.9%, MWt: 507.39, Formula: C20H22F9N3O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (246.36 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: ABX-1431 is a highly potent, selective, and orally available, CNS-penetrant monoacylglycerol lipase (MAGL) inhibitor with an IC50 of 14 nM.
IC50 & Target: IC50: 14 nM (human MGLL)[1]
In Vitro: ABX-1431 is a potent human MGLL inhibitor (IC50=0.014 µM) with >100-fold selectivity against ABHD6 and >200-fold selectivity against PLA2G7. ABX-1431 inhibits human PC3 cells with an IC50 of 0.0022 µM. In the cell-based assay, >100-fold selectivity for MGLL over ABHD6 (IC50=0.253 µM) and PLA2G7 (IC50=494 µM) is maintained[1].
In Vivo: ABX-1431 inhibits MGLL activity in rodent brain (ED50=0.5-1.4 mg/kg), increases brain 2-AG concentrations, and suppresses pain behavior in the rat formalin pain model[1].

Name: AUT1, CAS: 1311136-84-1, stock 22.1g, assay 98.9%, MWt: 341.36, Formula: C18H19N3O4, Solubility: DMSO : ≥ 250 mg/mL (732.36 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: AUT1 is a Kv3 potassium channel modulator, with pEC50s of 5.33 and 5.31 for human recombinant Kv3.1b and Kv3.2a, respectively, exhibits 10-fold lower potency at human recombinant Kv3.3 channel (pEC50, 4.5)[1].
IC50 & Target: pEC50: 5.33 (Human recombinant Kv3.1b), 5.31 (Human recombinant Kv3.2a), 4.5 (Human recombinant Kv3.3)[1]

Name: SRPKIN-1, CAS: 2089226-94-6, stock 29.8g, assay 98.9%, MWt: 472.53, Formula: C27H21FN2O3S, Solubility: DMSO : ≥ 110 mg/mL (232.79 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: SRPK, Biological_Activity: SRPKIN-1 is a covalent and irreversible SRPK1/2 inhibitor with IC50s of 35.6 and 98 nM, respectively. Anti-angiogenesis effect[1].
IC50 & Target: IC50: 35.6 nM (SRPK1), 98 nM (SRPK2)[1]
In Vitro: SRPKIN-1 treatment at 200 nM (10, 50, 100, 200 nM, 16 hours) significantly reduces SR protein phosphorylation at the steady state with or without washout[1].
SRPK-IN-1 potently converts VEGF from pro-angiogenic to anti-angiogenic isoform[1].
In Vivo: SRPKIN-1 (50 nM, 300 nM,1 μL, 5 times) blocks angiogenesis in a CNV mouse model through VEGF alternative splicing[1].

Name: Angelicain Norcimifugin, CAS: 49624-66-0, stock 9.6g, assay 99%, MWt: 292.28, Formula: C15H16O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angelicain (Norcimifugin) is a constituent of Cimicifuga foetida with anti-inflammatory activity[1].

Name: MAC13772, CAS: 4871-40-3, stock 17.2g, assay 98.3%, MWt: 227.24, Formula: C8H9N3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: MAC13772 is a potent inhibitor of the enzyme BioA (IC50=250 nM), the antepenultimate step in biotin biosynthesis. MAC13772 is a novel antibacterial compound[1].
IC50 & Target: IC50: 250 nM (BioA)[1]

Name: ESI-05 NSC 116966, CAS: 5184-64-5, stock 32.3g, assay 98.5%, MWt: 274.38, Formula: C16H18O2S, Solubility: DMSO : 83.33 mg/mL (303.70 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ESI-05 (NSC 116966) is a specific antagonist of EPAC2 (exchange protein directly activated by cAMP 2), with an IC50 of 0.4 µM. ESI-05 (NSC 116966) inhibits cAMP-mediated activation of EPAC2 as well as EAPC2 mediated Rap1 activation[1].
IC50 & Target: IC50: 0.4 µM (EPAC2)[1]

Name: SPHINX31, CAS: 1818389-84-2, stock 27.8g, assay 98.7%, MWt: 507.51, Formula: C27H24F3N5O2, Solubility: DMSO : 17.33 mg/mL (34.15 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: SRPK, Biological_Activity: SPHINX31 is a potent and selective inhibitor of serine/arginine-rich protein kinase 1 (SRPK1), with an IC50 of 5.9 nM. SPHINX31 inhibits phosphorylation of serine/arginine-rich splicing factor 1 (SRSF1). SPHINX31 is a potential topical therapeutic for neovascular eye disease[1].
IC50 & Target: IC50: 5.9 nM (SRPK1)[1].

Name: A-381393, CAS: 726174-00-1, stock 33.4g, assay 98.5%, MWt: 320.43, Formula: C20H24N4, Solubility: DMSO : 51.67 mg/mL (161.25 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: A-381393 is a potent, selective, brain penetrate dopamine D4 receptor antagonist, with Kis of 1.5, 1.9 and 1.6 nM for human dopamine D4.4, D4.2, and D4.7 receptor, respectively, >2700-fold selectivity over D1, D2, D3 and D5 dopamine receptors. A-381393 shows moderate affinity for 5-HT2A (Ki, 370 nM)[1].
IC50 & Target: Ki: 1.5 nM (D4.4 receptor), 1.9 nM (D4.2 receptor), 1.6 nM (D4.7 receptor)[1]
In Vitro: A-381393 exhibits weak affinity at 5-HT1A, Sigma 2, Adenoceptor α1A, Adenoceptor α2C, Histamine H1, with Kis of 1365, 8600, 2044, 1912 and 2962 nM, respectively[1].

Name: MBQ-167, CAS: 2097938-73-1, stock 11.3g, assay 98.5%, MWt: 338.41, Formula: C22H18N4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 155 mg/mL (458.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;GPCR/G Protein, Target: CDK;Ras, Biological_Activity: MBQ-167 is a dual Rac/Cdc42 inhibitor, with IC50s of 103 nM for Rac 1/2/3 and 78 nM for Cdc42 in MDA-MB-231 cells, respectively.
IC50 & Target: IC50: 103 nM (1/2/3), 78 nM (Cdc42)[1].
In Vitro: MBQ-167 (≥100 nM) induces a loss of polarity in metastatic breast cancer cells. Treatment with 500 nM MBQ-167 for 24 h results in ~95% cell rounding and detachment from the substratum in metastatic MDA-MB-231 cells. Moreover, MBQ-167 induces this phenotype in multiple mesenchymal cancer cell types including GFP-HER2-BM, MDA-MB-468, and Hs578t human breast cancer cells, as well as Mia-PaCa-2 pancreatic cancer cells, SKOV3 ovarian cancer cells, AGS and NCI-N87 gastric cancer cells, and SH-SY5Y neuroblastoma cells. Following treatment with 250 nM MBQ-167 for 24 h, the attached population of MDA-MB-231 cells demonstrate a ~25% decrease in Rac activation while the detached cells are more responsive with a ~75% decrease. At earlier times (6h), treatment with 250 or 500 nM MBQ-167, induce a inhibition in Rac activity in the attached cell population, while the detached population demonstrate a ~40-50% inhibition[1].
In Vivo: MBQ-167-treated mice demonstrate a statistically significant reduction in tumor growth. At sacrifice, 1.0 mg/kg BW of MBQ-167 results in a ~80% reduction in tumor growth, and the 10 mg/kg BW MBQ-167 treatment results in ~95% reduction in tumor growth. Since EHop-016 only exerts ~40% reduction of tumor growth at 10 mg/kg BW, MBQ-167 is 10X more effective than EHop-016. MBQ-167 treated mice demonstrate similar doubling times for both treatments (10 and 11 days)[1].

Name: CNT2 inhibitor-1, CAS: 880155-70-4, stock 39.7g, assay 98.2%, MWt: 448.47, Formula: C23H24N6O4, Solubility: DMSO : 75 mg/mL (167.24 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CNT2 inhibitor-1 is a potent concentrative nucleoside transporter 2 Inhibitor (CNT2), with an IC50 of 640 nM for hCNT2.
IC50 & Target: IC50: 640 nM (hCNT2)[1][2].
In Vitro: CNT2 inhibitor-1 (compound 48) exhibits 81-fold more potent inhibitory activity than the parent compound 12. In addition, CNT2 inhibitor-1 exhibits inhibitory activity 1500-fold more potent than that of 2’-deoxy-5-fluorouridine, phlorizin, and 7,8,3’-trihydroxyflavone, which are well-known hCNT2 inhibitors[1]. CNT2 inhibitor-1 (compound 1) is a potent inhibitor with poor solubility[2].

Name: GSK-J4 (hydrochloride), CAS: 1797983-09-5, stock 6.2g, assay 98.9%, MWt: 453.96, Formula: C24H28ClN5O2, Solubility: DMSO : 125 mg/mL (275.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: GSK-J4 hydrochloride is a potent dual inhibitor of H3K27me3/me2-demethylases JMJD3/KDM6B and UTX/KDM6A with IC50s of 8.6 and 6.6 μM, respectively. GSK-J4 hydrochloride inhibits LPS-induced TNF-α production in human primary macrophages with an IC50 of 9 μM. GSK-J4 hydrochloride is a cell permeable prodrug of GSK-J1[1][2][3].
IC50 & Target: IC50: 8.6 µM (JMJD3/KDM6B), 6.6 µM (UTX/KDM6A)[6]
In Vitro: GSK-J4 Hydrochloride has cellular activity in Flag-JMJD3-transfected HeLa cells, in which GSK-J4 prevents the JMJD3-induced loss of nuclear H3K27me3 immunostaining. Administration of GSK-J4 increases total nuclear H3K27me3 levels in untransfected cells. GSK-J4 significantly reduces the expression of 16 of 34 LPS-driven cytokines, including tumour-necrosis factor-α (TNF-α)[1]. 
GSK-J4 Hydrochloride (5 μM; 48 hours) causes a more than 3-fold increase in mouse podocyte H3K27me3 content. H3K27me3 levels in cultured podocytes, GSK-J4 reduces Jagged-1 mRNA and Jagged-1 protein levels. Correspondingly, when exposed podocytes to the inducer of dedifferentiation TGF-β1, pretreatment with GSK-J4 preventes both the increase in intracellular N1-ICD levels and the increase in α-SMA and the decrease in podocin mRNA levels[2]. 
GSK-J4 Hydrochloride (10, 25 nM) acts upon DCs promoting the differentiation of Treg cells, improving Treg stability and suppressive capacities, without affecting the differentiation of Th1 and Th17 cells[3]. 
GSK-J4 Hydrochloride inhibits JMJD3 expression that is induced by TGF-β1[4]. 
GSK-J4 Hydrochloride inhibits H3K4 demethylation at Xist, Nodal, and HoxC13 in female embryonic stem cells[5].
In Vivo: GSK-J4 Hydrochloride (10 mg/kg; i.p.; thrice-weekly for 10 weeks) attenuates the development of kidney disease in diabetic mice[2]. 
GSK-J4 Hydrochloride (0.5 mg/kg, i.p.) significantly reduces the severity and delays the onset of the disease of the mouse model of experimental autoimmune encephalomyelitis[3].

Name: Sulfosuccinimidyl oleate Sulfo-N-succinimidyl oleate, CAS: 135661-44-8, stock 22.5g, assay 98.8%, MWt: 459.60, Formula: C22H37NO7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Mitophagy, Biological_Activity: Sulfosuccinimidyl oleate (Sulfo-N-succinimidyl oleate) is a long chain fatty acid that inhibits fatty acid transport into cells. Sulfosuccinimidyl oleate is a potent and irreversible inhibitor of mitochondrial respiratory chain. Sulfosuccinimidyl oleate binds the CD36 receptor on the surface of microglia. Anti-inflammatory effect[1][2].
In Vitro: Sulfosuccinimidyl oleate (20 μM and 50 μM, 24 hours) alone does not alter the cellular viability. Exposure to 100 ng/ml LPS+5 ng/mL IFNγ modestly, yet significantly reduces the viability of the BV2 cells. Co-treatment with Sulfosuccinimidyl oleate prevents the LPS+IFNγ-induced reduction in the cell viability[1]. 
Sulfosuccinimidyl oleate (50 μM, 24 hours) co-treatment significantly reduces the LPS+IFNγ-induced expression of NOS2 and COX-2 in BV2 cells. Western blot analysis reveals a significant LPS/IFNγ-induced upregulation in the phosphorylated form of the p38, which is prevented by co-treatment with Sulfosuccinimidyl oleate (50 μM, 24 hours)[1]. 
In Vivo: Sulfosuccinimidyl oleate (50 mg/kg; administered once by single oral gavage) significantly reduces the cortical ischemic infarct size compared to vehicle-treated controls in male BALB/cABom mice with pMCAo model. In addition, Sulfosuccinimidyl oleate at 50 mg/kg is suitable to see a beneficial effect after stroke[1].

Name: Diacylglycerol acyltransferase inhibitor-1, CAS: 1610800-25-3, stock 23.1g, assay 98%, MWt: 377.44, Formula: C21H23N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: Diacylglycerol acyltransferase inhibitor-1 is a diacylglycerol acyltransferase (DGAT1) inhibitor.

Name: GW-406381, CAS: 221148-46-5, stock 8.5g, assay 98.8%, MWt: 393.46, Formula: C21H19N3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: GW406381, a highly selective cyclooxygenase-2 (COX-2) inhibitor, attenuates spontaneous ectopic discharge in sural nerves of rats following chronic constriction injury[1][2].
IC50 & Target: COX-2[1]

Name: Apratastat, CAS: 287405-51-0, stock 34.1g, assay 98.5%, MWt: 414.50, Formula: C17H22N2O6S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Apoptosis, Target: MMP;TNF Receptor, Biological_Activity: Apratastat is an orally active, potent, and reversible dual inhibitor of tumor necrosis factor-α converting enzyme (TACE) and matrix metalloproteinases (MMPs) . Apratastat can potently inhibit the release of TNF-α in vitro, ex vivo, and in vivo with IC50s of 144 ng/mL in vitro and 81.7 ng/mL ex vivo, respectively[1].

Name: Sucrose octaacetate, CAS: 126-14-7, stock 23g, assay 98.4%, MWt: 678.59, Formula: C28H38O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sucrose octaacetate is an acetylated derivative of sucrose with an intensely bitter tasting and can be used as bitter tasting surrogate. Sucrose octaacetate can be used as food additive and also used as an adhesive and plasticizer. Sucrose octaacetate also used in many pesticides, insecticides, and other toxic products as a deterrent to accidental poisoning. Sucrose octaacetate can also be used as an in situ seed and a soft template to synthesize polyaniline (PANI) nanofibers[1][2][3].
In Vitro: Sucrose octaacetate is nontoxic and has a number of uses based on its bitter taste. For example, sugar is rendered too bitter is eat at a concentration of 0.06% (w/w) Sucrose octaacetate. Sucrose octaacetate can form 255 different possible isomers and degradation products, all of which have a very low molar absorptivity[1]. 
Polyaniline (PANI) nanofibers and nanorods are obtained using 2 and 3 g Sucrose octaacetate, respectively. The nanostructures containing irregular-shaped agglomerates, such as particulate particles and scaffolds are observed with increasing the concentrations of Sucrose octaacetate. The presence of Sucrose octaacetate during polymerization could only induce a change in morphology, but could not influence the molecular structure of the resulting PANI. Compared with those derived with 1, 3, and 4 g Sucrose octaacetate, the polymerized PANI from 2 g Sucrose octaacetate possesses higher thermal stability and electrical conductivity due to its higher crystallinity and highly ordered structure[3].
In Vivo: No recombination has been found between Sucrose octaacetate-avoidance phenotype and PRP haplotype in any mouse population. Soa and Prp, therefore, are either very near each other or identical. To assess the latter possibility, two type-A, proline-rich protein genes (MP2 and M14), situated approximately 30 kb apart at the Prp locus, are separately transferred from a Sucrose octaacetate-taster inbred strain (SWR) to a Sucrose octaacetate-nontaster inbred strain (FVB). Five MP2-transgenic mice and seven M14-transgenic mice are insensitive to 1 mM Sucrose octaacetate in two-bottle tests, thus retaining the nontaster FVB phenotype. Expression of mRNAs for both type-A Prp genes alone or together do not enhance SOA taste sensitivity in nontaster mice[2].

Name: 1,4-Cineole, CAS: 470-67-7, stock 8.2g, assay 98%, MWt: 154.25, Formula: C10H18O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: 1,4-Cineole is a widely distributed, natural, oxygenated monoterpene[1]. 1,4-Cineole, present in eucalyptus oil, activates both human TRPM8 and human TRPA1[2].

Name: AZD-8055, CAS: 1009298-09-2, stock 7.9g, assay 98%, MWt: 465.54, Formula: C25H31N5O4, Solubility: DMSO : 33.33 mg/mL (71.59 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: Apoptosis;mTOR;Autophagy, Biological_Activity: AZD-8055 is a novel ATP-competitive inhibitor of mTOR kinase activity, with an IC50 of 0.8 nM. AZD-8055 inhibits both mTORC1 and mTORC2.
IC50 & Target: IC50: 0.8 nM (mTOR)[1]
In Vitro: The inhibitory activity of AZD-8055 (AZD8055) against mTOR is evaluated using two different assays. Using the truncated recombinant mTOR enzyme, the IC50 for AZD8055 is 0.13±0.05 nM. Using native mTOR enzyme complexes extracted from HeLa cells, the IC50 is 0.8±0.2 nM. AZD-8055 shows excellent selectivity (~1,000-fold) against all class I PI3K isoforms and other members of the PI3K-like kinase family. AZD-8055 inhibits the phosphorylation of mTORC1 substrates p70S6K and 4E-BP1 as well as phosphorylation of the mTORC2 substrate AKT and downstream proteins. The cellular IC50s for AZD8055 are calculated as 24±9 nM (n=13) for pAKT Ser473 and 27±3 nM (n=12) for pS6 Ser235/236 in MDA-MB-468 cells[1].
In Vivo: In mice bearing U87-MG (PTEN null) glioblastoma xenografts, oral treatment with AZD-8055 (AZD8055) results in a dose-dependent tumor growth inhibition of 33%, 48%, and 77% with 2.5, 5, and 10 mg/kg/d twice daily, respectively. A similar dose dependency is observed in nude mice bearing A549 xenografts: tumor growth inhibition is 44%, 55%, and 93% after 2.5, 5, and 10 mg/kg/d twice daily, respectively. AZD8055 also results in significant inhibition of tumor growth and/or regression in breast, lung, colon, prostate, and uterine xenograft models when administered either twice daily at 10 mg/kg or daily at a dose of 20 mg/kg[1]. AZD8055 markedly decreases the phosphorylation levels of mTOR and its substrates and the activation of microglia in vivo, and promotes the microglial polarization from M1 phenotype to M2 phenotype. In addition, administration of AZD8055 following subarachnoid hemorrhage (SAH) significantly ameliorates EBI, including neuronal apoptosis, neuronal necrosis, brain edema and blood-brain barrier permeability[2].

Name: TL02-59, CAS: 1315330-17-6, stock 19.7g, assay 98.4%, MWt: 609.64, Formula: C32H34F3N5O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis, Target: Src;Apoptosis, Biological_Activity: TL02-59 is an orally active, selective Src-family kinase Fgr inhibitor with an IC50 of 0.03 nM. TL02-59 also inhibits Lyn and Hck with IC50s of 0.1 nM and 160 nM, respectively. TL02-59 potently suppresses acute myelogenous leukemia (AML) cell growth[1].
IC50 & Target: IC50: 0.03 nM (Fgr)[1]
In Vitro: TL02-59 inhibits the growth and induced apoptosis of AML cell lines expressing this kinase with single-digit nM potency[1]. 
TL02-59 induces growth arrest in primary AML bone marrow samples[1]. 
TL02-59 (0.1-1000 nM; 6 hours) potently inhibits Fgr autophosphorylation in TF-1 cells, with paritial inhibition at 0.1-1 nM and complete inhibition above 10 nM. Hck, Lyn and Flt3 are inhibited in the 100 to 1000 nM range[1]. 
In Vivo: TL02-59 (oral administration; 1 and 10 mg/kg; for three weeks) completely eliminates AML cells from the spleen and peripheral blood in a mouse model of AML, while dramatically suppressing bone marrow involvement[1]. 
TL02-59 has a t1/2 of 5.7 h by i.v injection and 6.5 h by p.o. administration, respectively[1].

Name: Tifenazoxide NN414, CAS: 279215-43-9, stock 5g, assay 98.9%, MWt: 291.78, Formula: C9H10ClN3O2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Tifenazoxide (NN414) is a potent, orally active and SUR1/Kir6.2 selective KATP channels opener. Tifenazoxide has antidiabetic effect, can inhibit glucose stimulated insulin release in vitro and in vivo, and has a beneficial effect on glucose homeostasis[1][2].
IC50 & Target: KATP channels[1][2]
In Vitro: Tifenazoxide (NN414) hyperpolarises βTC3 cell membranes, and inhibits insulin release from βTC6, from isolated rat islets and from human islets at least a 100-fold more potent than Diazoxide[2]. 
The EC50 values for Tifenazoxide and diazoxide are 0.45 and 31 µM, respectively in the patch-clamp assay. Tifenazoxide (100 µM) activates Kir6.2/SUR1 channels, but not Kir6.2/SUR2A or Kir6.2/SUR2 channels, expressed in Xenopus oocytes both in whole-cell and inside-out macropatch recordings[2]. 
Tifenazoxide is a potent inhibitor of glucose stimulated insulin release from βTC6 cells (IC50 = 0.15 µM)[1].
In Vivo: Tifenazoxide (NN414; 1.5 mg/kg; oral administration; twice daily; for 3 weeks; male VDF Zucker (fa/fa) rat) treatment for 3 weeks in VDF rats reduces basal hyperglycemia, improves glucose tolerance, and reduces hyperinsulinemia during an oral glucose tolerance test (OGTT) and improves insulin secretory responsiveness ex vivo[1].

Name: Fosmidomycin sodium salt FR-31564, CAS: 66508-37-0, stock 31.4g, assay 98.4%, MWt: 205.08, Formula: C4H9NNaO5P, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Fosmidomycin sodium salt is a phosphonic acid antibiotic and a antimalarial drug, which is active against both Gram-negative and Gram-positive bacteria.
In Vitro: Fosmidomycin sodium salt is a phosphonic acid antibiotic[1][2], which is active against both Gram-negative and Gram-positive bacteria[3].
In Vivo: Animals treated intraperitoneally with dosages of >10 mg/kg of fosmidomycin are apparently free of parasites. After treatment with 5 mg/kg of fosmidomycin, parasitemias are <1%. Animals treated orally with 50 or 100 mg/kg of fosmidomycin are apparently free of parasites, and parasitemias are <1% after treatment with 20 mg/kg of drug. Recrudescence is observed when the treatment is terminated after 4 days. Mice treated with 30 mg/kg of fosmidomycin over a period of 8 days are totally cured[3].

Name: SX-682, CAS: 1648843-04-2, stock 17.3g, assay 98.5%, MWt: 467.20, Formula: C19H14BF4N3O4S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: SX-682 is an orally bioavailable, potent allosteric inhibitor of CXCR1 and CXCR2. SX-682 can block tumor myeloid-derived suppressor cells (MDSCs) recruitment and enhance T cell activation and antitumor immunity[1].

Name: VU0661013, CAS: 2131184-57-9, stock 11.6g, assay 98.6%, MWt: 712.66, Formula: C39H39Cl2N5O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 125 mg/mL (175.40 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: VU661013 is a potent and selective MCL-1 inhibitor.
IC50 & Target: MCL-1[1]
In Vitro: VU661013 exhibits a Ki of 97±30 pM to human MCL-1 in a TR-FRET assay by displacing a fluorescently labeled peptide derived from the pro-apoptotic protein BAK. However, VU661013 does not significantly inhibit BCL-xL (Ki>40 μM) or BCL-2 (Ki=0.73 μM)[1].
In Vivo: VU661013, a novel, potent, selective MCL-1 inhibitor that de-stabilizes BIM/MCL-1 association, leads to apoptosis in AML, and is active in Venetoclax-resistant cells and patient derived xenografts. After establishing disseminated leukemia, NSGS mice are dosed intraperitoneally with 10, 25 or 75 mg/kg of VU661013 daily for 21 days. Weekly chimerism analyses are conducted and the percentage of MV-4-11 cells are quantified in murine peripheral blood using anti-human CD45 (hCD45) and anti-hCD33 monoclonal antibodies. Twenty-eight days post-transplant, vehicle-treated mice have developed large leukemia burdens and thus, mice are sacrificed, and their organs are harvested for analysis. Vehicle mice treated died of xenografted AML, but have no evidence of VU661013-related toxicity in non target organs. VU661013 treatment of disseminated human AML results in a dose-dependent decrease in tumor burden, nearly eliminating the hCD45+ MV-4-11 cells at the 75 mg/kg dose in the blood (mean, 13.0±2.2% in vehicle vs 7.4±7.2% in 25mg/kg vs 0.17±0.12% in 75 mg/kg treated mice), bone marrow (mean, 40.7±13.9% in vehicle vs 33.46±4.0 % in 25 mg/kg vs 0.384±0.345 in 75 mg/kg treated mice), and spleen (mean, 46.22±13.3% in vehicle vs 13.31±10.0% in 25 mg/kg vs 1.588±1.51% in 75 mg/kg treated mice). Treatment with VU661013 reduces disease-associated splenomegaly (mean, vehicle vs. 75mg/kg, 0.17±0.02 vs 0.09±0.01g), and amendeding spleen to body weight ratio (vehicle vs 75mg/kg, 0.99 vs 0.50). In a second MV-4-11 xenograft study, mice are followed until death, and survival is evaluated by Kaplan-Meier analysis. In this study, NSGS mice are treated daily (starting 7 days after transplant) with vehicle only, 15 mg/kg or 75 mg/kg of VU661013. Analysis reveals an increase in survival in mice treated with the 75mg/kg dose (vehicle treated mice=31 days, vs 15 mg/kg=32 days, vs 75 mg/kg treated mice=43 Days)[1].

Name: Asp-AMS, CAS: 828288-98-8, stock 17.5g, assay 98.6%, MWt: 461.41, Formula: C14H19N7O9S, Solubility: DMSO : ≥ 100 mg/mL (216.73 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: Mitochondrial Metabolism;Aminoacyl-tRNA Synthetase, Biological_Activity: Asp-AMS, an analogue of aspartyl-adenylate, is an aspartyl-tRNA synthetase inhibitor and also a strong competitive inhibitor of the mitochondrial enzyme.
IC50 & Target: Aspartyl-tRNA synthetase, Mitochondrial enzyme [1].
In Vitro: Asp-AMS is a 500-fold stronger competitive inhibitor of the mitochondrial enzyme than aspartol-AMP (10 nM) and a 35-fold lower competitor of human and bovine cyt-AspRSs (300 nM). Asp-AMS is a strong inhibitor with Ki in the nanomolar (nM) range. Asp-AMS has also the highest inhibitory effect for the mitochondrial enzyme. Asp-AMS is the most active inhibitor with Ki values in the nanomolar range, with a stronger effect on bacterial AspRSs (E. coli and P. aeruginosa) than on human cytosolic AspRS[1].

Name: Gln-AMS, CAS: 209543-57-7, stock 25.3g, assay 98.5%, MWt: 474.45, Formula: C15H22N8O8S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aminoacyl-tRNA Synthetase, Biological_Activity: Gln-AMS is an aminoacyl-tRNA synthetases (AARS) inhibitor, which binds the A-domain within the NRPS enzymes.

Name: Arg-AMS, CAS: 301351-95-1, stock 13.6g, assay 99%, MWt: 502.51, Formula: C16H26N10O7S, Solubility: DMSO : ≥ 100 mg/mL (199.00 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aminoacyl-tRNA Synthetase, Biological_Activity: Arg-AMS is a potent nanomolar inhibitor of arginyl tRNA synthetase, which displays tightly bound inhibitory characteristics for the A-domains in non-ribosomal peptide synthetases (NRPS) enzymes.

Name: LY2828360, CAS: 1231220-79-3, stock 27.9g, assay 98.4%, MWt: 426.94, Formula: C22H27ClN6O, Solubility: DMSO : 20.83 mg/mL (48.79 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cannabinoid Receptor;Cannabinoid Receptor, Biological_Activity: LY2828360 is a slowly acting but efficacious G protein-biased cannabinoid (CB2) agonist, inhibiting cAMP accumulation and activating ERK1/2 signaling.
IC50 & Target: CB2[1].
In Vivo: In WT mice, acute systemic administration of LY2828360 suppresses paclitaxel-induced mechanical and cold allodynia in a dose-dependent manner. LY2828360 produces time-dependent suppressions of paclitaxel-evoked mechanical and cold hypersensitivities and suppression of allodynia is maintained for at least 4.5 h post-injection relative to drug pre-injection levels. At 24 h post-injection, paclitaxel-induced mechanical allodynia has returned to drug pre-injection levels of hypersensitivity. Residual suppression of cold allodynia was absent by 72 h post LY2828360 treatment. Previously chronic administration of LY2828360 blocks the development of tolerance to the antiallodynic effects of morphine in WT but not in CB2KO mice. Chronic LY2828360 treatment suppresses paclitaxel-induced mechanical and cold allodynia in WT mice but not in CB2KO mice previously render tolerant to morphine[1].

Name: Glycodeoxycholic acid monohydrate, CAS: 1079043-81-4, stock 24.7g, assay 98.6%, MWt: 467.64, Formula: C26H45NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Glycodeoxycholic acid monohydrate is a nuclear receptor ligand.

Name: Mito-TEMPO, CAS: 1334850-99-5, stock 36.3g, assay 98.1%, MWt: 510.03, Formula: C29H35ClN2O2P, Solubility: DMSO : 125 mg/mL (245.08 mM; Need ultrasonic); H2O : 60 mg/mL (117.64 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Mitochondrial Metabolism, Biological_Activity: Mito-TEMPO is a mitochondria-targeted superoxide dismutase mimetic with superoxide and alkyl radical scavenging properties.
In Vivo: Mito-TEMPO (MT) greatly attenuates the increase in ALT activities and reduces the areas of necrosis at both time points, indicating that the protection by Mito-TEMPO is sustained until at least 24 h post-APAP. Mito-Tempo could induce secondary apoptosis in the late phase of APAP hepatotoxicity. Mito-Tempo induces secondary apoptosis after APAP overdose by inhibition of RIP3[1].

Name: UT-155, CAS: 2031161-35-8, stock 7.9g, assay 98.2%, MWt: 405.35, Formula: C20H15F4N3O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 130 mg/mL (320.71 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: UT-155 is a selective and potent androgen receptor (AR) antagonist, with a Ki of 267 nM for UT-155 binding to AR-LBD.
IC50 & Target: Ki: 267 nM (AR-LBD)[1].
In Vitro: UT-155 binds to the AR-LBD at Ki of 267 nM. UT-155 potently inhibits the R1881-induced wildtype AR transactivation with 6-10-fold higher potency than enzalutamide. While UT-155 antagonizes both wildtype and mutant ARs comparably, enzalutamide is weaker by two fold with the W742L mutant AR relative to the wild type AR. Treatment of LNCaP cells with UT-155 inhibits 0.1 nM R1881-induced PSA and FKBP5 gene expression between 10 and 100 nM with 5-10-fold better potency than enzalutamide[1].
In Vivo: Consistent with the anti-proliferative effects in vitro, UT-155 significantly inhibits the growth of 22RV1 xenograft by 53%, while, as expected, enzalutamide has no effect on the growth of the 22RV1 tumors. Tumor weights and PSA and the expression of AR and AR-SV are significantly lower in UT-155-treated animals[1].

Name: Dansylamide, CAS: 1431-39-6, stock 21.3g, assay 98.6%, MWt: 250.32, Formula: C12H14N2O2S, Solubility: DMSO : 150 mg/mL (599.23 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dansyl amide is a fluorescent dye that is used in biochemistry and chemistry to label substances with the fluorescent dansyl group.

Name: AST2818 (mesylate), CAS: 2130958-55-1, stock 9g, assay 98.4%, MWt: 664.70, Formula: C29H35F3N8O5S, Solubility: DMSO : 5 mg/mL (7.52 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: AST2818 mesylate is an EGFR inhibitor.
IC50 & Target: EGFR[1]
In Vitro: AST2818 mesylate is designed to inhibit EGFR active mutations as well as the T790M acquired resistant mutation[1].

Name: 5'-GTP trisodium salt hydrate Guanosine 5'-triphosphate trisodium salt hydrate, CAS: 207300-85-4, stock 15g, assay 98.7%, MWt: 1000, Formula: C10H13N5Na3O14P3.xH2O, Solubility: H2O : ≥ 150 mg/mL, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5'-GTP trisodium salt hydrate is an activator of the signal transducing G proteins and also serves as an energy-rich precursor of mononucleotide units in the enzymatic biosynthesis of DNA and RNA.

Name: GDC-0927 Racemate SRN-927 Racemate, CAS: 1443983-36-5, stock 1.3g, assay 98.5%, MWt: 461.52, Formula: C28H28FNO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: GDC-0927 Racemate (SRN-927 Racemate) is a degrader of estrogen receptor, potently inhibits ER-α activity, with an IC50 of 0.2 nM, and is used in the research of ER-related diseases.
IC50 & Target: IC50: 0.2 nM (ER-α)[1]
In Vitro: GDC-0927 Racemate (Example 1) is a degrader of estrogen receptor, potently inhibits ER-α activity, with an IC50 of 0.2 nM, and is used in the research of ER-related diseases. GDC-0927 Racemate reduces the viability of MCF7 cells with an IC50 of 0.21 nM[1].

Name: IITZ-01, CAS: 1807988-47-1, stock 34.7g, assay 98.6%, MWt: 482.51, Formula: C26H23FN8O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (310.87 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;Autophagy, Target: PI3K;Apoptosis;Autophagy, Biological_Activity: IITZ-01 is a potent lysosomotropic autophagy inhibitor with single-agent antitumor activity, with an IC50 of 2.62 μM for PI3Kγ.
IC50 & Target: IC50: 2.62 μM (PI3Kγ), Autophagy[1].
In Vitro: IITZ-01 (0-2 μM, 24 h) enhances autophagosomes formation as indicated by increased expression of LC3-II levels time- and dose-dependently in triple-negative breast cancer (TNBC) cell lines (MDA-MB-231 and MDA-MB-453). IITZ-01 also demonstrates potent autophagy inhibitory activity in other breast, lung, and colon cancer cells[1].
In Vivo: IITZ-01 (45 mg/kg, i.p. every alternate day for 4 weeks) inhibits average breast tumor growth when compared with control from third day of treatment in triple-negative breast tumor models in mice[1].

Name: Boldenone Cypionate, CAS: 106505-90-2, stock 33.1g, assay 98.7%, MWt: 410.59, Formula: C27H38O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: Boldenone Cypionate is an androgenic anabolic steroid.

Name: DC1SMe, CAS: 501666-85-9, stock 2.6g, assay 98.4%, MWt: 684.23, Formula: C35H30ClN5O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Cytotoxin, Biological_Activity: DC1Sme, a DC1 derivative, exhibits IC50 values of 22 pM, 10 pM, 32 pM and 250 pM for Ramos, Namalwa, HL60/s and COLO 205 cancer cells, respectively. DC1, an analogue of the minor groove-binding DNA alkylator CC-1065, is a ADC Cytotoxin. DC1 can be used in synthesis of antibody-drug conjugates for the targeted treatment of cancer.

Name: N-(p-amylcinnamoyl) Anthranilic Acid ACA, CAS: 110683-10-8, stock 19.2g, assay 98.3%, MWt: 337.41, Formula: C21H23NO3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 125 mg/mL (370.47 mM), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel;Metabolic Enzyme/Protease;Neuronal Signaling, Target: TRP Channel;Phospholipase;TRP Channel, Biological_Activity: N-(p-amylcinnamoyl) Anthranilic Acid (ACA) is a broad spectrum Phospholipase A2 (PLA2) inhibitor and TRP channel blocker[1][2]. N-(p-amylcinnamoyl) Anthranilic Acid (ACA) is also an effective reversible inhibitor of calcium-activated chloride channels, has potential to treat arrhythmia[3].
IC50 & Target: PLA2[1][2]. 
TRP channel[1][2].
Calcium-activated chloride channels[3].
In Vitro: N-(p-amylcinnamoyl) Anthranilic Acid (ACA; 20 μM) completely blocks ADPR-induced whole-cell currents and H2O2-induced Ca2+ signals (IC50=1.7 μM) in HEK293cells transfected with human TRPM2[1]. 
N-(p-amylcinnamoyl) Anthranilic Acid (ACA; 20 μM) also blocks currents through human TRPM8 and TRPC6 expressed in HEK293 cells[1]. 
N-(p-amylcinnamoyl) Anthranilic Acid (ACA) modulates the activity of different TRP channels independent of PLA22 inhibition[1].

Name: BMS-1166 (hydrochloride), CAS: 2113650-05-6, stock 29.1g, assay 98.8%, MWt: 677.57, Formula: C36H34Cl2N2O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: PD-1/PD-L1, Biological_Activity: BMS-1166 hydrochloride is a potent PD-1/PD-L1 interaction inhibitor with an IC50 of 1.4 nM. BMS-1166 antagonizes the inhibitory effect of PD-1/PD-L1 immune checkpoint on T cell activation.
IC50 & Target: IC50: 1.4 nM (PD-1/PD-L1 interaction)[1].
In Vitro: BMS-1166 is a potent PD-1/PD-L1 interaction inhibitor with an IC50 of 1.4 nM in a homogenous time-resolved fluorescence binding assay[1]. BMS-1166 antagonizes the inhibitory effect of PD-1/PD-L1 immune checkpoint on T cell activation. BMS-1166 dose dependently abolishes the inhibition of ECs stimulation by sPD-L1[2].

Name: Thioisonicotinamide 4-Pyridylthioamide, CAS: 2196-13-6, stock 33g, assay 98.3%, MWt: 138.19, Formula: C6H6N2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Thioisonicotinamide (4-Pyridylthioamide) is a synthetic intermediate used for pharmaceutical synthesis.

Name: DO34, CAS: 1848233-58-8, stock 6.6g, assay 98.9%, MWt: 531.53, Formula: C26H28F3N5O4, Solubility: DMSO : ≥ 100 mg/mL (188.14 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DO34 is a highly potent, selective and centrally active diacylglycerol lipase (DAGL) inhibitor, with an IC50 of 6 nM for DAGLα conversion of SAG to 2-AG, and an IC50 for DAGLβ.
IC50 & Target: IC50: 6 nM (DAGLα), 3-8 nM (DAGLβ)[1].
In Vitro: DO34 is a highly potent, selective and centrally active DAGL inhibitor, with an IC50 of 6 nM for DAGLα conversion of SAG to 2-AG, as determined using a real-time, fluorescence-based natural substrate assay with membrane lysates from HEK293T cells expressing recombinant human DAGLα. It is also confirmed that and DO34 is a potent inhibitor of DAGLβ with IC50 of 3-8 nM[1].
In Vivo: DO34 (compound 39) prevents fasting-induced refeeding of mice, which is typical cannabinoid CB1-receptor mediated behavior. DO34 (comound 39) reduces brain 2-AG levels in dose- and time dependent manner[2]. DO34 could block the tonic CB1 activation. AM251 significantly increases basal PF-EPSCs in MAGL-TKO mice, and the effect of AM251 is blocked by the DAGL inhibitor DO34[3].

Name: C-176, CAS: 314054-00-7, stock 4.9g, assay 99%, MWt: 358.09, Formula: C11H7IN2O4, Solubility: DMSO : 150 mg/mL (418.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: STING, Biological_Activity: C-176 is a strong and covalent mouse STING inhibitor.
IC50 & Target: STING[1].
In Vitro: C-176 strongly reduces STING-mediated, but not RIG-I- or TBK1-mediated, IFNβ reporter activity. Pretreatment with C-176 markedly reduce the CMA-mediated induction of serum levels of type I IFNs and IL-6[1].
In Vivo: Notably, treatment of Trex1−/− mice with C-176 results in a significant reduction in serum levels of type I IFNs and in a strong suppression of inflammatory parameters in the heart. Wild-type mice on a two-week treatment with C-176 show no evident signs of overt toxicity. The three-month trial conducted with C-176 in Trex1−/− mice demonstrates marked amelioration of various signs of systemic inflammation[1].

Name: ODM-203, CAS: 1430723-35-5, stock 0.4g, assay 98.4%, MWt: 505.54, Formula: C26H21F2N5O2S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;FGFR, Biological_Activity: ODM-203 is a potent FGFR and VEGFR families inhibitor with IC50s of 11, 16, 6, 35 nM towards recombinant FGFR1, FGFR2, FGFR3 and FGFR4 as well as 26, 9, 5 nM towards VEGFR1, VEGFR2 and VEGFR3, respectively. ODM-203 exhibits strong anti-tumor activity and induces anti-tumor immunity[1].
IC50 & Target: IC50: 11 nM (FGFR1), 16 nM (FGFR2), 6 nM (FGFR3), 35 nM (FGFR4), 26 nM (VEGFR1), 9 nM (VEGFR2), 5 nM (VEGFR3)[1]

Name: Grp94 Inhibitor-1, CAS: 2234897-35-7, stock 20.6g, assay 98.1%, MWt: 352.47, Formula: C22H28N2O2, Solubility: DMSO : 250 mg/mL (709.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: Grp94 Inhibitor-1 is a potent, selective Grp94 inhibitor with an IC50 value of 2 nM, and over 1000-fold selectivity to Grp94 against Hsp90α[1].
IC50 & Target: IC50: 2 nM (Grp94)[1]

Name: Cav 2.2 blocker 1, CAS: 1567335-29-8, stock 18.7g, assay 98.4%, MWt: 424.96, Formula: C25H29ClN2O2, Solubility: DMSO : 20.83 mg/mL (49.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Cav 2.2 blocker 1 (compound 9) is a N-type calcium channel (Cav 2.2) blocker for the treatment of pain, with an IC50 of 1 nM[1].
IC50 & Target: IC50: 1 nM (Cav 2.2)[1].

Name: BRM/BRG1 ATP Inhibitor-1, CAS: 2270879-17-7, stock 24.3g, assay 99%, MWt: 318.27, Formula: C11H9F3N4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BRM/BRG1 ATP Inhibitor-1 is an allosteric dual brahma homolog (BRM)/SWI/SNF related matrix associated actin dependent regulator of chromatin subfamily A member 2 (SMARCA2) and brahma related gene 1 (BRG1)/SMARCA4 ATPase activity inhibitor, both IC50s are below 0.005 µM[1].
IC50 & Target: IC50: ﹤0.005 µM (BRM, BRG1)[1]

Name: mTOR inhibitor-1, CAS: 468747-17-3, stock 22g, assay 98.9%, MWt: 363.21, Formula: C16H15BrN2O3, Solubility: DMSO : 83.33 mg/mL (229.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Autophagy, Target: mTOR;Autophagy, Biological_Activity: mTOR inhibitor-1 is a novel mTOR pathway inhibitor which can suppress cells proliferation and inducing autophagy.
IC50 & Target: mTOR[1]

Name: Isotanshinone I, CAS: 20958-17-2, stock 37.1g, assay 98.9%, MWt: 276.29, Formula: C18H12O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucosidase, Biological_Activity: Isotanshinone I has inhibitory activity against α-glucosidase and formation of AGE, with IC50s of 1.13, 0.432 μM for α-glucosidase and AGE, respectively.
IC50 & Target: IC50: 1.13μM (α-glucosidase), 0.432 μM (AGE)[1].

Name: Isotanshinone IIA, CAS: 20958-15-0, stock 15.7g, assay 98.5%, MWt: 294.34, Formula: C19H18O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Isotanshinone IIA, an abietane-type diterpene metabolite, could non-competitively inhibit Protein Tyrosine Phosphatase 1B (PTP1B) activity with an IC50 0f 11.4 μM.
IC50 & Target: IC50: 11.4 μM (PTP1B)[1].

Name: Halopemide, CAS: 59831-65-1, stock 6.3g, assay 98.4%, MWt: 416.88, Formula: C21H22ClFN4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling;Metabolic Enzyme/Protease, Target: Dopamine Receptor;Dopamine Receptor;Phospholipase, Biological_Activity: Halopemide is a potent phospholipase D (PLD) inhibitor, with IC50s of 220 and 310 nM for human PLD1 and PLD2, respectively. Halopemid is a dopamine receptors antagonist, and acts a psychotropic agent[1][2].
In Vitro: Halopemide (1-2 μM; 21 day) affects calcification in transdifferentiated MOVAS cells[3].
In Vivo: Halopemide (10 mg/kg; p.o.) induces dyskinesias in the majority of monkeys tested[2].

Name: Papain, CAS: 9001-73-4, stock 28.8g, assay 98.7%, MWt: 1000, Formula: N/A, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : 50 mg/mL (Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Cathepsin, Biological_Activity: Papain is a cysteine protease of the peptidase C1 family, which is used in food, pharmaceutical, textile, and cosmetic industries.
In Vitro: Papain is a cysteine protease of the peptidase C1 family, which is used in food, pharmaceutical, textile, and cosmetic industries.

Name: Pevonedistat hydrochloride MLN4924 (hydrochloride), CAS: 1160295-21-5, stock 15.7g, assay 98.4%, MWt: 479.98, Formula: C21H26ClN5O4S, Solubility: DMSO : 100 mg/mL (208.34 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: NEDD8-activating Enzyme, Biological_Activity: Pevonedistat hydrochloride (MLN4924 hydrochloride) is a potent and selective NEDD8-activating enzyme (NAE) inhibitor, with an IC50 of 4.7 nM.
IC50 & Target: IC50: 4.7 nM (NAE)
In Vitro: Pevonedistat (MLN4924) is a potent inhibitor of NAE (half-maximal inhibitory concentration (IC50=0.004 μM), and is selective relative to the closely related enzymes UAE, SAE, UBA6 and ATG7 (IC50=1.5, 8.2, 1.8 and >10 μM, respectively). Pevonedistat (MLN4924) treatment inhibits overall protein turnover in cultured HCT-116 cells. Treatment of HCT-116 cells with Pevonedistat (MLN4924) for 24 h results in a dose-dependent decrease of Ubc12-NEDD8 thioester and NEDD8-cullin conjugates, with an IC50 < 0.1 μM, resulting in a reciprocal increase in the abundance of the known CRL substrates CDT1, p27 and NRF2 (also known as NFE2L2), but not non-CRL substrates[1]. Pevonedistat induces CLL cell apoptosis and circumvented stroma-mediated resistance. Pevonedistat promotes induction of Bim and Noxa in the CLL cells leading to rebalancing of Bcl-2 family members toward the proapoptotic BH3-only proteins[2]. Pevonedistat (MLN4924) rapidly inhibits cullin 1 neddylation and remarkably suppressed growth and survival as well as migration in a dose-and time-dependent manner in gastric cancer cells, and significantly suppresses migration by transcriptionally activating E-cadherin and repressing MMP-9[3].
In Vivo: Pevonedistat (MLN492410, 30 or 60 mg/kg, s.c.) leads to a dose- and time-dependent increase in the steady state levels of NRF2 and CDT1 in HCT-116 tumour-bearing mice, and decreases NEDD8-cullin levels in normal mouse tissue as illustrated in mouse bone marrow cells. Pevonedistat (MLN4924) administered on a BID schedule at 30 and 60 mg/kg inhibits tumour growth with T/C values of 0.36 and 0.15, respectively[1].

Name: Foliglurax (monohydrochloride) PXT002331 (monohydrochloride), CAS: 2133294-96-7, stock 18g, assay 98.6%, MWt: 457.97, Formula: C23H24ClN3O3S, Solubility: DMSO : 5 mg/mL (10.92 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: Foliglurax monohydrochloride (PXT002331 monohydrochloride) is a highly selective and potent, brain-penetrant metabotropic glutamate receptor 4 positive allosteric modulator (mGluR4 PAM) , with an EC50 of 79 nM[1]. Antiparkinsonian effect[1].
In Vitro: Foliglurax, a highly selective and potent mGlu4 receptor PAM with a marked brain-penetrance feature, might revolutionize the field of mGlu4 receptor drug targeting in CNS disorders[2].

Name: I-191, CAS: 1690172-25-8, stock 15.3g, assay 98.3%, MWt: 423.48, Formula: C23H26FN5O2, Solubility: DMSO : 8.33 mg/mL (19.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: I-191 is a potent, selective protease-activated receptor 2 (PAR2) antagonist[1].
IC50 & Target: Protease-activated receptor 2[1]
In Vitro: I-191 inhibits cytokine production as well as cytokine-related caspase cleavages via ERK1/2 signaling in HT29 colon cancer cells[1].

Name: 9-Ethyladenine, CAS: 2715-68-6, stock 16.5g, assay 98.8%, MWt: 163.18, Formula: C7H9N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 9-Ethyladenine is a partially effective inhibitor of APRT (adenine phosphoribosyltransferase)[1].
IC50 & Target: APRT[1]

Name: Chloramben 3-Amino-2,5-dichlorobenzoic acid, CAS: 133-90-4, stock 28.8g, assay 99%, MWt: 206.03, Formula: C7H5Cl2NO2, Solubility: DMSO : 250 mg/mL (1213.42 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chloramben (3-Amino-2,5-dichlorobenzoic acid) is a pre-emergence herbicide used to control the seedlings of annual grasses and broadleaf weeds[1].

Name: Bis-PEG4-acid, CAS: 31127-85-2, stock 19.3g, assay 98.6%, MWt: 294.30, Formula: C12H22O8, Solubility: DMSO : 300 mg/mL (1019.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: Bis-PEG4-acid is a PEG PROTAC linker.
IC50 & Target: PROTAC linker[1]

Name: 2-Iminobiotin Guanidinobiotin, CAS: 13395-35-2, stock 7.5g, assay 98.6%, MWt: 243.33, Formula: C10H17N3O2S, Solubility: DMSO : 12.5 mg/mL (51.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: 2-Iminobiotin (Guanidinobiotin) is a biotin (vitamin H or B7) analog. 2-Iminobiotin is a reversible nitric oxide synthases inhibitor with Kis of 21.8 and 37.5μM for murine iNOS and rat n-cNOS, respectively[1]. 2-Iminobiotin superimposes on hypothermia protects human neuronal cells from hypoxia-induced cell damage[2].
IC50 & Target: Nitric oxide synthases[1]

Name: PF-06424439 (methanesulfonate), CAS: 1469284-79-4, stock 32.2g, assay 98.9%, MWt: 536.05, Formula: C23H30ClN7O4S, Solubility: DMSO : 250 mg/mL (466.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: PF-06424439 methanesulfonate is an oral, potent and selective imidazopyridine diacylglycerol acyltransferase 2 (DGAT2) inhibitor with an IC50 of 14 nM[1]. PF-06424439 methanesulfonate is slowly reversible, time-dependent inhibitor, which inhibits DGAT2 in a noncompetitive mode with respect to the acyl-CoA substrate[2].
IC50 & Target: IC50: 14 nM (DGAT2)[1]
In Vivo: PF-06424439 methanesulfonate (p.o.; 60 mg/kg/day; for 3 days) reduces plasma TG and cholesterol levels and decreases nonsignificant in circulating lipids in mice (Ldlr-/-)[1]. 
PF-06424439 methanesulfonate (i.v.; 1 mg/kg) shows moderate clearance in rats following intravenous administration and moderate steady-state volume of distribution (Vdss) results in a short half-life[1].

Name: Asoprisnil J867, CAS: 199396-76-4, stock 0.9g, assay 98.9%, MWt: 449.58, Formula: C28H35NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Progesterone Receptor, Biological_Activity: Asoprisnil (J867), a selective progesterone receptor modulator, exhibits mixed progesterone agonist and antagonist effects on various progesterone targeted tissues in animal and human[1].

Name: Benzobicyclon, CAS: 156963-66-5, stock 23.6g, assay 98.9%, MWt: 446.97, Formula: C22H19ClO4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Benzobicyclon is a pro-herbicide, which acts as an inhibitor of 4-hydroxyphenylpyruvate dioxygenase (4-HPPD) in plant, and leads to bleaching and death[1].
IC50 & Target: 4-HPPD[1]

Name: Neridronate, CAS: 79778-41-9, stock 4.5g, assay 98.2%, MWt: 277.15, Formula: C6H17NO7P2, Solubility: H2O : 18.75 mg/mL (67.65 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Neridronate is an aminobisphosphonate, licensed in Italy for the treatment of osteogenesis imperfecta (OI) and Paget’s disease of bone (PDB). Neridronate is effective also in other skeletal diseases such as osteoporosis, algodystrophy, hypercalcemia of malignancy, and bone metastases[1][2].

Name: Exicorilant CORT 125281, CAS: 1781244-77-6, stock 24.2g, assay 98.8%, MWt: 589.56, Formula: C26H23F4N7O3S, Solubility: DMSO : 250 mg/mL (424.05 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: Exicorilant (CORT 125281) is a selective and oral active glucocorticoid receptor (GR) antagonist, with a Ki value of 7 nM[1]. Exicorilant (CORT 125281) has potential to overcome adiposity, glucose intolerance and dyslipidaemia[2].
IC50 & Target: Ki: 7 nM (GR)[1].
In Vitro: Exicorilant (CORT 125281) reverses corticosterone-mediated GR activity in murine brown adipocytes in vitro[1].
In Vivo: Exicorilant (CORT 125281) reduces body weight, fat mass and plasma lipids in HFD-fed mice[2]. 
Exicorilant (CORT 125281) (6, 20 or 60 mg/kg/d, for 3 weeks in mice) at different dosages reduce body weight, fat mass, plasma TG, cholesterol and FFA in a dose-dependent manner, with no effect on lean mass[2].

Name: Mavacoxib, CAS: 170569-88-7, stock 29.7g, assay 99%, MWt: 385.34, Formula: C16H11F4N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Mavacoxib is a selective, oral long-acting cyclooxygenase-2 (COX-2) inhibitor and a long-acting non-steroidal anti-inflammatory drug (NSAID). Mavacoxib is used to treat pain and inflammation associated with degenerative joint disease in dogs[1].
In Vitro: Mavacoxib (0-200 μM; 72 hours; CSKOS, U2OS, REM, K9TCC and T24 cells) treatment reduces cell viability in a dose-dependent manner. However, sensitivity to Mavacoxib varied between the cell lines, with IC50 values ranging from 34.5 μM to 157.7 μM. The IC50 values of U2OS, KTOSA5, CSKOS, REM, LILY, K9TCC, K9TCC-AXA, K9TCC-In, K9TCC-Sh, T24, 5637 and HT-1376 cells are 52.6 μM, 89.8 μM, 106.3 μM, 66.6 μM, 97.5 μM, 54.9 μM, 34.5 μM, 78.7 μM, 50.7 μM, 63.4 μM, 72.5 μM and 157.7 μM, respectively[1]. 
Mavacoxib (0-200 μM; 48 hours; KTOSA5, REM, LILY, K9TCC, U2OS, and T24 cells) treatment can induce caspase-dependent apoptosis in a number of cell lines[1]. 
Mavacoxib (0-75 μM; 24 hours; CSKOS, U2OS, REM, K9TCC and T24 cells) treatment down-regulates the expression of p-Akt in CSKOS cells in in a dose-dependent manner, as is total Akt in U2OS cells. In REM cells, both p-ERK and p-Akt are increased in expression with increasing doses of Mavacoxib, and in K9TCC cells p-ERK expression is also increased with Mavacoxib treatment[1].
In Vivo: Osteoarthritic dogs enrolled in the studies are randomized to receive treatment with Mavacoxib and daily placebo for carprofen or placebo for Mavacoxib and daily carprofen at a nominal dose of 4 mg/kg BW. Mavacoxib is administered in both studies with a 2-week interval between the first and second doses but with monthly dosing thereafter. The nominal Mavacoxib doses in Studies 1 and 2 are 4 and 2 mg/kg BW, respectively. Seven Mavacoxib doses are administered in Study 1, but only five doses in Study 2. In Study 1, Mavacoxib is administered without regard to the timing of meals, but in Study 2, all of the Mavacoxib doses are administered with food[2].

Name: Fluopyram, CAS: 658066-35-4, stock 37.4g, assay 98.7%, MWt: 396.71, Formula: C16H11ClF6N2O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (315.09 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Fluopyram is a succinate dehydrogenase inhibitor fungicide, inhibits the growth of F. virguliforme isolates with mean EC50 of 3.35 µg/mL[1].
IC50 & Target: Succinate dehydrogenase, Fungal[1]

Name: PF-06250112, CAS: 1609465-89-5, stock 10.8g, assay 98.5%, MWt: 438.43, Formula: C22H20F2N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: PF-06250112 is a potent, highly selective, orally bioavailable BTK inhibitor with an IC50 of 0.5 nM, shows inhibitory effect toward BMX nonreceptor tyrosine kinase and TEC with IC50s of 0.9 nM and 1.2 nM, respectively[1].
IC50 & Target: IC50: 0.5 nM (BTK), 0.9 nM (BMX), 1.2 nM (TEC)[1]

Name: Levetimide, CAS: 21888-99-3, stock 35.8g, assay 98.4%, MWt: 362.46, Formula: C23H26N2O2, Solubility: DMSO : ≥ 100 mg/mL (275.89 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Levetimide is a potent and stereoselective inhibitor of [3H](+)pentazocine binding, with a Ki of 2.2 nM[1].
In Vitro: Levetimide potently inhibits [3H]DTG binding although without stereoselectivity (Ki value of 103 nM) [1].

Name: Danicopan ACH-4471, CAS: 1903768-17-1, stock 12.5g, assay 99%, MWt: 580.41, Formula: C26H23BrFN7O3, Solubility: DMSO : 260 mg/mL (447.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Complement System, Biological_Activity: Danicopan (ACH-4471), a selective and orally active small-molecule factor D inhibitor, shows high binding affinity to human Factor D with Kd value of 0.54 nM. Danicopan (ACH-4471) inhibits alternative pathway of complement (APC) activity, has potential to block the alternative pathway of complement in paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS)[1].
IC50 & Target: Factor D[1]
In Vitro: Danicopan (ACH-4471) inhibits the proteolytic activity of purified Factor D against its natural substrate Factor B in complex with C3b, blocking production of Bb fragment in a dose-dependent manner with an IC50 value of 0.015 μM[1].
Danicopan (ACH-4471)potently inhibits hemolysis with IC50 values ranging from 0.0040 μM to 0.027 μM (IC90 values from 0.015 μM to 0.11 μM) [1].

Name: BC-1215, CAS: 1507370-20-8, stock 34.4g, assay 99%, MWt: 394.51, Formula: C26H26N4, Solubility: DMSO : 12.5 mg/mL (31.68 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for E3 Ligase, Biological_Activity: BC-1215 is an inhibitor of F-box protein 3 (FBXO3, a ubiquitin E3 ligase component, IC50=0.9 μg/mL for IL-1β release). BC-1215 decreases Fbxo3-Fbxl2 interaction and prevents SCFFbxo3 catalyzed Fbxl2 ubiquitination. BC-1215 inhibits the Fbxo3-TRAF activation pathway by destabilizing TRAF1–TRAF6. BC-1215, interacts with ApaG to profoundly inhibit secretion of a broad spectrum of TH1 panel cytokines from human PBMC[1].

Name: AZD9567, CAS: 1893415-00-3, stock 14.3g, assay 98.1%, MWt: 494.53, Formula: C27H28F2N4O3, Solubility: H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: AZD9567 (compound 15) is a potent, oral active, non-steroidal and selective glucocorticoid receptor modulator (SGRM), with an IC50 of 3.8 nM. Exhibits excellent efficacy in the streptococcal cell wall (SCW) reactivation model of joint inflammation[1].
IC50 & Target: IC50: 3.8 nM (Glucocorticoid receptor)[1].
In Vivo: AZD9567 (15 mg/kg/day, Oral gavage daily for 8 days) treatment shows excellent in vivo efficacy in a rat model of joint inflammation[1].

Name: GNE-207, CAS: 2158266-58-9, stock 6.5g, assay 98.9%, MWt: 510.59, Formula: C29H30N6O3, Solubility: DMSO : 200 mg/mL (391.70 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Epigenetic Reader Domain;Histone Acetyltransferase, Biological_Activity: GNE-207 is a potent, selective and orally bioavailable inhibitor of the bromodomain of CBP, with an IC50 of 1 nM, exhibits a selectively index of >2500-fold against BRD4 (1). GNE-207 shows excellent CBP potency, with an EC50 of 18 nM for MYC expression in MV-4-11 cells[1].
IC50 & Target: IC50: 1 nM (CBP)[1], 3.1 μM (BRD4 (1))[1]
In Vitro: GNE-207 is a potent, selective and orally bioavailable inhibitor of the bromodomain of CBP, with an IC50 of 1 nM, a selectively index of >2500-fold against BRD4 (1) (IC50, 3.1 μM)[1]. 
GNE-207 shows excellent CBP potency, with an EC50 of 18 nM for MYC expression in MV-4-11 cells[1].
In Vivo: GNE-207 (5 mg/kg) shows moderate clearance in PK, with acceptable oral bioavailability[1].

Name: GSK461364 GSK461364A, CAS: 929095-18-1, stock 10.2g, assay 98.4%, MWt: 543.60, Formula: C27H28F3N5O2S, Solubility: DMSO : 50 mg/mL (91.98 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: Polo-like Kinase (PLK), Biological_Activity: GSK461364 is a selective, reversible and ATP-competitive Polo-like kinase 1 (PLK1) inhibitor with a Ki value of 2.2 nM.
IC50 & Target: Ki: 2.2 nM (PLK1)[1]
In Vitro: GSK461364 is a potent, selective, and reversible ATP-competitive Plk1 inhibitor (Ki, 2.2 nM) with at least 390-fold greater selectivity for Plk1 than for Plk2 and Plk3 and 1,000-fold greater selectivity than for a panel of 48 other kinases[1]. GSK461364 (GSK461364A, 250 nM) inhibiting plk1 causes prolonged mitotic delay, aberrant mitotic exit, and p53 activation in A549 and PL45 cells. Knockdown of p53 significantly enhances the sensitivity of the cells to GSK461364A (30 or 300 nM) in preventing outgrowth in A549 and NCI-H460 cells, compared with cells with nonsilencing control siRNA[2]. GSK461364 can inhibits cell growth of most proliferating cancer cell lines, and suppresses 89% of cancer cell line (66 of 74 lines) proliferation, with a GI50 (concentration required to inhibit 50% cell growth) of ≤100 nM. GSK461364 (GSK461364A, >20 nM) blocks cells in G2-M phase with reduction of cells in G1 phase of A549 lung carcinoma line. GSK461364 (10-250 nM) blocks cells in G2 and M phases of the cell cycle and causes M-phase caspase-3/caspase-7 activation in cancer cells[3]. GSK461364 (0.5-2 μM) decreases level of PLK1 and pCDC25C, and cuases a dose- and time-dependent increase in pHisH3, an indicator of mitotic arrest in OS cell lines[4].
In Vivo: GSK461364 (50 mg/kg) exhibits various degrees of tumor growth delay (TGD) in multiple xenograft tumor models by i.p. one dose every 2 days repeated twelve times (q2d×12)[1].

Name: TM-25659, CAS: 260553-97-7, stock 5.5g, assay 98.5%, MWt: 500.60, Formula: C30H28N8, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 135 mg/mL (269.68 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TM-25659 is a transcriptional co-activator with PDZ-binding motif (TAZ) modulator. Anti-osteoporotic and anti-obesity activities[1].
IC50 & Target: TAZ[1]
In Vitro: TM-25659 (2, 10, 20, 100 μM) enhances nuclear TAZ localization in a dose-dependent manner and attenuates PPARγ-mediated adipocyte differentiation by facilitating PPARγ suppression activity of TAZ[1].
TM-25659 (2, 10, 50 μM) enhances osteogenic gene expression and thereby increases osteoblast differentiation[1].
In Vivo: TM-25659 (50 mg/kg, i.p., every other day for 2 weeks) suppresses bone loss in vivo and decreases weight gain in an obesity model[1].
TM-25659 has a favourable pharmacokinetic profile in rats. The plasma concentration of TM-25659 declines with an approximate t1/2 of 7 or 10 h following i.v or p.o. administration respectively. The systemic clearance (CL) is 0.21 L×h-1×kg-1 and the volume of distribution at steady-state (1.91 L×h-1×kg-1) is larger than the volume of total body fluids[1].

Name: GSK 366, CAS: 1953157-39-5, stock 10.9g, assay 98.8%, MWt: 361.78, Formula: C17H16ClN3O4, Solubility: DMSO : 250 mg/mL (691.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GSK 366 is a potent kynurenine-3-monooxygenase (KMO) inhibitor with IC50s of 2.3 nM and 0.7 nM for human KMO and P. fluorescens-KMO (Pf-KMO), respectively[1].
IC50 & Target: IC50: 2.3 nM (human KMO), 0.7 nM (Pf-KMO)[1]

Name: YKL-06-061, CAS: 2172617-15-9, stock 1.7g, assay 98.1%, MWt: 527.66, Formula: C30H37N7O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (118.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Salt-inducible Kinase (SIK), Biological_Activity: YKL-06-061 is a potent, selective, second-generation salt-inducible kinase (SIK) inhibitor with IC50 values of 6.56 nM/1.77 nM/20.5 nM for SIK1/2/3, respectively[1].
IC50 & Target: IC50: 6.56 nM/1.77 nM/20.5 nM (SIK1/2/3)[1].
In Vitro: YKL 06-061 yields a dose-dependent increase in MITF mRNA expression[1].

Name: PFE-360 PF-06685360, CAS: 1527475-61-1, stock 13g, assay 98.6%, MWt: 308.34, Formula: C16H16N6O, Solubility: DMSO : 10.42 mg/mL (33.79 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: LRRK2, Biological_Activity: PFE-360 (PF-06685360) is a potent, selective, brain penetrated and orally active leucine-rich repeat kinase 2 (LRRK2) inhibitor with a mean IC50 of 2.3 nM in vivo[1][2].
IC50 & Target: IC50: 2.3 nM (LRRK2 in vivo) [1][2].
In Vivo: PFE-360 (4 mg/kg and 7.5 mg/kg, orally, BID, 10-12 weeks) treatment potently decreases the LRRK2-pSer935/total LRRK2 ratio, with no significant adverse effects[1].

Name: R-10015, CAS: 2097938-51-5, stock 33.3g, assay 98.3%, MWt: 410.86, Formula: C20H19ClN6O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (152.12 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Anti-infection, Target: LIM Kinase (LIMK);Reverse Transcriptase, Biological_Activity: R-10015, a broad-spectrum antiviral compound for HIV infection, acts as a potent and selective inhibitor of LIM domain kinase (LIMK) and binds to the ATP-binding pocket, with an IC50 of 38 nM for human LIMK1[1].
IC50 & Target: IC50: 38 nM (human LIMK1)[1]
In Vitro: R-10015 (100 μM; 0-4 hours) inhibits cofilin phosphorylation directly through blocking LIM kinase in CEM-SS T cells[1]. 
R-10015 inhibits HIV-1 DNA synthesis, nuclear migration, and virion release[1]. 
R-10015 inhibits multiple viruses, including Zaire ebolavirus (EBOV), Rift Valley fever virus (RVFV), Venezuelan equine encephalitis virus (VEEV), and herpes simplex virus 1 (HSV-1) [1]. 
In Vivo: R-10015 (10 mg/kg; i.p.) displays none indication of toxicity. The result suggests the possibility of short-term use of LIMK inhibitors to block viral infections[1].

Name: MW-150 MW01-18-150SRM, CAS: 1628502-91-9, stock 9.3g, assay 99%, MWt: 381.47, Formula: C24H23N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: MW150 (MW01-18-150SRM) is a selective, CNS penetrant, and orally active inhibitor of p38α MAPK with a Ki of 101 nM. MW-150 inhibits the ability of the endogenous p38α MAPK to phosphorylate an endogenous substrate MK2 in activated glia[1].
IC50 & Target: Ki: 101nM (p38α MAPK)[1]
In Vitro: MW-150 inhibits in a concentration-dependent manner the ability of the endogenous p38α MAPK to phosphorylate an endogenous substrate MK2 in activated glia[1]. 
MW-150 blocks in a concentration-dependent manner the increased IL-1β production by activated glia. The IC50 values are 332 nM and 936 nM for MK2 and IL-1β, respectively[1].
In Vivo: MW-150 (2.5 mg/kg; oral daily for 3-4 months) improves the APP/PS1 transgenic (Tg) mice performance in radial arm water maze (RAWM) and contextual fear conditioning tests[1]. 
MW-150 (2.5 mg/kg; given i.p.; daily for 14 days) treatment in APPNLh/NLh × PSP264L/P264L knock-in mouse (with no overexpression of the amyloid precursor protein) exhibits RAWM behavior indistinguishable from WT mice[1].

Name: Metarrestin ML246, CAS: 1443414-10-5, stock 19.6g, assay 98.2%, MWt: 474.60, Formula: C31H30N4O, Solubility: DMSO : 31.25 mg/mL (65.84 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: Metarrestin (ML246) disrupts the nucleolar structure and inhibits RNA polymerase (Pol) I transcription, at least in part by interacting with the translation elongation factor eEF1A2. Metarrestin is a first-in-class perinucleolar compartment inhibitor with a favorable PK profile, which effectively suppresses metastasis[1][2].
IC50 & Target: RNA polymerase (Pol) I[1][2]

Name: 3-Deazaadenosine (hydrochloride), CAS: 86583-19-9, stock 7.8g, assay 98%, MWt: 302.71, Formula: C11H15ClN4O4, Solubility: DMSO : 41.67 mg/mL (137.66 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HIV, Biological_Activity: 3-Deazaadenosine (hydrochloride) is an inhibitor of S-adenosylhomocysteine hydrolase, with a Ki of 3.9 µM; 3-Deazaadenosine has anti-inflammatory, anti-proliferative and anti-HIV activity.
IC50 & Target: IC50: 0.15 (HIV-1, A012 isolate), 0.20 µM (HIV-1, A018 isolate)[1] 
Ki: 3.9 µM (S-adenosylhomocysteine hydrolase)[1]
In Vitro: 3-Deazaadenosine is an inhibitor of S-adenosylhomocysteine hydrolase, with a Ki of 3.9 µM. 3-Deazaadenosine shows anti-HIV effect, and inhibits p24 antigen in peripheral blood mononuclear (PBMCs) cells infected with HIV-1 isolates (A012 and A018) with IC50s of 0.15 and 0.20 µM, respectively[1]. 3-Deazaadenosine (1-100 µM) inhibits LPS-induced expression of TNF-α mRNA, increases DNA binding activity of NF-κB, and causes proteolytic degradation of IκBα, but Not IκBβ in RAW 264.7 cells. 3-Deazaadenosine (100 µM) enhances nuclear translocation of NF-κB, but blocks LPS-induced NF-κB transcriptional activity, and such inhibition is augmented by the addition of homocysteine[2]. 3-Deazaadenosine (50, 100 µM) dose-dependently inhibits the phosphorylation of Raf and ERK, protein-dependent kinase 1, protein kinase B (Akt), and forkhead transcription factor FoxO1a. 3-Deazaadenosine (50 µM) suppresses vascular smooth muscle cell (VSMC) proliferation via interfering with Ras signaling[3].

Name: DT-061, CAS: 1809427-19-7, stock 32.2g, assay 98.1%, MWt: 520.52, Formula: C25H23F3N2O5S, Solubility: DMSO : 125 mg/mL (240.14 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: DT-061 is an orally bioavailable activator of protein phosphatase 2A (PP2A) and could be applied in the therapy of KRAS-mutant and MYC-driven tumorigenesis[1].
IC50 & Target: PP2A[1].
In Vivo: DT-061 (5 mg/kg, oral gavage, 4 weeks) shows single-agent activity in inhibiting H358 or H441 xenograft growth. Additionally, the combination of DT-061 and AZD6244 is more significantly efficient[1].

Name: GNE-6640, CAS: 2009273-67-8, stock 13.7g, assay 98.6%, MWt: 330.38, Formula: C20H18N4O, Solubility: DMSO : 5 mg/mL (15.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: GNE-6640 is a selective and non-covalent inhibitor of ubiquitin epecific peptidase 7 (USP7), with IC50 values of 0.75 μM, 0.43 μM, 20.3 μM and 0.23 μM for full length USP7, USP7 catalytic domain, full length USP43 and Ub-MDM2, respectively.
IC50 & Target: IC50: 0.75 μM(full length USP7), 0.43 μM(USP7 catalytic domain), 20.3 μM(full length USP43), 0.23 μM(Ub-MDM2)[1].
In Vitro: GNE-6640 promotes endogenous MDM2 ubiquitination with Lys48 (K48)-linked polyubiquitin chains, which directs proteasomal degradation13. GNE-6640 targets cellular USP7, MDM2, and p53 signalling pathways. GNE-6640 decreases viability of 108 cell lines with IC50 ≤ 10 μM. Combining GNE-6640 with doxorubicin or cisplatin (DNA-damaging agents), which could activate the p53 response and enhance USP7 inhibitor efficacy. GNE-6640 could induce tumor cell death. GNE-6640 enhances cytotoxicity with chemotherapeutic agents and targeted compounds, including PIM kinase inhibitors[1].

Name: MM-589 (TFA), CAS: 2097887-21-1, stock 28.6g, assay 98.5%, MWt: 686.72, Formula: C30H45F3N8O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: MM-589 TFA is a potent inhibitor of WD repeat domain 5 (WDR5) and mixed lineage leukemia (MLL) protein-protein interaction. MM-589 binds to WDR5 with an IC50 of 0.90 nM and inhibits the MLL H3K4 methyltransferase activity with an IC50 of 12.7 nM[1].
IC50 & Target: IC50: 0.90 nM (WDR5), 12.7 nM (HMT)[1]
Ki: <1 nM (WDR5)[1]
In Vitro: MM-589 (0.01-10 µM, 4 days or 7 days) potently and selectively inhibits cell growth in human leukemia cell lines harboring MLL translocations[1].

Name: MLS0315771, CAS: 727664-91-7, stock 9.2g, assay 98.6%, MWt: 273.33, Formula: C15H12FNOS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MLS0315771 is a potent and biologically active competitive phosphomannose isomerase (MPI) inhibitor, with an IC50 ~1 μM and a Ki of 1.4 μM.
IC50 & Target: IC50: ~1 μM (MPI)[1].
In Vitro: MLS0315771 increases mannose flux toward glycosylation. 
MLS0315771 toxicity at higher concentrations is an off-target effect. 
MLS0315771 is toxic to the zebrafish embryos above 2 μM. At 8-10 μM, ~50% embryos appeare sick within 20 min, and most of them die by 30-60 min[1].

Name: Semaglutide, CAS: 910463-68-2, stock 21.1g, assay 98.9%, MWt: 4113.64, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: Glucagon Receptor, Biological_Activity: Semaglutide, a long-acting GLP-1 analogue, is a glucagon-like peptide-1 (GLP-1) receptor agonist that can be used in the treatment of type 2 diabetes.
IC50 & Target: GLP-1 receptor[1].
In Vitro: Semaglutide has two amino acid substitutions compared to human GLP-1 (Aib8, Arg34) and is derivatized at lysine 26. The GLP-1R affinity of Semaglutide is 0.38±0.06 nM[1]. Semaglutide is a GLP-1 analogue with 94% sequence omology to human GLP-1[3.
In Vivo: The plasma half-life of Semaglutide is 46h in mini-pigs following i.v. administration and semaglutide has an MRT of 63.6h after s.c. dosing to mini-pigs[1]. Semaglutide improves 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP)-induced motor impairments. In addition, Semaglutide rescues the decrease of tyrosine hydroxylase (TH) levels, alleviates the inflammation response, reduces lipid peroxidation, inhibits the apoptosis pathway, and also increases autophagy- related protein expression, to protect dopaminergic neurons in the substantia nigra and striatum. Moreover, the long-acting GLP-1 analogue semaglutide is superior to liraglutide in most parameters[2]. Semaglutide lowers blood glucose by stimulating the release of insulin and also lowers body weight[3].

Name: Ibiglustat (L-Malic acid) Venglustat (L-Malic acid);SAR402671 (L-Malic acid);GZ402671 (L-Malic acid), CAS: 1629063-78-0, stock 26.1g, assay 98.7%, MWt: 523.57, Formula: C24H30FN3O7S, Solubility: DMSO : ≥ 100 mg/mL (191.00 mM), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Ibiglustat L-Malic acid (Venglustat L-Malic acid), a potential therapy for PD Parkinson’s disease, SRT in Fabry’s and Gaucher’s, is a selective, allosteric inhibitor of glucosylceramide synthase (GCS) with ability to cross the blood-brain barrier[1][2][3].
IC50 & Target: Glucosylceramide synthase[1].
In Vitro: Ibiglustat (SAR402671) (1 μM, 15 days) treated FD cells are close to the physiological level in untreated WT cells in GL-3 levels, suggesting that Ibiglustat can prevent additional GL-3 accumulation and could serve to ameliorate the abundant levels of this sphingolipid in FD cardiomyocytes[4].

Name: GW843682X GW843682, CAS: 660868-91-7, stock 28.7g, assay 99%, MWt: 477.46, Formula: C22H18F3N3O4S, Solubility: DMSO : 33.33 mg/mL (69.81 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Polo-like Kinase (PLK), Biological_Activity: GW843682X is a selective, ATP-competitive inhibitor of PLK1 and PLK3, with IC50s of 2.2 nM and 9.1 nM, respectively, and is also >100-fold selective against ∼30 other kinases.
IC50 & Target: IC50: 2.2 nM (PLK1), 9.1 nM (PLK3)[1]
In Vitro: GW843682X (compound 1) is effective on inhibition of growth of tumor cells, with IC50s of 0.41, 0.57, 0.11, 0.38, and 0.70 μM for A549, BT474, HeLa, H460 and HCT116 cell lines. GW843682X dose-dependently inhibits PLK1 phosphorylation of Ser15-p53, with an IC50 of 0.14 μM. GW843682X (3 μM) causes a strong G2-M arres in HDF cells and H460 cells after treatment for 24, 48, and 72 h. GW843682X (5 μM) leads to apoptosis in H460 cells instead of HDF cells[1]. GW843682X inhibits proliferation of U937 cells with an EC50 of 120 nM. GW843682X (500 nM) in combination with 5 µM VP-16 suppresses 50% of entry into mitosis in U937 cells[2]. GW843682X (0.06-1 μM) has inhibitory activities against proliferation of acute leukemia cells, and potentiates the anti-proliferative activity of vincristine. Moreover, GW843682X (0.1-1 μM) induces apoptosis of leukemia cells in a dose- and time-dependent manner. GW843682X (0.5-1 μM) dephosphorylates Bcl-xl in leukemia cells[3].

Name: BI-671800, CAS: 1093108-50-9, stock 14.9g, assay 98.1%, MWt: 501.50, Formula: C25H26F3N5O3, Solubility: DMSO : 135 mg/mL (269.19 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Immunology/Inflammation;GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: BI-671800 is a highly specific and potent antagonist of chemoattractant receptor-homologous molecule on Th2 cells (DP2/CRTH2), with IC50 values of 4.5 nM and 3.7 nM for PGD2 binding to CRTH2 in hCRTH2 and mCRTH2 transfected cells, respectively[1]. BI-671800 has potential for the treatment of poorly controlled asthma[2].
IC50 & Target: CRTH2[1].
In Vitro: BI-671800 (compound A) exhibits low nM potency as an antagonist of human or mouse CRTH2 in transfected cells[1].
In Vivo: BI-671800 (compound A, 0.1-10 mg/kg, i.g.) shows significant inhibition of AHR in mice[1]. 
BI-671800 (compound A), effectively blocks edema formation and greatly reduces the inflammatory infiltrate and skin pathology observed in drug vehicle-treated animals[3].

Name: Rolziracetam CI-911, CAS: 18356-28-0, stock 0.6g, assay 98.2%, MWt: 139.15, Formula: C7H9NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Rolziracetam is a nootropic drug of the racetam family and improves short-term memory in rats and monkeys[1].

Name: CID 1375606, CAS: 313493-80-0, stock 29.8g, assay 98.4%, MWt: 385.24, Formula: C20H14Cl2N2O2, Solubility: DMSO : 53.33 mg/mL (138.43 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CID 1375606 is a surrogate agonist of orphan G protein-coupled receptor GPR27.
IC50 & Target: GPR 27[1].
In Vitro: CID 1375606 is a GPR27-specific surrogate agonist. GPR27 is characterized by a high level of conservation among vertebrates and a predominant expression in the central nervous system. In addition, it has recently been linked to insulin secretion[1].

Name: BI 2536, CAS: 755038-02-9, stock 25.3g, assay 98.1%, MWt: 521.65, Formula: C28H39N7O3, Solubility: DMSO : ≥ 55.5 mg/mL (106.39 mM), Clinical_Informat: Phase 2, Pathway: Apoptosis;Cell Cycle/DNA Damage;Epigenetics, Target: Apoptosis;Polo-like Kinase (PLK);Epigenetic Reader Domain, Biological_Activity: BI 2536 is a dual PLK1 and BRD4 inhibitor with IC50s of 0.83 and 25 nM, respectively[1]. BI-2536 suppresses IFNB (encoding IFN-β) gene transcription[4].
IC50 & Target: IC50: 0.83 nM (Plk1), 3.5 nM (Plk2/Snk), 9 nM (Plk3/Fnk)[1] 
IC50: 25 nM (BRD4)[2]
In Vitro: Exceeding a 100-fold concentration range starting at 10 nM, BI 2536 causes HeLa cells to accumulate with a 4N DNA content, indicative of a cell-cycle block in either G2 phase or mitosis. In addition to HeLa cells, BI 2536 potently inhibits the proliferation of a panel of 32 human cancer cell lines, representing diverse organ derivations (including carcinomas of the breast, colon, lung, pancreas, and prostate, melanomas, and hematopoietic cancers) and varied patterns of tumor suppressor or oncogene mutations (including RB1, TP53, PTEN, andKRAS status). The half-maximal effective concentration (EC50) values in this cell panel ranged 2-25 nM, whereas a concentration of 100 nM of BI 2536 is typically sufficient for inducing a complete mitotic arrest. The proliferation of exponentially growing hTERT-RPE1, human umbilical vein endothelial cells (HUVECs), and normal rat kidney (NRK) cells is blocked at EC50values ranging 12-31 nM, indicating a comparable sensitivity of cycling nontransformed cells to BI 2536[3].
In Vivo: BI 2536 (40-50 mg/kg, i.v.) blocks the growth of human cancer xenografts in immunodeficient, nu/nu mice. Consecutive cycles of 40-50 mg/kg BI 2536 given i.v. once or twice per week are found to be highly efficacious in diverse xenograft models, such as the HCT 116 colon cancer with complete tumor suppression with the twice per week schedule (treated versus the control (T/C) value 0.3%) and a T/C value of 16% with once per week treatment; both schedules are well-tolerated, as judged by clinical signs and absence of major body-weight changes[3].

Name: Coumarin-3-carboxylic Acid 2-Oxochromene-3-carboxylic acid, CAS: 531-81-7, stock 38.2g, assay 98.8%, MWt: 190.15, Formula: C10H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Coumarin-3-carboxylic acid (2- Oxochromene-3-carboxylic acid) is an important initial compound for the synthesis of coumarins which are well known natural products for their diverse biological activities. Lanthanide complexes of Coumarin-3-carboxylic acid exhibit antiproliferative activity towards K-562 cell line[1][2].

Name: SB 239063, CAS: 193551-21-2, stock 22.5g, assay 98.5%, MWt: 368.40, Formula: C20H21FN4O2, Solubility: DMSO : 33.33 mg/mL (90.47 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: SB 239063 is a potent, selective and orally active p38 MAPK inhibitor, exhibits an IC50 of 44 nM for recombinant purified human p38α, with equipotent inhibitory activity against p38α and p38β. SB 239063 has no effect on p38γ or p38δ. With anti-asthma activity and also be used to enhance memory which is impaired due to aging or medical conditions, such as, AD[1][2].
IC50 & Target: IC50: 44 nM (Human p38α)[1]
In Vitro: SB 239063 (0.1–10 μM ; 29 hours, 47 hours) increases apoptosis of eosinophils in a dose-related in the presence of 10 pM IL-5 at every time point from 21 hours onwards[1]. 
SB 239063 potently inhibits IL-1 and TNF- a production in LPS-stimulated human peripheral blood monocytes with IC50 values of 120 nM and 350 nM, respectively[1]. 
In Vivo: SB 239063 (12 mg/kg; p.o.; 1 hour before and 4 hours after OA challenge; b.i.d. for 3 days) significantly inhibits the resultant antigen-induced airway eosinophilia[1]. 
SB 239063 (12 mg/kg; p.o.) almost abolishes ovalbumin (OA)-induced airway eosinophilia (~ 93% inhibition) by inhalation[1]. 
SB 239063 is a potent inhibitor of LPS-induced TNF-alpha production in the mouse peritoneal cavity with an EC50 of 5.8 mg/kg (2.8–10.3; 95% CL)[1].

Name: DNA2 inhibitor C5, CAS: 35973-25-2, stock 20.6g, assay 98.9%, MWt: 234.17, Formula: C10H6N2O5, Solubility: DMSO : 31.25 mg/mL (133.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DNA2 inhibitor C5 is a potent, competitive and specific inhibitor of DNA2 nuclease activity with an IC50 of 20 μM. DNA2 inhibitor C5 inhibits nuclease, DNA dependent ATPase, helicase, and DNA binding activities of DNA2. DNA2 inhibitor C5 is a promising lead compound to develop sensitizers for cancer chemotherapeutics that cause replication stress[1].
IC50 & Target: IC50: 20 μM (DNA2 nuclease)[1]

Name: TAK-715, CAS: 303162-79-0, stock 12.6g, assay 98.5%, MWt: 399.51, Formula: C24H21N3OS, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (250.31 mM), Clinical_Informat: Phase 2, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: TAK-715 is a p38 MAPK inhibitor for p38α with IC50 of 7.1 nM, 28-fold more selective for p38α over p38β, no inhibition to p38γ/δ, JNK1, ERK1, IKKβ, MEKK1 or TAK1.
IC50 value: 7.1 nM [1]
Target: p38α MAPK
in vitro: TAK 715 inhibits LPS-stimulated release of TNF-alpha from THP-1 with IC50 of 48 nM [1]. TAK 715 (10 μM) inhibits Wnt-3a-induced hDvl2 phosphorylation and the hDvl2 shift in U2OS-EFC cells [2]. The amide NH of TAK 715 is hydrogen bonded to the main-chain carbonyl of Met109 of p38 alpha. TAK 715 binds relatively high in the ATP pocket, occupying the hydrophobic back pocket, the adenine region and the front pocket of p38 as well as extending to most of the length of the Gly-rich loop [3].
in vivo: TAK 715 (10 mg/kg, po) inhibits LPS-induced TNF-alpha production in mice with 87.6% inhibition. TAK 715 has a modest mouse bioavailability of 18.4% and a slightly improved rat bioavailability of 21.1%. TAK 715 has a modest mouse bioavailability of 18.4% and a slightly improved rat bioavailability of 21.1%. TAK 715 results in Cmax of 0.19 μg/mL and AUC(0-24 hours) of 1.16 μg·h/mL in rats. TAK 715 (30 mg/kg, po) significantly reduces the secondary paw volume with 25 % inhibition in a rat adjuvant-induced arthritis (AA) model [1].

Name: VX-702, CAS: 745833-23-2, stock 32.9g, assay 98.9%, MWt: 404.32, Formula: C19H12F4N4O2, Solubility: DMSO : ≥ 42 mg/mL (103.88 mM), Clinical_Informat: Phase 2, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: VX-702 is a highly selective inhibitor of p38α MAPK, 14-fold higher potency against the p38α versus p38β.

Name: Olaparib AZD2281;KU0059436, CAS: 763113-22-0, stock 0.2g, assay 98.7%, MWt: 434.46, Formula: C24H23FN4O3, Solubility: DMSO : ≥ 33.33 mg/mL (76.72 mM), Clinical_Informat: Launched, Pathway: Epigenetics;Cell Cycle/DNA Damage;Autophagy;Autophagy, Target: PARP;PARP;Autophagy;Mitophagy, Biological_Activity: Olaparib (AZD2281;KU0059436) is a potent and oral PARP inhibitor with IC50s of 5 and 1 nM for PARP1 and PARP2, respectively.
IC50 & Target: IC50: 5/1 nM (PARP-1/2)[1]
In Vitro: Olaparib (AZD2281) is a single digit nanomolar inhibitor of both PARP-1 and PARP-2 that shows standalone activity against BRCA1-deficient breast cancer cell lines. Olaparib is applied to SW620 cell lysates, and identified the IC50 for PARP-1 inhibition to be around 6 nM and the total ablation of PARP-1 activity to be at concentrations of 30−100 nM[1].
In Vivo: Animals bearing SW620 xenografted tumors are treated with Olaparib (10 mg/kg, p.o.) in combination with NSC 362856 (TMZ) (50 mg/kg, p.o.) once daily for 5 consecutive days, after which the tumors are left to grow out[1]. Olaparib increases vascular perfusion in Calu-6 tumors established in a DWC model. Administration of olaparib(50 mg/kg, p.o.) as a single agent (top panel) or in combination with radiation (bottom panel) results in an increase in fluorescence intensity in the Calu-6 tumors[2].

Name: Veliparib ABT-888, CAS: 912444-00-9, stock 7.2g, assay 98.4%, MWt: 244.29, Formula: C13H16N4O, Solubility: DMSO : ≥ 29 mg/mL (118.71 mM), Clinical_Informat: Phase 3, Pathway: Epigenetics;Cell Cycle/DNA Damage;Autophagy, Target: PARP;PARP;Autophagy, Biological_Activity: Veliparib is a potent PARP inhibitor, inhibiting PARP1 and PARP2 with Kis of 5.2 and 2.9 nM, respectively.
IC50 & Target: Ki: 5.2 nM (PARP1), 2.9 nM (PARP2)[1]
In Vitro: Veliparib (ABT-888) is also tested against SIRT2, an enzyme that also uses NAD+ for catalysis, and found to be inactive (>5,000 nM). The receptor profile of Veliparib is determined in a panel of 74 receptor-binding assays at a concentration of 10 μM. Veliparib displaces control-specific binding at 50% or greater at the human H1(61%), the human 5-HT1A (91%), and the human 5-HT7 (84%) sites only. The IC50s for these three receptors are 5.3, 1.5, and 1.2 μM, respectively[1]. c-Met knockdown cells show 4.2- (shMet-A; 95% CI=4-4.5) or 4.6-fold (shMet-B; 95% CI=4.4-4.8) growth inhibition when treated with 60 μM Veliparib (ABT-888). When treated with 38 μM Veliparib, c-Met knockdown cells show 2- (shMet-A; 95% CI=1.5-2.5) or 1.9-fold (shMet-B; 95% CI=1.3-2.5) growth inhibition[2]. In HaCaT cells, at 6 h post-treatment by Veliparib (ABT-888), cell viability is significantly increases under 1,000 µM sulfur mustard (SM) exposure, whereas Veliparib does not protect cell viability under 100 µM SM exposure. Moreover, the addition of Veliparib no longer shows the protective effect at 24 h post SM exposure[3].
In Vivo: Veliparib (ABT-888) is a potent inhibitor of PARP, has good oral bioavailability, can cross the blood-brain barrier in syngeneic and xenograft tumor models[1]. In MDA-MB-231 xenograft tumor models, combination treatment (AG014699/PF-02341066 and Veliparib (ABT-888)/Foretinib) substantially reduced tumor growth compared to either inhibitor alone[2].

Name: Galactose 1-phosphate Potassium salt, CAS: 19046-60-7, stock 8.5g, assay 98.3%, MWt: 336.32, Formula: C6H11K2O9P, Solubility: H2O : 125 mg/mL (371.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Galactose 1-phosphate Potassium salt is is an intermediate in the galactose metabolism and nucleotide sugars.

Name: Veliparib (dihydrochloride) ABT-888 dihydrochloride, CAS: 912445-05-7, stock 33.9g, assay 98.9%, MWt: 317.21, Formula: C13H18Cl2N4O, Solubility: DMSO : ≥ 3.2 mg/mL (10.09 mM); H2O : ≥ 50 mg/mL (157.62 mM), Clinical_Informat: Phase 3, Pathway: Epigenetics;Cell Cycle/DNA Damage;Autophagy, Target: PARP;PARP;Autophagy, Biological_Activity: Veliparib (dihydrochloride) is a potent inhibitor of PARP1 and PARP2 with Ki of 5.2 nM and 2.9 nM in cell-free assays, respectively.
IC50 & Target: Ki: 5.2 nM (PARP1), 2.9 nM (PARP2)[1]
In Vitro: Veliparib is inactive to SIRT2 (>5 μM)[1]. Veliparib inhibits the PARP activity with EC50 of 2 nM in C41 cells[2]. Veliparib can decrease the PAR levels in both irradiated and nonirradiated H460 cells. Veliparib reduces clonogenic survival and inhibits DNA repair by PARP-1 inhibition in H460 cells. Veliparib increases apoptosis and autophagy in H460 cells when combination with radiation[3]. Veliparib inhibits PARP activity in H1299, DU145 and 22RV1 cells and the inhibition is independent of p53 function. Veliparib (10 μM) suppresses the surviving fraction (SF) by 43% in the clonogenic H1299 cells. Veliparib shows effective radiosensitivity in oxic H1299 cells. Veliparib can attenuate the SF of hypoxic-irradiated cells including H1299, DU145 and 22RV1[4].
In Vivo: The oral bioavailability of Veliparib is 56%-92% in mice, SD rats, beagle dogs, and cynomolgus monkeys after oral administration[1]. Veliparib (25 mg/kg, i.p.) can improve tumor growth delay in a NCI-H460 xenograft model. Combination with radiation, veliparib decreases the tumor vessel formation[3]. Veliparib reduces intratumor PAR levels by more than 95% at a dose of 3 and 12.5 mg/kg in A375 and Colo829 xenograft models and the suppression can be maintained over time[4].

Name: EC359, CAS: 2012591-09-0, stock 37.2g, assay 98.2%, MWt: 540.68, Formula: C36H38F2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: EC359 is a potent, selective, high affinity and orally active leukemia inhibitory factor receptor (LIFR) inhibitor with a Kd of 10.2 nM, which directly interacts with LIFR to effectively block LIF/LIFR interactions[1].
IC50 & Target: Kd: 10.2 nM (leukemia inhibitory factor receptor)[1]
In Vitro: EC359 (0-100 nM; 3 days; BT-549, SUM-159, MDA-MB-231, MDA-MB-468, and HCC1806 cells) treatment reduces cell viability in a dose-dependent manner[1]. 
EC359 (20 nM, 25 nM; 72 hours; MDA-MB-231 and BT-549 cells) treatment significantly increases caspase-3/7 activity and Annexin V-positive cells in both MDAMB-231 and BT-549 cells. EC359 exhibits significant inhibitory activity on invasion and promotes apoptosis of TNBC cells[1]. 
EC359 (100 nM; 12 hours; BT549 cells) treatment significantly reduces the expression of several (such as STAT1 TGFB1, JUNB, MCL-1, etc) known STAT3 target genes[1]. 
EC359(100 nM; 1 hour; MDA-MB-231 and BT-549 cells) treatment substantially reduces the LIF activation of STAT3, also reduces the STAT3 activation by OSM and CNTF. EC359 treatment substantially decreases the phosphorylation of AKT, mTOR, S6, and ERK1/2 in MDA-MB231 and BT-549 cells. EC359 treatment also increases the phosphorylation of proapoptotic p38MAPK in BT549 cells[1].
In Vivo: EC359 (5 mg/kg; subcutaneous injection; 3 days per week; for 25 days; female athymic nude mice) treatment significantly reduces the tumor progression. The body weights of mice in EC359-treated groups remains unchanged confirming the low toxicity of EC359[1].

Name: AZ084, CAS: 929300-19-6, stock 39.8g, assay 98.4%, MWt: 434.57, Formula: C26H34N4O2, Solubility: DMSO : 250 mg/mL (575.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: AZ084 is a potent, selective, allosteric and oral active CCR8 antagonist, with a Ki of 0.9 nM. Has potential to treat asthma[1].

Name: SAG (hydrochloride), CAS: 2095432-58-7, stock 37.2g, assay 98.6%, MWt: 526.52, Formula: C28H29Cl2N3OS, Solubility: DMSO : 21.67 mg/mL (41.16 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: Smo, Biological_Activity: SAG (hydrochloride) is a potent Smo receptor agonist, and activates the Hedgehog signaling pathway, with a Kd of 59 nM.
IC50 & Target: Kd: 59 nM (Smo)[1].
In Vitro: SAG (hydrochloride) acts downstream of Ptch1 in the Hh pathway and counteracts cyclopamine inhibition of Smo. SAG induces firefly luciferase expression in Shh-LIGHT2 cells with an EC50 of 3 nM and then inhibits expression at higher concentrations. In Smo-expressing Cos-1 cells, SAG yields an apparent dissociation constant (KD) of 59 nM for the SAG/Smo complex[1]. SAG and purmorphamine verride the inhibitory effect of robotnikinin since Smo functions downstream of Shh/Ptc1[2].
In Vivo: In CD-1 mice, SAG (1.0 mM) or NELL-1 (600 μg/ml) alone results in increased bone formation at 4 and 8 weeks, but significantly greater bone formation with both components combined (SAG + NELL-1). The combination of the two compounds exhibits a significant increase in new bone formation, accompanied by increased defect vascularization[3]. SAG (15, 17, or 20 mg/kg, i.p.) induces pre-axial polydactyly prevalently. The highest SAG dose is effective in ca. 80% of the embryos and increased Gli1 and Gli2 mRNA expression in the limb bud, with Gli1 mRNA being the most upregulated[4].

Name: KT182, CAS: 1402612-62-7, stock 30.6g, assay 98.4%, MWt: 438.52, Formula: C27H26N4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: KT182 is a potent and selective inhibitor of α/β-hydrolase domain containing 6 (ABHD6), with an IC50 of 0.24 nM in Neuro2A cells[1].
IC50 & Target: IC50: 0.24 nM (ABHD6 in Neuro2A cells)[1].

Name: VU0467485 AZ13713945, CAS: 1451994-10-7, stock 38.9g, assay 98.7%, MWt: 360.41, Formula: C17H17FN4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: VU0467485 (AZ13713945) is a potent, selective, and orally bioavailable muscarinic acetylcholine receptor 4 (M4) positive allosteric modulator (PAM). VU0467485 (AZ13713945) potentiates activity of ACh at M4 with EC50s of 26.6 nM and 78.8 nM at rat and human M4 receptors, respectively. VU0467485 (AZ13713945) shows selectivity for M4 over human and rat M1/2/3/5. VU0467485 (AZ13713945) displays moderate to high CNS penetration. VU0467485 (AZ13713945) has antipsychotic-like activity[1].
In Vivo: VU0467485 (1-10 mg/kg; p.o.) has antipsychotic-like activity in an amphetamine-induced hyperlocomotion (AHL) rat model[1]. 
VU0467485 (3 mg/kg; p.o.) treatment displays that the Cmax, AUCo-inf and elimination t1/2 were 1.2 μM, 3.8 μM•h and 4.2 hours, respectively[1].

Name: BI8626, CAS: 1875036-75-1, stock 33.5g, assay 98.3%, MWt: 440.54, Formula: C25H28N8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: E1/E2/E3 Enzyme, Biological_Activity: BI8626 is a specific inhibitor of the ubiquitin ligase HUWE1 with an IC50 of 0.9 μM[1].
IC50 & Target: IC50: 0.9 μM (HUWE1)[1]
In Vitro: BI8626 induces HUWE1 ectopically expresses to abolishe ubiquitination of MCL1 in HeLa cells[1]. 
BI8626 suppresses colony formation of Ls174T cells with estimated IC50 value of 0.7 μM, and BI8622 (1-4 days) treatment retards passage of Ls174T cells through all phases of the cell cycle, with the effect being strongest for G1[1]. 
BI8626 (0-50 μM; 0-6 hours) retards the degradation of MCL1 in response to UV irradiation to the same extent as depletion of HUWE1 in U2OS cells[1].

Name: PLX5622, CAS: 1303420-67-8, stock 33.4g, assay 98.6%, MWt: 395.41, Formula: C21H19F2N5O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (252.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Fms, Biological_Activity: PLX5622 is a highly selective brain penetrant and oral active CSF1R inhibitor with an Ki of 5.9 nM, for extended and specific microglial elimination, preceding and during pathology development. PLX5622 demonstrates desirable PK properties in varies animals[1][2].
IC50 & Target: CSF1R[1]
In Vivo: PLX5622 (oral gavage; 65 mg/kg/day; for 14 days) causes paw withdrawal threshold high in mice, indicating that PLX5622 prevents the development of injury-associated mechanical allodynia[2].

Name: MC-DOXHZN hydrochloride Doxorubicin(6-maleimidocaproyl)hydrazone hydrochloride, CAS: 480998-12-7, stock 38g, assay 98.9%, MWt: 787.21, Formula: C37H43ClN4O13, Solubility: DMSO : 125 mg/mL (158.79 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: Topoisomerase;Drug-Linker Conjugates for ADC, Biological_Activity: MC-DOXHZN hydrochloride is an albumin-binding prodrug of Doxorubicin (DNA topoisomerase II inhibitor), with acid-sensitive properties[1].

Name: Propineb Zinc propylenebis(dithiocarbamate), CAS: 12071-83-9, stock 27.8g, assay 98.5%, MWt: 289.77, Formula: C5H8N2S4Zn, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Propineb (Zinc propylenebis) is a compound widely used in fruit and vegetables cultures, due to its large spectrum of activity against fungal plant diseases[1].
In Vivo: Propineb (Zinc propylenebis) has a moderate to low acute toxicity with a specific goitrogenic effect in rats. long-term exposure, oral or by inhalation is related to carcinogenicity, teratogenicity, malfunction of the reproductive system and malformation of their vitals[2].

Name: DO-264, CAS: 2301866-59-9, stock 19.4g, assay 98.1%, MWt: 558.40, Formula: C23H20Cl2F3N5O2S, Solubility: DMSO : ≥ 100 mg/mL (179.08 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: DO-264 is a selective and in vivo-active inhibitor of Abhydrolase Domain Containing 12 (ABHD12), with an IC50 of 11 nM.
IC50 & Target: IC50: 11 nM (ABHD12)[1].
In Vitro: DO-264 displays an IC50 value of 11 nM (9.6 nM-13 nM). DO-264 blocks lyso-PS hydrolysis activities of recombinant mouse and human ABHD12 in transfected HEK293T cell lysates (DO-264 IC50 values of ~30 and 90 nM against mouse and human ABHD12, respectively) and the ABHD12-dependent lyso-PS lipase activity of membrane lysates from mouse brain (IC50=2.8 nM, 2.4 nM-3.3 nM) and human THP-1 cells (IC50= 8.6 nM, 6.3 nM-12 nM)[1].
In Vivo: Mice treated with DO-264 display dose-dependent increases in brain lyso-PS and 20:4 PS content that are qualitatively similar to the changes observed in ABHD12–/– mice. DO-264-treated mice, however, show minimal impairment in auditory function following four weeks of drug exposure. Both ABHD12–/– and DO-264-treated mice display exacerbated immunopathology following infection with the lymphocytic choriomeningitis virus (LCMV) clone 13, resulting in severe inflammatory lung damage, heightened chemokine production, and, in some cases, death[1].

Name: KT203, CAS: 1402612-64-9, stock 24.8g, assay 98.1%, MWt: 466.53, Formula: C28H26N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: KT203 is a potent and selective inhibitor of α/β-hydrolase domain containing 6 (ABHD6), with an IC50 of 0.31 nM in Neuro2A cells[1].
IC50 & Target: IC50: 0.31 nM (ABHD6 in Neuro2A cells)[1].

Name: diABZI STING agonist-1 (trihydrochloride), CAS: 2138299-34-8, stock 4.9g, assay 98.3%, MWt: 959.32, Formula: C42H54Cl3N13O7, Solubility: DMSO : 125 mg/mL (130.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: STING, Biological_Activity: diABZI STING agonist-1 (trihydrochloride) is a selective stimulator of interferon genes (STING) receptor agonist, with an EC50s of 130 for human PBMCs.
IC50 & Target: STING[1].
In Vitro: diABZI STING agonist-1 is a selective stimulator of interferon genes (STING) receptor agonist, with EC50s of 130, 186 nM for human and mouse, respectively. At a concentration of 1 μM, diABZI STING agonist-1 (compound 3) demonstrates high selectivity against more than 350 kinases tested[1].
In Vivo: diABZI STING agonist-1 trihydrochloride (subcutaneous injection; 2.5 mg/kg) induces STING-dependent activation of type-I interferon and pro-inflammatory cytokines in vivo[1].
diABZI STING agonist-1 trihydrochloride (intravenous injection; 3 mg/kg) exhibits systemic exposure with a half-life of 1.4 h and achieves systemic concentrations greater than the half-maximal effective concentration (EC50) for mouse STING (200 ng/ml)[1].
diABZI STING agonist-1 trihydrochloride (intravenous injection; 1.5 mg/kg; days 1, 4 and 8; 43 days) results in significant tumour growth inhibition and significantly improves survival (P < 0.001) with 8 out of 10 mice remaining tumor free at the end of the study on day 43[1].

Name: CCT020312, CAS: 324759-76-4, stock 3g, assay 98.4%, MWt: 650.40, Formula: C31H30Br2N4O2, Solubility: DMSO : 125 mg/mL (192.19 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Autophagy, Target: PERK;Autophagy, Biological_Activity: CCT020312 is a selective EIF2AK3/PERK activator. CCT020312 elicits EIF2A phosphorylation in cells.
IC50 & Target: EIF2AK3/PERK[1][2].
In Vitro: Treatment of HT29 cells with CCT020312 for 24 hours reveals a concentration-dependent loss of P-S608-pRB signal, with a linear response between 1.8 and 6.1 μM[1]. 
CCT020312 treatment effectively inhibits cell proliferation (as measured at 96 hours) even if treatment is for 2 hours only with subsequent compound washout, indicating that CCT020312 is capable of eliciting durable rather than transient cytostasis[1]. 
Treatment of HT29 cells with 10 μM CCT020312 for 24 hours reduces the amount of the G1/S cyclins D1, D2, E and A as well as the CDK catalytic subunit CDK2 and increased the level of the CDK inhibitor p27KIP1 present in such cells[1].
In Vivo: Treatment of 15-week-old wildtype mice with the PERK activator CCT020312 (1-5 mg/kg; i.p.; once daily for 3 days) leads to increased levels of phosphorylated PERK and NRF2 in brain homogenates[2]. 
P301S transgenic mice treated with CCT020312 (2 mg/kg; i.p.; once daily for 6 weeks) performes significantly better in Morris water maze[2].

Name: LY2794193, CAS: 2173037-97-1, stock 8.2g, assay 98.1%, MWt: 334.32, Formula: C16H18N2O6, Solubility: H2O : 2 mg/mL (5.98 mM; ultrasonic and adjust pH to 14 with NaOH), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: LY2794193 is a highly potent and selective mGlu3 receptor agonist (hmGlu3 Ki=0.927 nM，EC50=0.47 nM; hmGlu2 Ki=412 nM，EC50=47.5 nM)[1].

Name: GB-88, CAS: 1416435-96-5, stock 35.7g, assay 98.7%, MWt: 546.70, Formula: C32H42N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: GB-88 is an oral, selective non-peptide antagonist of PAR2, inhibits PAR2 activated Ca2+ release with an IC50 of 2 µM[1].
IC50 & Target: PAR2[1]
In Vitro: GB-88 inhibits iCa2+ release induced in HT29 cells by trypsin, 2f-LIGRLO-NH2 and GB110 (PAR2 agonists). And antagonism by GB-88 is agonist dependent[1]. 
In Vivo: GB-88 (10 mg/kg, p.o. in olive oil) is both orally active and anti-inflammatory in vivo, with specific antagonist activity against four structurally and mechanistically different PAR2 agonists (2f-LIGRLO-NH2, trypsin, SLIGRL-NH2 and GB110)[1]. 
GB-88 inhibits PAR2-induced acute inflammation in vivo[1].

Name: BAY-850, CAS: 2099142-76-2, stock 7.3g, assay 98.8%, MWt: 654.24, Formula: C38H44ClN5O3, Solubility: DMSO : 62.5 mg/mL (95.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BAY-850 is a potent and isoform selective ATPase family AAA domain-containing protein 2 (ATAD2) inhibitor, with an IC50 of 166 nM.
IC50 & Target: ATAD2[1].
In Vitro: BAY-850 competes with the binding of a mono-acetylated Histone H4 N-terminal peptide to ATAD2 BD with an IC50 of 166 nM measured in TR-FRET assay. BAY-850 displaces the tetra-acetylated peptide with an IC50 of 157 nM and a KD of 115 nM respectively. The unprecedented isoform selectivity of BAY-850 suggests a different mode of action to those exhibited by canonical BD inhibitors[1].

Name: Pronase E Pronase, CAS: 9036-06-0, stock 18.4g, assay 98.8%, MWt: 1000, Formula: N/A, Solubility: H2O : 20 mg/mL (Need ultrasonic); DMSO : 50 mg/mL (Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Pronase E is a mixture of proteolytic enzymes that is obtained from Streptomyces griseus and could digest protein into individual amino acids.

Name: H-Val-Pro-Pro-OH, CAS: 58872-39-2, stock 5.3g, assay 98.3%, MWt: 311.38, Formula: C15H25N3O4, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: H-Val-Pro-Pro-OH, a milk-derived proline peptides derivative, is an inhibitor of Angiotensin I converting enzyme (ACE), with an IC50 of 9 μM.
IC50 & Target: IC50: 9 μM (ACE)[1].
In Vitro: H-Val-Pro-Pro-OH, a proline peptides derivative, could inhibit Angiotensin I converting enzyme (ACE), with an IC50 of 9 μM[1]. H-Val-Pro-Pro-OH could enhance insulin sensitivity and prevent insulin resistance in 3T3-F442A pre-adipocytes. H-Val-Pro-Pro-OH also has anti-hypertensive and anti-inflammatory functions. H-Val-Pro-Pro-OH further enhances the expression of glucose transporter 4 (GLUT4) in adipocytes and restores glucose uptake in TNF-treated adipocytes[2].

Name: KY-226, CAS: 1621673-53-7, stock 26.9g, assay 98.5%, MWt: 481.67, Formula: C27H31NO3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: KY-226 is a potent, selective, orally active and allosteric protein tyrosine phosphatase 1B (PTP1B) inhibitor with an IC50 of 0.25 μM, and without PPARγ agonist activity. KY-226 exerts anti-diabetic and anti-obesity effects by enhancing insulin and leptin signaling, respectively. KY-226 also protects neurons from cerebral ischemic injury[1][2].
IC50 & Target: IC50: 0.25 μM (Protein tyrosine phosphatase 1B (PTP1B))[2]
In Vitro: In human hepatoma-derived cells (HepG2), KY-226 (0.3-10 μM) increases the phosphorylated insulin receptor (pIR) produced by insulin[1]. 
KY-226 (1 μM; 24 hours; bEnd.3 cells) treatment rescues lipopolysaccharide-induced reduction of mRNA and protein levels of ZO-1. KY-226 treatment restores phosphorylation of pAkt (T308) and its downstream target forkhead box protein O1 (FoxO1) (S256) in bEnd.3 cells[2].
In Vivo: KY-226 (10-30 mg/kg/day; oral administration; daily; for 4 weeks; male db/db mice) treatment significantly reduces plasma glucose and triglyceride levels as well as hemoglobin A1c values without increasing body weight gain[1]. 
KY-226 attenuates plasma glucose elevations in the oral glucose tolerance test. KY-226 also increases pIR and phosphorylated Akt in the liver and femoral muscle[1].

Name: BI-1347, CAS: 2163056-91-3, stock 21.1g, assay 98.2%, MWt: 356.42, Formula: C22H20N4O, Solubility: DMSO : 125 mg/mL (350.71 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: BI-1347 is a potent CDK8 inhibitor extracted from patent WO2017202719A1, product I-003, has an IC50 of 1.1 nM[1].
IC50 & Target: IC50: 1.1 nM (CDK8)[1]

Name: Thrombin, CAS: 9002-04-4, stock 1.5g, assay 98.9%, MWt: 1000, Formula: N/A, Solubility: H2O, Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Thrombin, Biological_Activity: Thrombin is a trypsin-like allosteric serine protease. Thrombin enables site-specific cleavage of fusion proteins with an accessible Thrombin recognition sequence and can be used to digest GST-tagged proteins.
In Vitro: One unit of enzyme cleaves > 90% of 100 µg of a test GST-tagged protein when incubated in 1× PBS at 22°C for 16 h. 
Thrombin solution: Dissolve 500 units in 0.5 mL of PBS prechilled to 4°C. Swirl gently. Store solution in small aliquots at -80°C to preserve activity. 
Cleavage buffer: PBS (140 mM NaCl, 2.7 mM KCl, 10 mM Na2HPO4, 1.8 mM KH2PO4) pH 7.3. 
Elution buffer: 50 mM Tris-HCl, 10 mM reduced glutathione, pH 8.0

Name: AZD-0284, CAS: 2101291-07-8, stock 4g, assay 98.6%, MWt: 524.43, Formula: C21H18F6N2O5S, Solubility: DMSO : 100 mg/mL (190.68 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: ROR, Biological_Activity: AZD-0284 is an inverse agonist of the nuclear receptor RORγ. In development for the treatment of plaque psoriasis vulgaris and respiratory tract disorders[1].
IC50 & Target: RORγ[1]

Name: Bifenazate, CAS: 149877-41-8, stock 30g, assay 98.4%, MWt: 300.35, Formula: C17H20N2O3, Solubility: DMSO : ≥ 250 mg/mL (832.36 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Bifenazate is a carbazate acaricide that control 100% of mites at a concentration of 25 ppm[1]. Bifenazate is a positive allosteric modulator of GABA receptor[2].
IC50 & Target: GABA receptor[2].

Name: DJ-V-159, CAS: 2253744-53-3, stock 39.6g, assay 98.2%, MWt: 502.37, Formula: C24H12F6N4O2, Solubility: DMSO : 25 mg/mL (49.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: DJ-V-159 is an agonist for G protein-coupled receptor family C group 6 member A (GPRC6A).
IC50 & Target: GPRC6A[1].
In Vitro: DJ-V-159 activates ERK in HEK-293 transfected with GPRC6A but not in non-transfected HEK-293 cells, with potency similar to L-Arg. In addition, DJ-V-159 dose-dependently stimulates cAMP production in GPRC6A expressing HEK-293 cells, achieving a response a 0.2 nM concentrations in the media. DJ-V-159 stimulates insulin secretion in mouse beta-cell MIN-6 cells. The DJ-V-159 increased insulin stimulation index (SI) in MIN-6 cells similar to the effects of Ocn, known ligand of GPRC6A[1].
In Vivo: DJ-V-159 at the dose of 10 mg/kg reduces blood glucose levels in wildtype mice at 60 and 90 minutes after intraperitoneal administration of 10 mg/kg, whereas the vehicle (95% PEG + 5% DMSO) has no effect on blood glucose. DJ-V-159 reduces blood glucose levels in wild-type mice by 43.6% and 41.9% at 60 and 90 minutes, respectively, after intraperitoneal administration of 10 mg/kg. The mice tolerated this short-term exposure to DJ-V-159 without any overt side-effects. DJ-V-159, however, is almost in or on the boundary of the Lipinski's Rule of Five[1].

Name: Diprotin A (TFA) Ile-Pro-Pro (TFA), CAS: 209248-71-5, stock 4.9g, assay 98.5%, MWt: 455.47, Formula: C19H32F3N3O6, Solubility: H2O : ≥ 77.5 mg/mL (170.15 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Dipeptidyl Peptidase, Biological_Activity: Diprotin A (TFA) is an inhibitor of dipeptidyl peptidase IV (DPP-IV).
IC50 & Target: DPP-IV[1].
In Vitro: Diprotin A increases the phosphorylation of Src and vascular endothelial-cadherin (VE-cadherin) in human endothelial cells and disrupts endothelial cell-to-cell junctions, which are attenuated by CXCR4 (receptor of SDF-1α)-blocker or Src-inhibitor[1].
In Vivo: In the model of retinopathy of prematurity, Diprotin A increases not only retinal vascularity but also leakage. Additionally, in the murine diabetic retinopathy model, Diprotin A increases the phosphorylation of Src and VE-cadherin and aggravates vascular leakage in the retinas. Collectively, Diprotin A induces vascular leakage by augmenting the SDF-1α/CXCR4/Src/VE-cadherin signaling pathway[1].

Name: Barbadin, CAS: 356568-70-2, stock 5.9g, assay 98.1%, MWt: 333.41, Formula: C19H15N3OS, Solubility: DMSO : 50 mg/mL (149.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Barbadin is a novel and selective β-arrestin/β2-adaptin interaction inhibitor, has IC50 values of 19.1 μM for β-arrestin1 and 15.6 μM for β-arrestin2. Barbadin blocks agonist-promoted endocytosis of the prototypical β2-adrenergic, V2-vasopressin and angiotensin-II type-1 receptors[1].
IC50 & Target: IC50: 19.1 μM (β-arrestin1); 15.6 μM (β-arrestin2)[1]

Name: 2-D08, CAS: 144707-18-6, stock 23.8g, assay 98.4%, MWt: 270.24, Formula: C15H10O5, Solubility: DMSO : 150 mg/mL (555.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Protein Tyrosine Kinase/RTK, Target: E1/E2/E3 Enzyme;TAM Receptor, Biological_Activity: 2-D08 is a cell permeable, mechanistically unique inhibitor of protein SUMOylation. 2-D08 also inhibits Axl with an IC50 of 0.49 nM.
IC50 & Target: IC50: 0.49 nM (Axl)[2]
In Vitro: 2-D08 inhibits sumoylation by preventing transfer of SUMO from the UBC9-SUMO thioester to the substrate[1]. 2-D08 decreases the ratio of p-Axl to t-Axl in a dose-dependent manner. Suppression of Axl kinase activity by 2D08 disrupts the cytoskeleton and actin filaments with re-organization at cellular junctions[2].

Name: TVB-3166, CAS: 1533438-83-3, stock 32.6g, assay 98.9%, MWt: 384.47, Formula: C24H24N4O, Solubility: DMSO : 62.5 mg/mL (162.56 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Fatty Acid Synthase (FAS), Biological_Activity: TVB-3166 is an orally-available, reversible, and selective fatty acid synthase (FASN) inhibitor with IC50s of 42 nM and 81 nM for biochemical FASN and cellular palmitate synthesis, respectively. TVB-3166 induces apoptosis, and inhibits in-vivo xenograft tumor growth[1].
IC50 & Target: IC50: 42 nM (FASN) and 81 nM (cellular palmitate synthesis)[1]
In Vitro: TVB-3166 (0.001-10 μM; 24 hours) causes cell death in CALU-6 non-small-cell lung tumor cells with a cellular IC50 value of 0.10 μM[1]. 
TVB-3166 (0.02 or 0.20 μM; 7 days) inhibits palmitate synthesis and tumor cell viability in a dose-dependent manner[1]. 
TVB-3166 (0.2 μM; 48 hours) inhibits β-catenin pathway signal transduction and transcriptional activity[1]. 
In Vivo: TVB-3166 (Oral gavage; 30-100 mg/kg/day) inhibits xenograft tumor growth[1]. 
TVB-3166 (Oral gavage; 30-100 mg/kg/day) has the concentration is approximately 3-fold higher in plasma than tumor. The 100 and 30 mg/kg groups had plasma and tumor concentrations of 7 and 2.9 μM, respectively[1].

Name: Ikarugamycin, CAS: 36531-78-9, stock 12.6g, assay 98.6%, MWt: 478.62, Formula: C29H38N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ikarugamycin is an antibiotic and a inhibitor of clathrin-mediated endocytosis (CME)[1].
IC50 & Target: Clathrin-mediated endocytosis[1]
In Vitro: Ikarugamycin has an IC50 of 2.7 μM in H1299 cells[1].

Name: D609, CAS: 83373-60-8, stock 11.1g, assay 98.9%, MWt: 266.46, Formula: C11H15KOS2, Solubility: DMSO : 100 mg/mL (375.29 mM; Need ultrasonic); H2O : 2 mg/mL (7.51 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phospholipase, Biological_Activity: D609 is a selective competitive inhibitor of phosphatidyl choline-specific phospholipase C (PC-PLC), with Ki of 6.4 μM, used for antiviral and antitumor research.
IC50 & Target: Ki: 6.4 μM (PC-PLC)

Name: Psicofuranine, CAS: 1874-54-0, stock 22.1g, assay 98%, MWt: 297.27, Formula: C11H15N5O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Bacterial;Parasite, Biological_Activity: Psicofuramine a nucleoside antibiotic and has the inhibition of xanthosine 5'-phosphate aminase. Psicofuranine also specifically inhibits GMP synthase, and interrupts parasite growth. Psicofuranine exhibits a dose-dependent inhibition of P. falciparum growth[1][2].
IC50 & Target: Xanthosine 5'-phosphate aminase[2] 
P. falciparum[1] 
E. coli[1]
In Vitro: Psicofuranine specifically inhibits bacterial GMP synthase as demonstrated by isolation of Psicofuranine-resistant Escherichia coli mutants with mutations in the gene encoding GMP synthase and inhibition of bacterial growth. Psicofuranine exhibits a dose-dependent inhibition of P. falciparum growth with an IC50 of 0.3 mM. The Psicofuranine inhibitory concentration is similar to that of E. coli[1].

Name: Terphenyllin, CAS: 52452-60-5, stock 36.7g, assay 98.2%, MWt: 338.35, Formula: C20H18O5, Solubility: DMSO : 83.33 mg/mL (246.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucosidase, Biological_Activity: Terphenyllin is a naturally abundant p-terphenyl metabolite isolated from the coral derived fungus Aspergillus candidus, has signiﬁcant α-glucosidase inhibitory activity[1].
IC50 & Target: α-glucosidase[1]

Name: Trofosfamide, CAS: 22089-22-1, stock 28.1g, assay 98.6%, MWt: 323.58, Formula: C9H18Cl3N2O2P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Trofosfamide is an orally bioavailable oxazaphosphorine derivative with antineoplastic activity[1].

Name: WRG-28, CAS: 1913291-02-7, stock 22.3g, assay 98.4%, MWt: 410.44, Formula: C21H18N2O5S, Solubility: DMSO : 17.86 mg/mL (43.51 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Discoidin Domain Receptor, Biological_Activity: WRG-28 is a selective, extracellularly acting DDR2 allosteric inhibitor with an IC50 of 230 nM. WRG-28 uniquely inhibits receptor-ligand interactions via allosteric modulation of the receptor. WRG-28 inhibits tumor invasion and migration, as well as tumor-supporting roles of the stroma, and inhibits metastatic breast tumor cell colonization in the lungs by targeting DDR2[1].

Name: Alizarin Red S (sodium) ARS (sodium), CAS: 130-22-3, stock 30.7g, assay 98.7%, MWt: 342.26, Formula: C14H7NaO7S, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alizarin Red S sodium (ARS sodium) is an anthraquinone dye that has been widely used to evaluate calcium deposits in cell culture[1].

Name: BMS-193885, CAS: 186185-03-5, stock 35.4g, assay 98.9%, MWt: 590.71, Formula: C33H42N4O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: BMS-193885 is a potent, selective, competitive, and brain penetrant neuropeptide Y1 receptor antagonist with a Ki of 3.3 nM, and has an IC50 of 5.9 nM for hY1, which displays > 100, > 160, > 160 and > 160-fold selectivity over α1, hY2, hY4 and hY5 receptors, respectively [1] [2].
IC50 & Target: Ki: 3.3 nM (Neuropeptide Y1 receptor)[1] 
IC50: 5.9 nM (hY1)[1]

Name: BMS-1001 (hydrochloride), CAS: 2113650-04-5, stock 9.7g, assay 98.6%, MWt: 631.11, Formula: C35H35ClN2O7, Solubility: DMSO : 12.5 mg/mL (19.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: PD-1/PD-L1, Biological_Activity: BMS-1001 hydrochloride is an orally active human PD-L1/PD-1 immune checkpoint inhibitor. BMS-1001 hydrochloride exhibits low-toxicity in cells[1].
IC50 & Target: PD-L1/PD-1[1].
In Vitro: BMS-1001 binds to human PD-L1 and blocks its interaction with PD-1. BMS-1001 presents low toxicity towards tested cell lines and block the interaction of soluble PD-L1 with the cell surface-expressed PD-1. BMS-1001 alleviates the inhibitory effect of the soluble PD-L1 on the T-cell receptor-mediated activation of T-lymphocytes[1].

Name: Luciferase, firefly, CAS: 61970-00-1, stock 11.1g, assay 98.9%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Luciferase, firefly is the light-emitting enzyme responsible for the bioluminescence of fireflies and click beetles.
In Vitro: Firefly luciferase is the light-emitting enzyme responsible for the bioluminescence of fireflies and click beetles. The enzyme catalyses the oxidation of firefly luciferin, requiring oxygen and ATP. Because of the requirement of ATP, firefly luciferases have been used extensively in biotechnology.

Name: (S,R,S)-AHPC-C4-NH2 (hydrochloride) VH032-C4-NH2 (hydrochloride);VHL Ligand-Linker Conjugates 13;E3 ligase Ligand-Linker Conjugates 28, CAS: 2245697-83-8, stock 11.8g, assay 98.9%, MWt: 566.16, Formula: C27H40ClN5O4S, Solubility: H2O : ≥ 50 mg/mL (88.31 mM); DMSO : ≥ 109.6 mg/mL (193.58 mM), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: (S,R,S)-AHPC-C4-NH2 hydrochloride is a synthesized E3 ligase ligand-linker conjugate that incorporates the (S,R,S)-AHPC based VHL ligand and a linker used for EED-Targeted PROTAC[1].

Name: PF-06873600, CAS: 2185857-97-8, stock 23.6g, assay 98%, MWt: 471.52, Formula: C20H27F2N5O4S, Solubility: DMSO : 83.33 mg/mL (176.73 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: PF-06873600 is a selective and orally bioavailable inhibitor of cyclin-dependent kinase (CDK), with Ki values of 0.09 nM, 0.13 nM and 0.16 nM for CDK2, CDK4 and CDK6, respectively. PF-06873600 has potential antineoplastic activity[1][2].
IC50 & Target: Ki: 0.09 nM (CDK2), 0.13 nM (CDK4), 0.16 nM (CDK6)[1].
In Vitro: PF-06873600 (Example 8) is an orally bioavailable, cyclin-dependent kinase (CDK) inhibitor, with potential antineoplastic activity[1]. PF-06873600 selectively targets, binds to and inhibits the activity of CDKs. Inhibition of these kinases leads to cell cycle arrest, induction of apoptosis and inhibition of tumor cell proliferation. CDKs, ATP-dependent serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation, are frequently overexpressed in tumor cells[2].

Name: RU.521 RU320521, CAS: 2262452-06-0, stock 6.4g, assay 98.7%, MWt: 415.23, Formula: C19H12Cl2N4O3, Solubility: DMSO : ≥ 125 mg/mL (301.04 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: RU.521 (RU320521) is a potent and selective cyclic GMP-AMP synthase (cGAS) inhibitor and inhibits cGAS-mediated interferon upregulation. RU.521 suppresses dsDNA-activated reporter activity with an IC50 of 700 nM. RU.521 reduces constitutive expression of interferon in macrophages from a mouse model of Aicardi-Goutières syndrome (AGS)[1].
IC50 & Target: IC50: 700 nM (dsDNA)[1]

Name: IRAK4-IN-4, CAS: 1850276-58-2, stock 5.7g, assay 98.6%, MWt: 340.37, Formula: C22H16N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Protein Tyrosine Kinase/RTK, Target: IRAK;IRAK, Biological_Activity: IRAK4-IN-4 is an interleukin-1 receptor–associated kinase 4 (IRAK4) inhibitor extracted from patent CN107163044A, Compound15, has an IC50 of 2.8 nM. IRAK4-IN-4 also inhibits cyclic GMP-AMP synthase (cGAS) with an IC50 of 2.1 nM[1].
IC50 & Target: IC50: 2.8 nM (IRAK4), 2.1 nM (cGAS)[1]

Name: PROTAC FAK degrader 1, CAS: 2301916-69-6, stock 16.7g, assay 98.2%, MWt: 996.13, Formula: C47H56F3N9O8S2, Solubility: DMSO : 200 mg/mL (200.78 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;PROTAC, Target: FAK;PROTAC, Biological_Activity: PROTAC FAK degrader 1 is a selective and potent focal adhesion kinase (Fak) degrader with an IC50 of 6.5 nM, DC50 of 3 nM[1].
IC50 & Target: IC50: 6.5 nM (Focal adhesion kinase) 
DC50: 3 nM (Focal adhesion kinase)[1]

Name: RIPK1-IN-7, CAS: 2300982-44-7, stock 39.1g, assay 99%, MWt: 481.47, Formula: C25H22F3N5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (129.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: RIP kinase, Biological_Activity: RIPK1-IN-7 is a potent and selective RIPK1 inhibitor with a Kd of 4 nM and an enzymatic IC50 of 11 nM. RIPK1-IN-7 exhibits excellent antimetastasis activity in the experimental B16 melanoma lung metastasis model[1].
IC50 & Target: IC50: 11 nM (RIPK1)[1] 
Kd: 4 nM (RIPK1)[1]
In Vitro: RIPK1-IN-7 shows potent cell protection effect in the TSZ-induced HT29 cell necroptosis model with an EC50 of 2nM[1]. 
RIPK1-IN-7 displays considerable activity against several other kinases, such as Flt4, TrkA, TrkB, TrkC, Axl, HRI, Mer, and MAP4K5 with IC50s of 20, 26, 8, 7, 35, 26, 29, and 27 nM, respectively[1].

Name: GLPG2451, CAS: 2055015-61-5, stock 3.9g, assay 98.4%, MWt: 419.38, Formula: C16H16F3N3O5S, Solubility: DMSO : 270 mg/mL (643.81 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Autophagy;Membrane Transporter/Ion Channel, Target: Autophagy;CFTR, Biological_Activity: GLPG2451 is a cystic fibrosis transmembrane conductance regulator (CFTR) potentiator, which effectively potentiates low temperature rescued F508del CFTR with an EC50 of 11.1 nM[1].
IC50 & Target: Cystic fibrosis transmembrane conductance regulator[1]
In Vitro: GLPG2451 has an EC50 value of 675 nM and an efficacy level of 147% of that of VX770 in G551D/F508del cells[1].

Name: ROCK inhibitor-2, CAS: 1127308-52-4, stock 16g, assay 98.9%, MWt: 332.40, Formula: C21H20N2O2, Solubility: DMSO : 250 mg/mL (752.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: ROCK;ROCK;ROCK, Biological_Activity: ROCK inhibitor-2 is a selective dual ROCK1 and ROCK2 inhibitor with IC50s of 17 nM and 2 nM, respectively[1].
IC50 & Target: IC50: 17 nM (ROCK1), 2 nM (ROCK2)[1]

Name: GW284543 UNC10225170, CAS: 790186-68-4, stock 37.2g, assay 98.7%, MWt: 372.42, Formula: C23H20N2O3, Solubility: DMSO : 125 mg/mL (335.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MEK, Biological_Activity: GW284543 (UNC10225170) is a selective MEK5 inhibitor. GW284543 (UNC10225170) reduces pERK5, and decreases endogenous MYC protein[1].

Name: Cetaben, CAS: 55986-43-1, stock 34g, assay 98.7%, MWt: 361.56, Formula: C23H39NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cetaben, an exceptional type of peroxisome proliferator, is a peroxisome proliferator-activated receptor α (PPARα)-independent peroxisome proliferator. Cetaben is a non-fibrate hypolipidemic drug and potently reduces the concentration of cholesterol and triglycerides[1][2].
In Vitro: Cetaben (10 µM; 24 hours) induces severe micromorphological and ultrastructural changes in HepG2 and MH1C1 cells. After treatment with 100 µM cetaben, cells contained several Golgi regions, most of them disintegrated into vesicles[2]. 
Cetaben-treated (10 µM; 24 hours) cells were characterized by a striking heterogeneity of the peroxisomal population with the occurrence of dumbbell-shaped and cup-shaped peroxisomal profiles in MH1C1cells[2]. 
In Vivo: Cetaben reveales a significant rise in the activities of peroxisomal enzymes in both the liver and kidney at doses of 50-100 mg/kg body over 10 days, but the maximal effect is observed at 250 mg/kg[1].

Name: Caracemide NSC-253272, CAS: 81424-67-1, stock 23.1g, assay 98.4%, MWt: 189.17, Formula: C6H11N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Cell Cycle/DNA Damage, Target: Bacterial;DNA/RNA Synthesis, Biological_Activity: Caracemide (NSC-253272) is a novel anticancer agent derived from a hydroxamic acid. Caracemide inactivates R1 by covalent modification at the substrate-binding site and inhibits the enzyme ribonucleotide reductase of Escherichia coli. Caracemide has demonstrated to produce severe central nervous system (CNS) toxicity. Caracemide has a toxic metabolite, methylisocyanate (MIC), in vivo[1][2].
In Vivo: The mercapturic acid derivative AMCC was identified in urine rats following administration to rats of a single i.p. dose (6.6 mg/kg) of caracemide (NSC-253272)[1]. .

Name: BX-912, CAS: 702674-56-4, stock 24.9g, assay 98.7%, MWt: 471.35, Formula: C20H23BrN8O, Solubility: DMSO : ≥ 100 mg/mL (212.16 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR, Target: Apoptosis;PDK-1, Biological_Activity: BX-912 is a direct, selective, and ATP-competitive PDK1 inhibitor (IC50=26 nM). BX-912 blocks PDK1/Akt signaling in tumor cells and inhibits the anchorage-dependent growth of a variety of tumor cell lines in culture or induces apoptosis[1].
IC50 & Target: IC50: 26 nM (PDK1)[1]
In Vitro: BX-912 promotes a block at the G2/M phase of the cell cycle in MDA-468 cells[1]. 
BX-912 binds to the ATP binding site of PDK1, and is 9-fold selective for PDK1 relative to PKA. BX-912 blocks PDK1 activity in PTEN-negative PC-3 cells. PTEN-negative PC-3 cells display constitutive activation of Akt which is reflected in high levels of the PDK1 product, phospho-Thr308-Akt[1]. 
BX-912 is identified in a coupled assay measuring PDK1- and PtdIns-3,4-P2-mediated Akt activation, which can detect inhibitors of PDK1, AKT2, or other steps critical for activation of AKT2[1].

Name: APX-115 Ewha-18278, CAS: 1395946-75-4, stock 38.6g, assay 98.2%, MWt: 315.80, Formula: C17H18ClN3O, Solubility: DMSO : ≥ 250 mg/mL (791.64 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: NADPH Oxidase, Biological_Activity: APX-115 (Ewha-18278) is a potent, orally active pan NADPH oxidase (Nox) inhibitor with Ki values of 1.08 μM, 0.57 μM, and 0.63 μM for Nox1, Nox2 and Nox4, respectively. APX-115 effectively prevents kidney injury[1].
IC50 & Target: Ki: 1.08 μM (Nox1), 0.57 μM (Nox2) and 0.63 μM (Nox4)[1]
In Vitro: APX-115 (5 μM; 60 min) almost completely suppresses high glucose-induced proinflammatory and profibrotic molecule expression in the mouse podocyte cell line[2]. 
In the kidney, APX-115 attenuates Nox gene upregulation and protein expression while improving inflammatory and fibrotic processes[2]. 
In Vivo: APX-115 (oral gavage; 60 mg/kg/day; for 12 weeks) significantly improves insulin resistance in diabetic mice[2]. 
APX-115 treatment decreases the urinary excretion of albumin and plasma creatinine levels[2].

Name: Daltroban BM-13505;SKF 96148, CAS: 79094-20-5, stock 29g, assay 98.9%, MWt: 353.82, Formula: C16H16ClNO4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Daltroban (BM-13505) is a selective and specific thromboxane A2 (TXA2) receptor antagonist. Daltroban increase intracellular calcium in vascular smooth muscle cells. Daltroban shows protective effect in reperfusion injury[1][2].
In Vivo: Daltroban (BM-13505) (1 mg/kg; i.v.; per hour) exerts protective effect in reperfusion injury following acute myocardial ischemia in cats[2]. 
In comparison with vehicle (physiological saline)-treated cats, Daltroban (20 mg/kg per hour i.v.) reduces the ischaemia-induced rise in the ST segment and prevented the development of a Q-wave in the ECG during reperfusion. Daltroban protects the myocardium from ischaemic injury and that this effect involves prevention of ischaemia-induced leukocytosis[3].

Name: DMNQ, CAS: 6956-96-3, stock 23.5g, assay 98.9%, MWt: 218.21, Formula: C12H10O4, Solubility: DMSO : 50 mg/mL (229.14 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), 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: DMNQ is a redox cycling agent that generates both superoxide and hydrogen peroxide intracellularly in a concentration dependent manner. DMNQ increases ROS generation[1].

Name: ARN-3236, CAS: 1613710-01-2, stock 19.6g, assay 98.7%, MWt: 336.41, Formula: C19H16N2O2S, Solubility: DMSO : 130 mg/mL (386.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Salt-inducible Kinase (SIK), Biological_Activity: ARN-3236 is an oral active and selective inhibitor of salt-inducible kinase 2 (SIK2), with IC50s of <1 nM, 21.63 nM and 6.63 nM for SIK2, SIK1 and SIK3, respectively. Has anti-cancer activity[1][2].
IC50 & Target: IC50: < 1 nM (SIK2)[1][2].
In Vitro: ARN-3236 inhibits SIK2 activity with an IC50 <1 nM[2]. 
ARN-3236 inhibits cell growth and increases NSC 125973 sensitivity in ovarian cancer cells[2].
In Vivo: ARN-3236 (60 mg/kg, orally) sensitizes ovarian cancer to NSC 125973 in vivo[2].

Name: Zidebactam WCK-5107, CAS: 1436861-97-0, stock 20.7g, assay 98.3%, MWt: 391.40, Formula: C13H21N5O7S, Solubility: H2O : 50 mg/mL (127.75 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Zidebactam (WCK-5107) is a potent β-lactamase inhibitor[1]. Zidebactam also is a penicillin-binding protein2 (PBP2) inhibitor with an IC50 of 0.26 μg/mL[2].
IC50 & Target: IC50: 0.26 μg/mL (P. aeruginosa PAO1 PBP2)[2]
In Vitro: Zidebactam (WCK-5107) inhibits WT Enterobacteriaceae with a MIC50 of 0.25 mg/L. Zidebactam alone exhibits variable activity when tested against E. coli (MIC50/90 0.12/0.12 mg/L) and Enterobacter spp. (MIC50/90 0.12/0.25 mg/L)[1].

Name: Chrysene, CAS: 218-01-9, stock 21.1g, assay 98.6%, MWt: 228.29, Formula: C18H12, Solubility: DMSO : 5 mg/mL (21.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chrysene is a high molecular weight (HMW), polycyclic aromatic hydrocarbon (PAH) known for its recalcitrance and carcinogenic properties[1].

Name: Aclacinomycin A hydrochloride Aclarubicin hydrochloride, CAS: 75443-99-1, stock 23.2g, assay 98.9%, MWt: 848.33, Formula: C42H54ClNO15, Solubility: DMSO : ≥ 125 mg/mL (147.35 mM), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: Proteasome;Topoisomerase, Biological_Activity: Aclacinomycin A hydrochloride (Aclarubicin hydrochloride), a fluorescent molecule and the first described non-peptidic inhibitor showing discrete specificity for the CTRL (chymotrypsin-like) activity of the 20S proteasome[1]. Aclacinomycin A hydrochloride is also a dual inhibitor of topoisomerase I and II[2]. An effective anthracycline chemotherapeutic agent for hematologic cancers and solid tumors[3].
IC50 & Target: 20S proteasome[1]. 
Topoisomerase I and II[2].

Name: Imrecoxib BAP-909, CAS: 395683-14-4, stock 36.8g, assay 98.8%, MWt: 369.48, Formula: C21H23NO3S, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Imrecoxib (BAP-909) is a novel and selective cyclooxygenase 2 (COX-2) inhibitor with an IC50 value of 18 nM, it also inhibits COX1- activity with an IC50 value of 115 nM. Imrecoxib (BAP-909) has anti-inflammatory effect[1].
In Vitro: Imrecoxib (BAP-909) (0.1-10 µM; 24 hours) decreases COX-2 mRNA level induced by PMA+LPS at a dose dependent manner in U937 cells[1].
In Vivo: Imrecoxib (BAP-909) (gastrointestinal administration; 5-20 mg/kg; 1 hour before carrageenan injection) inhibits carrageenan-induced acute inflammation, and the inhibitory effect is maximal at 4 hours[1].
Imrecoxib (BAP-909) (gastrointestinal administration; 5-20 mg/kg; started on day 7; 26 days) diminishes the secondary paw swelling and inhibits heat-inactivated BCG induced-inflammtory polyarthritis[1].

Name: delta-Valerobetaine, CAS: 6778-33-2, stock 23.8g, assay 98%, MWt: 159.23, Formula: C8H17NO2, Solubility: H2O : 125 mg/mL (785.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: delta-Valerobetaine is a precursor of trimethylamine N-oxide (TMAO).
In Vitro: The levels of delta-valerobetaine were by far higher in ruminant than in non-ruminant meat and, among ruminants, cattle present higher levels of the substance than sheep and goat. The levels of delta-valerobetaine in milk of ruminants are much lower than in their meat. However, delta-valerobetaine content in milk of ruminants is noticeably higher than that observed in non-ruminant milk. It is showed that incubation of ruminal fluid with labeled Nε-trimethyllysine leads to a rapid formation of labeled delta-valerobetaine[1].

Name: BI8622, CAS: 1875036-74-0, stock 22.8g, assay 98%, MWt: 426.51, Formula: C25H26N6O, Solubility: DMSO : 125 mg/mL (293.08 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: E1/E2/E3 Enzyme, Biological_Activity: BI8622 is a specific inhibitor of the ubiquitin ligase HUWE1 with an IC50 of 3.1 μM[1].
IC50 & Target: IC50: 3.1 μM (HUWE1)[1]
In Vitro: BI8622 induces HUWE1 ectopically expresses to abolish ubiquitination of MCL1 with an IC50 value of 6.8 μM in HeLa cells[1]. 
BI8622 suppresses colony formation of Ls174T cells with estimated IC50 value of 8.4 μM[1]. 
BI8622 (10 μM; 1-4 days) treatment retards passage of Ls174T cells through all phases of the cell cycle, with the effect being strongest for G1[1]. 
BI8622 (0-50 μM; 16 hours) retards the degradation of MCL1 in response to UV irradiation by inhibiting HUWE1 in HeLa cells[1]. 
BI8622 inhibits MYC-dependent transactivation in colorectal cancer cells[1].

Name: C25-140, CAS: 1358099-18-9, stock 19.2g, assay 98.2%, MWt: 457.57, Formula: C26H31N7O, Solubility: DMSO : ≥ 130 mg/mL (284.11 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Apoptosis, Target: E1/E2/E3 Enzyme;TNF Receptor, Biological_Activity: C25-140, a first-in-class, fairly selective TRAF6-Ubc13 inhibitor, directly binds to TRAF6, and blocks the interaction of TRAF6 with Ubc13. C25-140 lowers TRAF6 activity, reduces NF-κB activation, and combats autoimmunity[1].
IC50 & Target: TRAF6-Ubc13[1]
In Vitro: C25-140 dose-dependently impedes TRAF6-Ubc13 interaction[1]. 
C25-140 (10-30 μM; 2 hours) effectively reduces TRAF6-mediated ubiquitin chain formation[1]. 
C25-140 affects TNFα-induced phosphorylation of IκBα as well as NF-κB-induced target gene expression[1]. 
C25-140 efficiently inhibits IL-1β- and TNFα-mediated receptor signaling in the context of cytokine activation[1].
In Vivo: C25-140 (~1.5 mg/kg; topically to the shaved back and the right ear; twice daily for 6 days) ameliorates symptoms of autoimmune psoriasis in R 837-induced psoriasis mouse model[1]. 
C25-140 (6-14 mg/kg; given i.p.; twice daily for 14 days) shows a dose-dependent improvement of RA disease outcome in Collagen-induced arthritis (CIA) model[1].

Name: Dactolisib BEZ235;NVP-BEZ235, CAS: 915019-65-7, stock 20.2g, assay 98.4%, MWt: 469.54, Formula: C30H23N5O, Solubility: DMSO : 5.2 mg/mL (11.07 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR;Autophagy, Target: PI3K;mTOR;Autophagy, Biological_Activity: Dactolisib (BEZ235) is a dual pan-class I PI3K and mTOR kinase inhibitor with IC50s of 4 nM/5 nM/7 nM/75 nM, and 20.7 nM for p110α/p110γ/p110δ/p110β and mTOR, respectively. Dactolisib (BEZ235) inhibits both mTORC1 and mTORC2.
IC50 & Target: IC50: 4 nM (p110α), 5 nM (p110γ), 7 nM (p110δ), 75 nM (p110β), 20.7 nM (mTOR)[1] 
mTORC1, mTORC2[1]
In Vitro: Dactolisib (BEZ235) potently inhibits PI3K in an ATP Competitive Manner. Dactolisib (BEZ235) (250 nM) significantly reduced the phosphorylation levels of the mTOR activated kinase p70S6K. Dactolisib (BEZ235) also leads to a reduction of S235/S236P-RPS6 levels with an IC50 of 6.5 nM, suggesting that Dactolisib (BEZ235) can directly inhibit the mTOR kinase, as the kinase domain of mTOR is highly homologous to the one of class IA PI3K. The activity of Dactolisib (BEZ235) against mTOR is confirmed using a biochemical mTOR K-LISA assay (IC50, 20.7 nM)[1]. The IC50s of Dactolisib (BEZ235) for HCT116, DLD-1, and SW480 cell lines are 14.3±6.4, 9.0±1.5, and 12.0±1.6 nM, respectively[2].
In Vivo: Dactolisib (BEZ235) (45 mg/kg, p.o.) treatment induces colonic tumor regression in a GEM model for sporadic PIK3CA wild-type CRC[2]. Dactolisib (BEZ235) (45 mg/kg) is administered to MENX rats (n=2 each group) by oral gavage and animals are sacrificed 1 or 6 hours after treatment. Immunostains for P-AKT and P-S6 show considerable reduction of the two proteins, and particularly of P-S6, 6 hours after administration of Dactolisib (BEZ235) when compares with PEG-treated rats. At 6 hours after treatment, the pituitary adenomas of Dactolisib (BEZ235)-treated rats has a proteomic profile significantly different from the tumors of placebo-treated rats[3].

Name: (3-Carboxypropyl)trimethylammonium chloride γ-Butyrobetaine hydrochloride, CAS: 6249-56-5, stock 24.9g, assay 98.8%, MWt: 181.66, Formula: C7H16ClNO2, Solubility: DMSO : 30 mg/mL (165.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (3-Carboxypropyl)trimethylammonium chloride is angiopathic substance produced as an intermediary metabolite by gut microbiota that feed on carnitine in dietary red meat.
In Vivo: (3-Carboxypropyl)trimethylammonium chloride is produced as an intermediary metabolite by gut microbes of L-Carnitine to TMAO[1]. (3-Carboxypropyl)trimethylammonium chloride is implicated in arteriosclerosis and long-term cardiovascular death[2].

Name: Olutasidenib FT-2102, CAS: 1887014-12-1, stock 20g, assay 98.9%, MWt: 354.79, Formula: C18H15ClN4O2, Solubility: DMSO : 125 mg/mL (ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Isocitrate Dehydrogenase (IDH), Biological_Activity: Olutasidenib is a highly potent, selective inhibitor of mutant Isocitrate dehydrogenase 1 (IDH1) that could be used in the treatment of acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
IC50 & Target: IDH1[1].

Name: PROTAC BET degrader-2, CAS: 2093388-33-9, stock 19g, assay 98.9%, MWt: 770.84, Formula: C41H42N10O6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (64.86 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: PROTAC BET degrader-2 is a highly potent degrader of Bromodomain and Extra-Terminal (BET) proteins with an IC50 value of 9.6 nM in cell growth inhibition in the RS4;11 cells and capable of achieving tumor regression.
IC50 & Target: IC50: 9.6 nM (BET in the RS4;11 leukemia cell line)[1].
In Vitro: PROTAC BET degrader-2 (compound 25) is a highly potent degrader of Bromodomain and Extra-Terminal (BET) proteins with an IC50 value of 9.6 nM in cell growth inhibition in the RS4;11 cells and capable of achieving tumor regression[1].

Name: AZD3229 Tosylate, CAS: 2248003-71-4, stock 24.5g, assay 98.4%, MWt: 651.71, Formula: C31H34FN7O6S, Solubility: DMSO : ≥ 100 mg/mL (153.44 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Kit, Biological_Activity: AZD3229 Tosylate is a potent pan-KIT mutant inhibitor for the treatment of gastrointestinal stromal tumors.
IC50 & Target: KIT[1].
In Vitro: AZD3229 is a potent, pan-KIT mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant KIT driven Ba/F3 cell lines (GI50=1-50 nM). AZD3229 demonstrates potent single digit nM growth inhibition across a broad cell panel, with good margin to KDR-driven effects. Selectivity over KDR can be rationalised predominantly by the interaction of water molecules with the protein and ligand in the active site and its kinome selectivity is similar to the best of the approved GIST agents[1].

Name: USL311, CAS: 1373268-67-7, stock 35.9g, assay 98.8%, MWt: 422.57, Formula: C24H34N6O, Solubility: DMSO : 25 mg/mL (59.16 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: USL311 is a selective CXCR4 antagonist, with anti-tumor activity. USL311 prevents the binding of stromal-cell derived factor-1 (SDF-1 or CXCL12) to CXCR4[1].

Name: Se-Methylselenocysteine Methylselenocysteine;Se-Methylseleno-L-cysteine, CAS: 26046-90-2, stock 18.6g, assay 98.1%, MWt: 182.08, Formula: C4H9NO2Se, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Se-Methylselenocysteine, a precursor of Methylselenol, has potent cancer chemopreventive activity and anti-oxidant activity. Se-Methylselenocysteine is orally bioavailable, and induces apoptosis[1][2].
In Vitro: Se-Methylselenocysteine (100-400 μM; 3 days) induces apoptosis in SKOV-33 cells[1]. 
Se-Methylselenocysteine (100-400 μM; 3 days) induces caspase-3 mediated apoptosis[1].
In Vivo: Se-Methylselenocysteine (0.2 mg/mouse; p.o.; daily for 14 days) potentiates the antitumour activity of CDDP and Cyclophosphamide in nude mice bearing human FaDu and A253 head and neck xenografts[2]. 
Alzheimer's disease (AD) mice are treats with Se-Methylselenocysteine (0.75 mg/kg BW per day) in their drinking water for 10 months. Se-Methylselenocysteine reduces oxidative stress and neuro-inflammation; Se-Methylselenocysteine modulates the distribution and levels of several metal ions; Se-Methylselenocysteine decreases amyloid-β peptide (Aβ) generation by inhibiting the expression of its precursor protein APP and β-secretase (BACE1), and attenuates tau hyperphosphorylation and neurofibrillary tangles (NFT) formation via promoting protein phosphatase 2A (PP2A) activity, thereby preserving synaptic proteins and neuron activities and finally improving spatial learning and memory deficits in AD model mice[3].

Name: RGX-104 (free Acid), CAS: 610318-54-2, stock 28g, assay 98.2%, MWt: 596.08, Formula: C34H33ClF3NO3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 130 mg/mL (218.09 mM), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: LXR, Biological_Activity: RGX-104 free Acid is an orally bioavailable and potent liver-X nuclear hormone receptor (LXR) agonist that modulates innate immunity via transcriptional activation of the ApoE gene.
IC50 & Target: LXR[1]
In Vivo: Oral administration of RGX-104 (100 mg/kg, daily) to animals bearing palpable tumors significantly suppresses the growth of multiple cancer types. Co-administration of RGX-104 with anti-PD-1 is superior to administration of either RGX-104 or anti-PD-1 alone. Importantly, co-administration of RGX-104 with anti-PD-1 therapy is well tolerated by mice, with no overt signs of toxicity[1].

Name: LY3295668 AK-01, CAS: 1919888-06-4, stock 38.3g, assay 98.7%, MWt: 489.95, Formula: C24H26ClF2N5O2, Solubility: DMSO : 150 mg/mL (306.15 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: LY3295668 is a potent, orally active and highly specific Aurora-A kinase inhibitor, with Ki values of 0.8 nM and 1038 nM for AurA and AurB, respectively.
IC50 & Target: Ki: 0.8 nM (AurA)[1].
In Vitro: LY3295668 is a highly specific Aurora-A kinase inhibitor, with Ki values of 0.8 nM and 1038 nM for AurA and AurB, respectively. LY3295668, a highly specific AurA inhibitor, can kill Rb-deficient cancer cells at doses that have minimal effects on normal cells. In a kinome-wide survey, only 5 of 386 kinases are potently inhibited by LY3295668 (<10 nM)[1].

Name: HS-10296 hydrochloride, CAS: 2134096-03-8, stock 37g, assay 98.1%, MWt: 562.11, Formula: C30H36ClN7O2, Solubility: DMSO : 83.33 mg/mL (148.25 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: HS-10296 hydrochloride is an orally available and third-Generation inhibitor of epidermal growth factor receptor (EGFR)-activating mutations and T790M-resistant mutation with limited activity against wild-type EGFR.
IC50 & Target: EGFR[1].
In Vitro: HS-10296 hydrochloride is an orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity, which canbe used to treat NSCLC[1]. Additionaly, HS-10296 could also inhibit other EGFR sensitive mutations, including G719X, del19, L858R and L861Q[2].

Name: NXT629, CAS: 1454925-59-7, stock 14.6g, assay 98.8%, MWt: 609.78, Formula: C35H39N5O3S, Solubility: DMSO : 125 mg/mL (204.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: NXT629 is a potent, selective, and competitive PPAR-α antagonist, with an IC50 of 77 nM for human PPARα, shows high selectivity over other nuclear hormone receptor, such as PPARδ, PPARγ, ERβ, GR and TRβ, IC50s are 6.0, 15, 15.2, 32.5 and >100 μM, respectively[1]. NXT629 has potent anti-tumor activity and inhibits experimental metastasis of cancer cell in animal models[2].
In Vitro: NXT629 (Compound 33) is a potent, selective PPAR-α antagonist, with an IC50 of 77 nM for human PPARα, shows high selectivity over other nuclear hormone receptor, such as PPARδ, PPARγ, Erβ, GR and TRβ, IC50s are 6.0, 15, 15.2, 32.5 and >100 μM, respectively[1]. NXT629 also competitively inhibits mousse PPARα, PPARβ/δ and PPARγ, with IC50s of 2.3, 35.1, 6.9 μM, resepctively[2].
In Vivo: NXT629 (Compound 33; 30 mg/kg, i.p.) exhibits good pharmacokinetics in mouse, and significantly decreases Fgf21 (Fibroblast growth factor 21), a PPARα target gene in fasted mice[1]. 
NXT629 has poor oral bioavailability in mice and rats. NXT629 (30 mg/kg, i.p., daily for 6 weeks) delays growth of subcutaneous SKOV-3 tumors in nude mice, inhibits growth of subcutaneous B16F10 tumors in C57Bl/6 mice. NXT629 (30 mg/kg, i.p.) is weakly anti-angiogenic against FGF-induced angiogenesis. NXT629 (3, 30 mg/kg, i.p.) inhibits experimental metastasis of B16F10 melanoma cells to the mouse lung[2].

Name: Cbz-B3A, CAS: 1884710-81-9, stock 3.6g, assay 98.2%, MWt: 706.87, Formula: C35H58N6O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: mTOR, Biological_Activity: Cbz-B3A is a potent and selective inhibitor of mTORC1 signaling that appear to bind to ubiquilins 1, 2, and 4, and Cbz-B3A inhibits the phosphorylation of eIF4E-binding protein 1 (4EBP1).
IC50 & Target: mTORC1 signaling[1].
In Vitro: Cbz-B3A slows cellular growth of some human leukemia cell lines, but is not cytotoxic. 
Cbz-B3A has a larger effect on the phosphorylation of 4EBP1 than p70S6k compared to repamycin. Cbz-B3A inhibits mTOR through Ubiquilins. 
Cbz-B3A decreases the incorporation of [35S]methionine/cysteine into protein in a dose-dependent manner, with maximal inhibition of 68% observed at 10 μM, and an EC50 of ~3 μM.

Name: S55746 (hydrochloride) BLC201 (hydrochloride), CAS: 1448525-91-4, stock 36.1g, assay 98.4%, MWt: 747.28, Formula: C43H43ClN4O6, Solubility: 10 mM in H2O, Clinical_Informat: Phase 1, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: S55746 hydrochloride (BLC201 hydrochloride) is a potent, orally active and selective BCL-2 inhibitor, with a Ki of 1.3 nM and a Kd of 3.9 nM. S55746 hydrochloride (BLC201 hydrochloride) has antitumor activity with low toxicity[1].
IC50 & Target: Ki: 1.3 nM (BCL-2), 520 nM (BCL-XL)[1] 
Kd: 3.9 nM (BCL-2), 186 nM (BCL-XL)[1]
In Vitro: S55746 (0-1 μM) potently and selectively induces cell death[1]. 
S55746 selectively induces apoptosis through BCL-2 inhibition in a BAX/BAK-dependent manner[1].
In Vivo: S55746 is a highly efficacious and well-tolerated (even at doses up to 300 mg/kg) orally active BCL-2 inhibitor [1]. 
S55746 (20-100 mg/kg, p.o.) inhibits xenograft growth in RS4;11 and Toledo models time- and dose-dependently[1].

Name: CP-532623, CAS: 261947-38-0, stock 15.4g, assay 98%, MWt: 598.50, Formula: C27H27F9N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: CETP, Biological_Activity: CP-532623 is a CETP inhibitor and elevates high-density lipoprotein cholesterolion. CP-532623 is a close structural analogue of Torcetrapib. CP-532623 has highly lipophilic properties[1][2][3].
IC50 & Target: CETP[1]
In Vitro: CP-532623 is highly lymphatically transported (28% of dose), and lymphatic transport is closely correlated with drug affinity for ex-vivo lymph lipoproteins or triglyceride emulsions and poorly relates to solubility in mixtures of lipoprotein core and/or surface lipids. CP-532623 alters the kinetics of lymph lipid transport and decreases lymph lipid transport in chylomicrons[2].
In Vivo: CP-532623 (50 mg; oral administration; adult male greyhound dogs) treatment substantially transports into the lymphatic system (>25% dose) in fed and fasted dogs. Food enhances oral bioavailability (from 44 to 58%, respectively) and the proportion of the absorbed dose transports via the lymph (from 61 to 86% and from 68 to 83%, respectively). Lymphatic triglyceride transport is significantly lower in fed dogs administered CP-532623[3].

Name: Pictilisib GDC-0941, CAS: 957054-30-7, stock 29.6g, assay 98.1%, MWt: 513.64, Formula: C23H27N7O3S2, Solubility: DMSO : ≥ 100 mg/mL (194.69 mM), Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR;Apoptosis;Autophagy, Target: PI3K;Apoptosis;Autophagy, Biological_Activity: Pictilisib (GDC-0941) is a potent inhibitor of PI3Kα/δ with an IC50 of 3 nM, with modest selectivity against p110β (11-fold) and p110γ (25-fold).
IC50 & Target: IC50: 3 nM (PI3Kα), 3 nM (PI3Kδ)[5]
In Vitro: Pictilisib (GDC-0941) and RP-56976 reduce tumor cell viability by 80% or greater in the breast cancer cell lines than single-agent treatment. GDC-0941 inhibits Akt phosphorylation and downstream targets of Akt signaling such as pPRAS40 and pS6 in Hs578T1.2 (PI3Kα wild-type), MCF7-neo/HER2 (PI3Kα-mutant), and MX-1 (PTEN-null) tumor models. Pictilisib (GDC-0941) decreases the time of RP-56976-induced mitotic arrest prior to apoptosis[1]. Pictilisib (GDC-0941) shows a high efficacy of antitumor activity in two ZD1839-resistant non-small cell lung cancer (NSCLC) cell lines, A549 and H460. Pictilisib (GDC-0941) is highly efficacious in combination with U0126 in inducing cell growth inhibition, G0-G1 arrest and cell apoptosis. H460 cells with activating mutations of PIK3CA are relatively more sensitive to Pictilisib (GDC-0941) than A549 cells with wild-type PIK3CA[3]. Pictilisib (GDC-0941) reduces PI3K pathway activity in both cell lines, illustrated by decreased pAK. Pictilisib (GDC-0941) significantly reduces secreted VEGF detected in the medium after hypoxic/anoxic exposure in all cells[4].
In Vivo: Pictilisib (GDC-0941) (150 mg/kg, p.o.) leads to tumor stasis in MCF7-neo/HER2-bearing animals model. Pictilisib (GDC-0941) and RP-56976 result in tumor regressions during the treatment period leading to enhanced antitumor responses[1]. Tumours in the Pictilisib (GDC-0941)-treated mice show a marked non-linear shrinkage, and when the Pictilisib (GDC-0941) treatment ceased, the tumours in the test cohort mice grow again[2]. Pictilisib (GDC-0941) (25 or 50 mg/kg) reduces tumor growth and PI3K and HIF-1 pathway activity in eGFP-FTC133 tumor-bearing mice[4].

Name: (-)-(S)-B-973B, CAS: 2244989-34-0, stock 21.7g, assay 98.7%, MWt: 452.50, Formula: C24H26F2N6O, Solubility: DMSO : 67.5 mg/mL (149.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: (-)-(S)-B-973B is a potent allosteric agonist and positive allosteric modulator of α7 nAChR, with antinociceptive activity[1].
IC50 & Target: α7 nAChR[1]

Name: MC180295 (rel)-MC180295, CAS: 2237942-08-2, stock 30.5g, assay 98.5%, MWt: 358.41, Formula: C17H18N4O3S, Solubility: DMSO : 100 mg/mL (279.01 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: MC180295 ((rel)-MC180295) is a potent and selective CDK9-Cyclin T1 inhibitor, with an IC50 of 5 nM, at least 22-fold more selective for CDK9 over other CDKs. MC180295 also inhibits GSK-3α and GSK-3β. MC180295 ((rel)-MC180295) has potent anti-tumor effect[1].
IC50 & Target: IC50: 5 nM (CDK9-Cyclin T1), 138 nM (CDK1-Cyclin B), 233 nM (CDK2-Cyclin A), 367 nM (CDK2-Cyclin E), 399 nM (CDK3-Cyclin E), 112 nM (CDK4-Cyclin D), 159 nM (CDK5-P35), 186 nM (CDK5-P25), 712 nM (CDK6-Cyclin D3), 555 nM (CDK7-CycH/MAT1)[1]
In Vitro: MC180295 is a potent and selective CDK9-Cyclin T1 inhibitor, with an IC50 of 5 nM, at least 22-fold more selective for CDK9 over other CDKs, such as CDK1-Cyclin B (IC50, 138 nM), CDK2-Cyclin A (IC50, 233 nM), CDK2-Cyclin E (IC50, 367 nM), CDK3-Cyclin E (IC50, 399 nM), CDK4-Cyclin D (IC50, 112 nM), CDK5-P35 (IC50, 159 nM), CDK5-P25 (IC50, 186 nM), CDK6-Cyclin D3 (IC50, 712 nM), and CDK7-CycH/MAT1 (IC50, 555 nM). MC180295 also inhibits GSK-3α and GSK-3β[1]. 
MC180295 (500 nM) reactivates epigenetically silenced genes by targeting CDK9 without affecting DNA methylation[1]. 
MC180295 (0.1 μM) inhibits the proliferation in cancer cells[1].
In Vivo: MC180295 (20 mg/kg, i.p., qod) inhibits significant anti-tumor activity in mice bearing SW48 cells, shows no inhibitory activity against human T cell growth in vivo[1].

Name: TAS-115 mesylate TAS-115 methanesulfonate, CAS: 1688673-09-7, stock 27.4g, assay 98.5%, MWt: 614.66, Formula: C28H27FN4O7S2, Solubility: DMSO : 75 mg/mL (122.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;VEGFR, Biological_Activity: TAS-115 mesylate is a potent VEGFRand hepatocyte growth factor receptor (c-Met/HGFR)-targeted kinase inhibitor, with IC50s of 30 and 32 nM for rVEGFR2 and rMET, respectively.
IC50 & Target: IC50: 30 nM (rVEGFR2), 32 nM (rMET)[1]
In Vitro: TAS-115 powerfully suppresses the VEGF-dependent proliferation of HUVECs (IC50=0.019 μM) as a VEGFR-targeted inhibitor and powerfully suppresses the proliferation of MET-amplified cancer cells (GI50=0.032-0.362 μM) as a MET-targeted inhibitor. TAS-115 has much less toxicity in various normal cell lines when compared with other VEGFR-targeted kinase inhibitors[1]. Crizotinib and TAS-115 inhibit Met phosphorylation and reverse erlotinib resistance and VEGF production triggered by HGF in PC-9 and HCC827 cells[2].
In Vivo: TAS-115 completely suppresses the progression of MET-inactivated tumor by blocking angiogenesis without toxicity when given every day for 6 weeks, even at a serum-saturating dose of TAS-115. TAS-115 induces marked tumor shrinkage and prolonges survival in MET-amplified human cancer–bearing mice[1].

Name: Fluorofenidone AKF-PD, CAS: 848353-85-5, stock 5.5g, assay 98.5%, MWt: 203.21, Formula: C12H10FNO, Solubility: DMSO : 140 mg/mL (688.94 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fluorofenidone (AKF-PD), an analogue of AMR69, shows equivalent antifibrotic activity, lower toxicity and longer half-life. Fluorofenidone (AKF-PD) attenuates the progression of renal interstitial fibrosis partly by suppressing NADPH oxidase and extracellular matrix (ECM) deposition via the PI3K/Akt signalling pathway[1][2].

Name: BI-167107, CAS: 1202235-68-4, stock 37.6g, assay 98.7%, MWt: 370.44, Formula: C21H26N2O4, Solubility: DMSO : 75 mg/mL (202.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: BI-167107 is a high affinity, full agonist that binds to the β2 adrenergic receptor (β2AR) with a dissociation constant Kd of 84 pM[1].
IC50 & Target: Kd: 84 pM (β2AR)[1]
In Vitro: Compared to other βAR ligands, BI-167107 displays nanomolar affinities and slow off-rates[1].

Name: Diacetoxyscirpenol, CAS: 2270-40-8, stock 13.1g, assay 98.3%, MWt: 366.41, Formula: C19H26O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diacetoxyscirpenol (DAS) is a trichothecene mycotoxin, a secondary metabolite product of fungi. Diacetoxyscirpenol (DAS) consumption induces haematological disorders (neutropenia, aplastic anemia) in human and animals[1].

Name: PXS-5153A, CAS: 2125956-82-1, stock 6.5g, assay 98%, MWt: 475.41, Formula: C20H25Cl2FN4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: PXS-5153A is a potent, selective, orally active and fast-acting lysyl oxidase like 2/3 enzymatic (LOXL2/LOXL3) inhibitor, with an IC50 of <40 nM for LOXL2 across all mammalian species and an IC50 of 63 nM for human LOXL3. PXS-5153A could reduce crosslinks and ameliorates fibrosis.
IC50 & Target: IC50: <40 nM (LOXL2 across all mammalian species), 63 nM (human LOXL3)[1].
In Vitro: PXS-5153A exhibits an IC50 of <40 nM for LOXL2 across all mammalian species tested. PXS-5153A also inhibits human LOXL3 with an IC50 value of 63 nM. PXS-5153A is >40-fold selective for LOXL2 over both LOX and LOXL1 and >700-fold selective over other related amine oxidases. PXS-5153A is a fast acting inhibitor, with enzymatic activity almost entirely blocked within 15 minutes [1].
In Vivo: As expected, rhLOXL2 dose-dependently induce oxidation of collagen with PXS-5153A dose-dependently impeding collagen oxidation. Therapeutic treatment of PXS-5153A substantially reduces immature crosslink formation compared with the CCl4 treated animals. Mature crosslink formation is also reduced by PXS-5153A treatment. All groups with therapeutic treatment of PXS-5153A show a significant reduction in DHLNL formation compared to the CCl4 treated animals. Treatment with PXS-5153A causes a significantly reduction in HYP compared to the CCl4 group. In addition, the amount of fibrillar collagen is markedly augmented by disease as seen by the 2.2-fold increase in percentage coverage area by Picrosirius red staining, which is reduced by PXS-5153A[1].

Name: Carebastine, CAS: 90729-42-3, stock 12.9g, assay 98.2%, MWt: 499.64, Formula: C32H37NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: Carebastine is the active metabolite of Ebastine. Carebastine is a histamine H1 receptor antagonist. Carebastine inhibits VEGF-induced HUVEC and HPAEC proliferation, migration and angiogenesis in a dose-dependent manner[1]. Carebastine suppresses the expression of macrophage migration inhibitory factor[2].
IC50 & Target: Histamine H1 receptor[1]

Name: Halofuginone (hydrobromide) RU-19110 (hydrobromide), CAS: 64924-67-0, stock 38.7g, assay 98.1%, MWt: 495.59, Formula: C16H18Br2ClN3O3, Solubility: DMSO : 50 mg/mL (100.89 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Stem Cell/Wnt;TGF-beta/Smad;Cell Cycle/DNA Damage, Target: TGF-beta/Smad;TGF-beta/Smad;DNA/RNA Synthesis, Biological_Activity: Halofuginone hydrobromide (RU-19110 hydrobromide) is a less-toxic form of Febrifugine, which is isolated from the plant Dichroa febrifuga[1]. Halofuginone inhibits prolyl-tRNA synthetase in an ATP-dependent manner with a Ki of 18.3 nM[2]. Halofuginone attenuates osteoarthritis (OA) by inhibition of TGF-β activity[3].
IC50 & Target: Ki: 18.3±0.5 nM (prolyl-tRNA synthetase)[2]
In Vitro: Halofuginone competitively inhibits prolyl-tRNA synthetase by occupying both the prolineand tRNA-binding pockets of prolyl-tRNA synthetase[1]. 
The IC50s of Halofuginone (1, 10, 100, 1000, 10000 nM; 48 hours) are 114.6 and 58.9 nM in KYSE70 and A549 cells, respectively. 
The IC50s of Halofuginone (1, 10, 100, 1000 nM; 24 hours) for NRF2 protein are 22.3 and 37.2 nM in KYSE70 and A549 cells, respectively. The IC50 of Halofuginone for global protein synthesis is 22.6 and 45.7 nM in KYSE70 and A549 cells, respectively[1]. 
In Vivo: Halofuginone (0.2, 0.5, 1 or 2.5 mg/kg; injected intraperitoneally every other day for 1 month) attenuates progression of OA in anterior cruciate ligament transection (ACLT) mice. Lower concentration (0.2 or 0.5 mg/kg) has minimal effects on subchondral bone and higher concentration (2.5 mg/kg) induces proteoglycan loss in articular cartilage[3]. 
Halofuginone (0.25 mg/kg; intraperitoneally injected; every day; 16 days) decreases NRF2 protein levels in tumors. While the tumor volumes do not change substantially between treatments with the vehicle, Halofuginone (0.25 mg/kg, intraperitoneally injected, every day) or cisplatin alone. Combined treatment with Halofuginone and Cisplatin significantly suppresses the tumor volume compared to treatment with Halofuginone or cisplatin alone[1].

Name: Lodenafil Hydroxyhomosildenafil, CAS: 139755-85-4, stock 36.2g, assay 98.1%, MWt: 504.60, Formula: C23H32N6O5S, Solubility: DMSO : ≥ 250 mg/mL (495.44 mM), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Lodenafil is a potent phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (ED)[1].
IC50 & Target: PDE5[1].

Name: PF-06305591, CAS: 1449473-97-5, stock 0.9g, assay 98.7%, MWt: 274.36, Formula: C15H22N4O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: PF-06305591 is a potent and highly selective voltage gated sodium channel NaV1.8 blocker, with an IC50 of 15 nM. An excellent preclinical in vitro ADME and safety profile[1].
IC50 & Target: IC50: 15 nM (NaV1.8)[1].
In Vitro: PF-06305591 (compound 9) has a highly attractive profile with respect to NaV selectivity, hERG activity, passive permeability and in vitro metabolic stability[1].
In Vivo: PF-06305591 (compound 9) has good rat bioavailability. PF-06305591 offers the possibility of investigating higher IC50 multiples of Nav1.8 blockade in the clinic, and therefore a more thorough evaluation of the role of NaV1.8 in the treatment of pain[1].

Name: S26131, CAS: 296280-56-3, stock 18.7g, assay 98.4%, MWt: 498.61, Formula: C31H34N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melatonin Receptor;Melatonin Receptor, Biological_Activity: S26131 (compound 5) is a potent and selective MT1 melatoninergic ligand, and the Ki values are 0.5 and 112 nM for MT1 and MT2, respectively. S26131 behaves as an MT1 and MT2 antagonist[1].
In Vitro: S26131 behaves as an antagonist on MT1 and MT2 receptors with KB values of 5.32 and 143 nM, respectively[1].

Name: CCB02, CAS: 2100864-57-9, stock 18.8g, assay 98.2%, MWt: 235.24, Formula: C14H9N3O, Solubility: DMSO : 20 mg/mL (85.02 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: CCB02 is a selective CPAP-tubulin interaction inhibitor, binding to tubulin and competing for the CPAP binding site of β-tubulin, with an IC50 of 689 nM, and shows potent anti-tumor activity. CCB02 shows no inhibition on the cell cycle- and centrosome-related kinases, or the phosphorylation status of Aurora A, Plk1, Plk2, CDK2, and CHK1[1].
IC50 & Target: IC50: 689 nM (CPAP-tubulin)[1]
In Vitro: CCB02 perturbs CPAP PN2-3-tubulin interaction with an IC50 of 0.441 μM in a PN2-3 CPAP-GST pull-down assay[1]. 
CCB02 shows no inhibition on the cell cycle- and centrosome-related kinases, or the phosphorylation status of Aurora A, Plk1, Plk2, CDK2, and CHK1[1]. 
CCB02 (0.1-15 μM, 72 hours) inhibits the proliferation of cancer cells with extra centrosomes, IC50s are 0.86-2.9 μM[1]. 
CCB02 activates spindle assembly checkpoint, induces PCM proteins recruitment to centrosomes, and enhances microtubule nucleation activities of centrosomes[1].
In Vivo: CCB02 (30 mg/kg, p.o. daily for 24 days) shows potent anti-tumor effect in nude mice bearing subcutaneous human lung (H1975T790M cells) tumor xenografts[1]. 
CCB02 also suppresses MDA-MB-231 cell migration and cuases multipolar mitosis in mouse xenografts[1].

Name: Pictilisib (dimethanesulfonate) GDC-0941 (dimethanesulfonate) ;GDC-0941 (2 MeSO3H salt), CAS: 957054-33-0, stock 29.7g, assay 98.6%, MWt: 705.85, Formula: C25H35N7O9S4, Solubility: DMSO : 50 mg/mL (70.84 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR;Autophagy, Target: PI3K;Autophagy, Biological_Activity: Pictilisib dimethanesulfonate (GDC-0941 dimethanesulfonate) is a potent inhibitor of PI3Kα/δ with IC50 of 3 nM, with modest selectivity against p110β (11-fold) and p110γ (25-fold).
IC50 & Target: IC50: 3 nM (PI3Kα), 3 nM (PI3Kδ)[5]
In Vitro: Pictilisib (GDC-0941) and RP-56976 reduce tumor cell viability by 80% or greater in the breast cancer cell lines than single-agent treatment. GDC-0941 inhibits Akt phosphorylation and downstream targets of Akt signaling such as pPRAS40 and pS6 in Hs578T1.2 (PI3Kα wild-type), MCF7-neo/HER2 (PI3Kα-mutant), and MX-1 (PTEN-null) tumor models. Pictilisib (GDC-0941) decreases the time of RP-56976-induced mitotic arrest prior to apoptosis[1]. Pictilisib (GDC-0941) shows a high efficacy of antitumor activity in two ZD1839-resistant non-small cell lung cancer (NSCLC) cell lines, A549 and H460. Pictilisib (GDC-0941) is highly efficacious in combination with U0126 in inducing cell growth inhibition, G0-G1 arrest and cell apoptosis. H460 cells with activating mutations of PIK3CA are relatively more sensitive to Pictilisib (GDC-0941) than A549 cells with wild-type PIK3CA[3]. Pictilisib (GDC-0941) reduces PI3K pathway activity in both cell lines, illustrated by decreased pAK. Pictilisib (GDC-0941) significantly reduces secreted VEGF detected in the medium after hypoxic/anoxic exposure in all cells[4].
In Vivo: Pictilisib (GDC-0941) (150 mg/kg, p.o.) leads to tumor stasis in MCF7-neo/HER2-bearing animals model. Pictilisib (GDC-0941) and RP-56976 result in tumor regressions during the treatment period leading to enhanced antitumor responses[1]. Tumours in the Pictilisib (GDC-0941)-treated mice show a marked non-linear shrinkage, and when the Pictilisib (GDC-0941) treatment ceased, the tumours in the test cohort mice grow again[2]. GDC-0941Pictilisib (GDC-0941) (25 or 50 mg/kg) reduces tumor growth and PI3K and HIF-1 pathway activity in eGFP-FTC133 tumor-bearing mice[4].

Name: COH000, CAS: 1534358-79-6, stock 34.9g, assay 98.8%, MWt: 419.47, Formula: C25H25NO5, Solubility: DMSO : 35.71 mg/mL (85.13 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: E1/E2/E3 Enzyme, Biological_Activity: COH000 is an allosteric, covalent and irreversible inhibitor of ubiquitin-like 1-activating enzyme (SUMO-activating enzyme) (E1), with an IC50 of 0.2 μM for SUMOylation in vitro[1].
IC50 & Target: IC50: 0.2 μM (SUMO-activating enzyme)[1].
In Vitro: COH000 has over 500-fold selectivity for SUMOylation than ubiquitylation. COH000 inhibits SUMO adenylation without directly competing with ATP or SUMO1 binding. COH000 has an extremely slow off-rate and is consistent with it being covalently bound to the enzyme[1].

Name: A1874, CAS: 2064292-12-0, stock 37.1g, assay 98.7%, MWt: 1173.59, Formula: C58H62Cl3F2N9O7S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (127.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: A1874 is a nutlin-based and BRD4-degrading PROTAC with a DC50 of 32 nM (induce BRD4 degradation in cells). Effective in inhibiting many cancer cell lines proliferation[1].
IC50 & Target: DC50: 32 nM (induce BRD4 degradation in cells)[1].
In Vitro: Treatment of HCT116 cells of A1874 (0-10 μM, 24 hours) induces a dose-dependent knockdown of BRD4 levels, with near-maximum knockdown by 100 nmol/L and a maximum degradation (Dmax) of BRD4 of 98% of the levels in control (0.1% DMSO-treated) cells[1]. 
Treatment of HCT116 cells of A1874 (0-10 μM, 24 hours) increases p53 levels in the HCT116 cells and showed dose-dependent p53 stabilization[1].

Name: Actein, CAS: 18642-44-9, stock 9.5g, assay 99%, MWt: 676.83, Formula: C37H56O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: JNK;Apoptosis;Akt;Autophagy, Biological_Activity: Actein is a triterpene glycoside isolated from the rhizomes of Cimicifuga foetida. Actein suppresses cell proliferation, induces autophagy and apoptosis through promoting ROS/JNK activation, and blunting AKT pathway in human bladder cancer. Actein has little toxicity in vivo[1][2].

Name: MD-224, CAS: 2136247-12-4, stock 11.3g, assay 98.8%, MWt: 889.80, Formula: C48H43Cl2FN6O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Apoptosis;PROTAC, Target: E1/E2/E3 Enzyme;MDM-2/p53;PROTAC, Biological_Activity: MD-224 is a first-in-class and highly potent small-molecule human murine double minute 2 (MDM2) degrader based on the proteolysistargeting chimera (PROTAC) concept. MD-224 induces rapid degradation of MDM2 at concentrations <1 nM in human leukemia cells, and achieves an IC50 value of 1.5 nM in inhibition of growth of RS4;11 cells. MD-224 has the potential to be a new class of anticancer agent[1].
In Vitro: MD-224 (1-30 nM; 2 hours) effectively induces depletion of MDM2 protein and concurrently accumulation of p53 protein in a dose-dependent manner in RS4;11 cells[1].
MD-224 (30 nM; 6 hours) is more potent than MI-1061 in induction of transcriptional upregulation of these p53 target genes but have no effect on TP53 itself in RS4;11 cells[1].
MD-224 (0.001-1 μM; 24 hours) induces robust apoptosis at ≤10 nM in a dose-dependent manner upon a 24 hours treatment[1].

Name: Trifloxystrobin CGA 279202, CAS: 141517-21-7, stock 21.8g, assay 98.9%, MWt: 408.37, Formula: C20H19F3N2O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (306.09 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Trifloxystrobin (CGA 279202) is a fungicide, with EC50s of 23.0 μg/L and 1.7 μg/L for Daphnia magna neonate and embryos, respectively, after treatment for 48 h[1].
IC50 & Target: EC50: 23.0 μg/L (Daphnia magna neonate), 1.7 μg/L (Daphnia magna embryos)[1]

Name: DPM-1001, CAS: 1471172-27-6, stock 10.2g, assay 98.5%, MWt: 567.85, Formula: C35H57N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: DPM-1001 is a potent, specific, orally bioavailable and non-competitive inhibitor of protein-tyrosine phosphatase (PTP1B) with an IC50 of 100 nM, an an analog of the specific PTP1B inhibitor trodusquemine (MSI-1436; IC50=600 nM). DPM-1001 has anti-diabetic property[1].
IC50 & Target: IC50: 100 nM (PTP1B)[1]

Name: S-Nitroso-N-acetyl-DL-penicillamine SNAP, CAS: 67776-06-1, stock 17.7g, assay 98.2%, MWt: 220.25, Formula: C7H12N2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: S-Nitroso-N-acetyl-DL-penicillamine (SNAP) is a nitric oxide donor and acts as a stable inhibitor of platelet aggregation[1][2][3][4].
In Vitro: S-Nitroso-N-acetyl-DL-penicillamine (10 mM; 8 hours) induces toxicity of about 80% after 6 hours under normoxic conditions by releasing nitric oxide (NO)[1]. 
S-Nitroso-N-acetyl-DL-penicillamine has a half-time about 6 hours in in isolated rat ventricular myocytes[3]. 
S-Nitroso-N-acetyl-DL-penicillamine (100 µM; 30 minutes) causes sustained decrease in the basal pHi in isolated rat ventricular myocytes[3]. 
In Vivo: SNAP (100μM, 300μM) causes small but significant increases of the electrically evoked [3H]-acetylcholine release in guinea-pig tracheal[4].

Name: SGC-GAK-1, CAS: 2226517-76-4, stock 19.7g, assay 98.2%, MWt: 389.24, Formula: C18H17BrN2O3, Solubility: DMSO : ≥ 125 mg/mL (321.14 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SGC-GAK-1 is a potent, selective cyclin G-associated kinase (GAK) inhibitor with a Ki of 3.1 nM. SGC-GAK-1 is a chemical probe for GAK[1].
IC50 & Target: Ki: 3.1 nM (GAK)[1]
In Vitro: SGC-GAK-1 potently binds cyclin G-associated kinase (GAK), adaptor protein 2-associated kinase (AAK1), serine/threonine kinase 16 (STK16) with Kis of 3.1 nM, 53 µM, 51 µM, respectively[1]. 
SGC-GAK-1 potently binds cyclin G-associated kinase (GAK), receptor-interacting protein kinase 2 (RIPK2), AarF domain containing kinase 3 (ADCK3), and nemo-like kinase (NLK) with KDs of 1.9 nM, 110 nM, 190 nM, and 520 nM, respectively[1]. 
SGCGAK-1 (0.1, 1, and 10 µM, 48 hours or 72 hours) shows strong growth inhibition in LNCaP, VCaP, and 22Rv1 cells at 10 µM, but minimal effect in PC3 and DU145 cells[1].

Name: TAK-071, CAS: 1820812-16-5, stock 15.3g, assay 98.8%, MWt: 421.46, Formula: C24H24FN3O3, Solubility: DMSO : 135 mg/mL (320.32 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: TAK-071 is a novel, potent and highly selective muscarinic acetylcholine receptor 1 (M1R) positive allosteric modulator. EC50 of TAK-071 M1R agonist activities is 520 nM[1].
IC50 & Target: EC50: 520 nM (M1R)[1]
In Vivo: TAK-071 increase hippocampal inositol monophosphate production through M1R activation and improved DB00747
-induced cognitive deficits in rats at 0.3 mg/kg[1].
TAK-071 also induce diarrhea at 10 mg/kg in rats[1].
Combining sub-effective doses of TAK-071 (3 mg/kg) with an acetylcholinesterase inhibitor significantly ameliorates DB00747-induced cognitive deficits in rats[1].

Name: ML367, CAS: 381168-77-0, stock 0.1g, assay 98.6%, MWt: 334.32, Formula: C19H12F2N4, Solubility: DMSO : ≥ 125 mg/mL (373.89 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ML367 is a potent inhibitor of ATPase family AAA domain-containing protein 5 (ATAD5) stabilization, acts as a probe molecule that has low micromolar inhibitory activity. ML367 blocks DNA repair pathways, suppresses general DNA damage responses including RPA32-phosphorylation and CHK1-phosphorylation in response to UV irradiation[1].
IC50 & Target: ATAD5[1]
In Vitro: ML367 (0-40 μM, 16 hours) inhibits FLAG-ATAD5 stabilization in HEK293T cells in the presence or absence of 20 μM 5-FUrd[1].

Name: JHU-083, CAS: 1998725-11-3, stock 35.5g, assay 98.7%, MWt: 312.36, Formula: C14H24N4O4, Solubility: DMSO : 100 mg/mL (320.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glutaminase, Biological_Activity: JHU-083 is a selective glutaminase antagonist. JHU-083 blocks glutaminase activity in brain CD11b+ cells and experimental cerebral malaria (ECM) resulting in a net decrease of glutamate levels in the animals[1][2].
IC50 & Target: Glutamine[2]

Name: (+)-Penbutolol (R)-Penbutolol;(+)-Isopenbutolol, CAS: 38363-41-6, stock 19.6g, assay 99%, MWt: 291.43, Formula: C18H29NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: (+)-Penbutolol is a β-adrenoceptor antagonist, with an IC50 of 0.74 μM[1]. (+)-Penbutolol is an optical isomer of l-penbutolol with Na+ channel-blocking action[2].
IC50 & Target: IC50: 0.74 μM (β-adrenoceptor)[1].
In Vitro: (+)-penbutolol on the [Ca2+]i-increase induced by LPC is concentration-dependent[1]. 
(+)-penbutolol inhibits the rounding of cells dose dependently (8±4%, 56±4% and 66±2% at the concentrations of 10-6 M, 5×10-6 M and 10-5 M, respectively)[2].

Name: CGP 36742 SGS-742, CAS: 123690-78-8, stock 36.2g, assay 98.4%, MWt: 179.20, Formula: C7H18NO2P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: CGP 36742 is a selective GABAB receptor antagonist that can penetrate the blood–brain barrier after peripheral administration, with an IC50 of 32 μM. CGP 36742 is useful in treatment of depression[1].
IC50 & Target: IC50: 32 μM (GABAB)[1]

Name: Enocitabine, CAS: 55726-47-1, stock 5.4g, assay 98.9%, MWt: 565.78, Formula: C31H55N3O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA Stain, Biological_Activity: Enocitabine, a nucleoside analog, is a potent DNA replication inhibitor and a DNA chain terminator. Enocitabine can be used as an effective chemotherapeutic agent for the treatment of acute myelogenous leukaemia and lymphocytic leukaemias[1].
IC50 & Target: IC50: DNA replication[1]

Name: Resorufin NSC 12097, CAS: 635-78-9, stock 9.6g, assay 98.8%, MWt: 213.19, Formula: C12H7NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Resorufin (NSC 12097) is a highly fluorescent pink dye.

Name: CYT-1010, CAS: 213769-33-6, stock 38.5g, assay 98.8%, MWt: 624.73, Formula: C35H40N6O5, Solubility: DMSO : 125 mg/mL (200.09 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: CYT-1010 is a mu-opioid receptor agonist extracted from patent WO2013173730A2, with EC50s of 13.1 nM and 0.0053 nM on beta-arrestin recruitment and inhibition of cAMP production, respectively[1].
IC50 & Target: EC50: 13.1 nM (beta-arrestin), 0.0053 nM (cAMP)[1]

Name: ZK824859, CAS: 2271122-53-1, stock 1.1g, assay 98.7%, MWt: 428.43, Formula: C23H22F2N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: PAI-1, Biological_Activity: ZK824859 is an oral available and selective urokinase plasminogen activator (uPA) inhibitor with IC50s of 79 nM, 1580 nM and 1330 nM for human uPA, tPA, and plasmin, respectively[1].
IC50 & Target: IC50: 79 nM (human uPA), 1580 nM (human tPA), 1330 nM (human plasmin)[1].
In Vitro: ZK824859 is 5 fold less potent and has lost selectivity in mouse: uPA IC50=410 nM; tPA IC50=910 nM; plasmin IC50=1600 nM compared to human IC50 values of 79 nM, 1580 nM and 1330 nM respectively[1].
In Vivo: ZK824859 (50, 25 and 10 mg/kg; b.i.d.; 25 days) is used in a chronic mouse EAE model. ZK 824859 completely prevents the development of disease. However, two lower doses (25 and 10 mg/kg) have no effect on clinical scores[1].

Name: Ibrutinib-MPEA, CAS: 1710768-30-1, stock 6.6g, assay 98%, MWt: 581.71, Formula: C32H39N9O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ibrutinib-MPEA (Compound 20) is ibrutinib derivative. Ibrutinib is a covalent and irreversible inhibitor of Bruton's tyrosine kinase (BTK) that has been used to treat haematological malignancies[1].

Name: ZSTK474, CAS: 475110-96-4, stock 0.3g, assay 98.2%, MWt: 417.41, Formula: C19H21F2N7O2, Solubility: DMSO : 2 mg/mL (4.79 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR;Autophagy;Autophagy, Target: PI3K;Autophagy;Autophagy, Biological_Activity: ZSTK474 is an ATP-competitive pan-class I PI3K inhibitor with IC50s of16 nM, 44 nM, 4.6 nM and 49 nM for PΙ3Κα, PI3Kβ, PI3Kδ and PI3Kγ, respectively.
IC50 & Target: IC50: 16 nM (PI3Kα), 44 nM (PI3Kβ), 4.6 nM (PI3Kδ), 49 nM (PI3Kγ)[1]
In Vitro: Lineweaver-Burk plot analysis revealed that ZSTK474 inhibits all four PI3K isoforms in an ATP-competitive manner. The Ki values determined for the four PI3K isoforms showed that ZSTK474 inhibited the PI3Kδ isoform most effectively with a Ki of 1.8 nM, whereas the other isoforms are inhibited with 4-10-fold higher Ki values. Therefore, ZSTK474 should be regarded as a pan-PI3K inhibitor. We also determined the IC50 values for inhibiting the four PI3K isoforms with ZSTK474 and LY294002. The IC50 values of ZSTK474 (16, 44, 4.6 and 49 nM for PI3Kα, PI3Kβ, PI3Kδ and PI3Kγ, respectively) are shown to be consistent with the Ki values (6.7, 10.4, 1.8 and 11.7 nM for PI3Kα, PI3Kβ, PI3Kδ and PI3Kγ, respectively), which further supported the idea that ZSTK474 inhibits PI3Kδ most potently. Even at a concentration of 100 µM, ZSTK474 inhibits mTOR activity rather weakly[1].
In Vivo: In mice subjected to MCAO, treatment with ZSTK474 is tested at dosages of 50, 100, 200, and 300 mg/kg. Since the 200 mg/kg dose produces significant improvement and no obvious toxic effects (P<0.01), mice are treated with ZSTK474 at a dose of 200 mg/kg/day daily for three post-MCAO days during the remaining experiments of this study. Neurological function is examined in mice suffered from MCAO followed by 24, 48, and 72 h of reperfusion. In the ZSTK474 group, neurological function scores are significantly better than the control group except the corner test[2].

Name: Patulin Terinin, CAS: 149-29-1, stock 24.6g, assay 98.5%, MWt: 154.12, Formula: C7H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Patulin (Terinin) is a mycotoxin produced by fungi including the Aspergillus, Penicillium, and Byssochlamys species, is suspected to be clastogenic, mutagenic, teratogenic and cytotoxic. Patulin (Terinin) induces autophagy-dependent apoptosis through lysosomal-mitochondrial axis, and causes DNA damage[1][2][3][4].

Name: Kinase inhibitor-1, CAS: 2135696-72-7, stock 37.7g, assay 98.8%, MWt: 461.74, Formula: C19H18BrClN6O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (216.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kinase inhibitor-1 (Compound 5) is a kinase inhibitor[1].
IC50 & Target: Kinase[1]
In Vitro: Kinases represent a large family of enzymes that catalyse the phosphorylation of proteins, lipids and metabolites and play a central role in the regulation of a wide variety of cellular processes. Abnormal kinase activity has been related to a wide range of disorders, including cancers[1].

Name: IU1-47, CAS: 670270-31-2, stock 10.8g, assay 98.2%, MWt: 330.85, Formula: C19H23ClN2O, Solubility: DMSO : 16.67 mg/mL (50.39 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: IU1-47 is a potent and specific USP14 inhibitor with an IC50 of 0.6 μM. IU1-47 inhibits IsoT/USP5 with an IC50 of 20 μM. IU1-47 induces tau elimination in cultured neurons[1].
IC50 & Target: IC50: 0.6 μM (USP14), 20 μM (IsoT/USP5)[1]
In Vitro: IU1-47 is essentially inactive on free USP14 (USP14 that is not bound to the proteasome). IU1-47 (25 μM) antagonizes USP14 deubiquitinating activity and stimulates substrate degradation in vitro[1]. 
IU1-47 stimulates tau degradation principally via the ubiquitin-proteasome system. IU1-47 (3 μM, 10 and 30 μM; 48 hours) significantly decreases Tau and phosphotau species Ser-202/Thr-205 levels in murine cortical primary neurons. The level of USP14 itself does not change[1].

Name: DLK-IN-1, CAS: 1620574-24-4, stock 10.4g, assay 98.1%, MWt: 423.43, Formula: C20H24F3N5O2, Solubility: DMSO : 62.5 mg/mL (147.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MAP3K, Biological_Activity: DLK-IN-1 is a selective, orally active inhibitor of dual leucine zipper kinase (DLK, MAP3K12), with a Ki of 3 nM. DLK-IN-1 retains excellent CNS penetration and is well tolerated following multiple days of dosing at concentrations that exceed those required for DLK inhibition in the brain. DLK-IN-1 has activity in a model of Alzheimer’s Disease.
IC50 & Target: Ki: 3 nM (DLK)[1].

Name: Glutaminase-IN-1 CB839 derivative, CAS: 2247127-79-1, stock 1.5g, assay 98.1%, MWt: 618.47, Formula: C26H24F3N7O3Se, Solubility: DMSO : 125 mg/mL (202.11 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glutaminase, Biological_Activity: Glutaminase-IN-1 (CB839 derivative), a CB839 derivative, is an allosteric inhibitor of 1,3,4-selenadiazole-containing kidney-type glutaminase (KGA), with an IC50 of 1 nM. Glutaminase-IN-1 (CB839 derivative) shows improved cellular uptake and antitumor activity.
IC50 & Target: IC50: 1 nM (KGA)[1].
In Vitro: Glutaminase-IN-1 (CPD20), a CB839 derivative, is an allosteric inhibitor of 1,3,4-selenadiazole-containing kidney-type glutaminase (KGA), with an IC50 of 1 nM. Glutaminase-IN-1 shows improved cellular uptake and antitumor activity. The IC50 values of Glutaminase-IN-1 are 17 nM, 6.78 μM, 19 nM and 9 nM in A549, H2, Caki-1 and HCT116 cell lines, respectively. Glutaminase-IN-1 has better KGA inhibitory activity than the corresponding BPTES and CB839[1].
In Vivo: Glutaminase-IN-1(10 mg/kg, s.c.) reduced the size and weight of the HCT116 tumor, and statistical analysis showed that the 40% reduction in tumor weight by CPD20 is statistically significant. Glutaminase-IN-1 could statistically significantly prolong the survival of H22-bearing mice[1].

Name: Cyclosporin A-Derivative 1 (Free base), CAS: 286852-20-8, stock 22g, assay 98.5%, MWt: 1276.69, Formula: C65H117N11O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cyclosporin A-Derivative 1 (Free base) is a crystalline intermediate derived from the opening of cyclosporin A extracted from patent WO 2013167703 A1. Cyclosporin A is an immunosuppressive agent which can bind to the cyclophilin and inhibit calcineurin.
In Vitro: Cyclosporin A-Derivative 1 is a non-immunosuppressive Cyclosporin A derivative. The cyclosporin is acylated on the butenyl-methyl-threonine side chain and then subjected to a ring-opening reaction (the ring opens between the sarcosine and the N-methyl-leucine residues). Cyclosporin A-Derivative 1 is a linear peptide intermediate[1].

Name: Triphala, CAS: 857906-76-4, stock 21.9g, assay 99%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;NF-κB, Target: Fungal;NF-κB, Biological_Activity: Triphala, an Ayurvedic polyherbal formulation comprising of equiproportional fruit parts of Terminalia chebula, Terminalia bellerica, and Phyllanthus emblica[1]. Triphala inhibits NF-κB activation. Triphala exerts antifungal action[2]. Anti-adipogenic, anti-inflammatory, and anti-neoplastic activities.
IC50 & Target: NF-κB[2] 
Antifungal[2]
In Vitro: Triphala regulates adipogenesis through modulation of expression of adipogenic genes in 3T3-L1 cell line. Triphala significantly decreases the adipogenesis in 3T3-L1 cells by reducing lipid accumulation and inhibiting the expression of adipogenic genes. The 3T3-L1 cells treated with Triphala show ~1.43-, 1.67-, and 2.5-fold decreases in lipid content at 1, 10, and 100 μg/mL concentrations, respectively, compared to the cells treated with induction cocktail alone. Triphala regulates lipid accumulation by down regulating expression of adipogenic genes, resulting into prevention of adipogenesis[1]. 
Triphala reduces expression of inflammatory mediators such as IL-17, COX-2, and RANKL through inhibition of NF-κB activation[2].
Triphala exerts antifungal action against Asperigillus species and has been reported to inhibit the fungus by up to 37.96% in vitro[2].

Name: Enocyanin, CAS: 11029-12-2, stock 11.3g, assay 98.5%, MWt: 1000, Formula: N/A, Solubility: DMSO : ≥ 50 mg/mL; H2O : 5 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Enocyanin is an anthocyanin extracted from grapes. Enocyanin shows inhibitory effect on the leucine aminopeptidase, acid phosphatase, γ-glutamyl transpeptidase and esterase activity[1].
IC50 & Target: Acid phosphatase[1]
In Vitro: Enocyanin (0.1%) affects the leucine aminopeptidase, acid phosphatase, γ-glutamyl transpeptidase and esterase activity by 63%, 100%, 134% and 99%, respectively[1].

Name: CDK4/6-IN-2, CAS: 1800506-48-2, stock 31g, assay 98.6%, MWt: 506.59, Formula: C27H32F2N8, Solubility: DMSO : 5.2 mg/mL (10.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CDK4/6-IN-2 is a potent CDK4 and CDK6 inhibitor extracted from patent US20180000819A1, Compound 1, has IC50s of 2.7 and 16 nM for CDK4 and CDK6, respectively[1].
In Vitro: CDK4/6-IN-2 inhibits H358, H441, PC3, MV-4-11, JeKo-1, SW780, and HGC-27 cells with IC50s of 290.9, 147.8, 260.5, 139, 36.98, 162.5, and 316.4 nM, respectively[1].

Name: CCG-222740, CAS: 1922098-69-8, stock 16.8g, assay 98.8%, MWt: 444.86, Formula: C23H19ClF2N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage;GPCR/G Protein, Target: ROCK;ROCK;ROCK;Ras, Biological_Activity: CCG-222740 is a potent and selective Rho/myocardin-related transcription factor (MRTF) pathway inhibitor[1]. CCG-222740 also is a potent inhibitor of alpha-smooth muscle actin protein expression. CCG-222740 effectively reduces fibrosis in skin and blocks melanoma metastasis[2].
IC50 & Target: Rho/MRTF pathway[1]
In Vitro: CCG-222740 (10, 20 μM; for 72 hours) increases the protein levels of p27 and decreased cyclin D1. CCG-222740 decreases cell viability of CAFs, with an IC50 of ~10 μM[1]. 
CCG-222740 (10, 25 μM) is potent at decreasing αSMA protein expression in human conjunctival fibroblasts[2]. 
CCG-222740 has an IC50 of 5 μM in a fibroblast-mediated collagen contraction assay, and it is less cytotoxic[2]. 
In Vivo: CCG-222740 (Oral gavage; 100 mg/kg daily for 7 days) significantly reduces α-SMA levels in the pancreas of caerulein-stimulated KC mice[1].

Name: 6-Hydroxy-4-methylcoumarin, CAS: 2373-31-1, stock 20.4g, assay 98.1%, MWt: 176.17, Formula: C10H8O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-Hydroxy-4-methylcoumarin (compound 9) is a coumarins secondary metabolites and has anticancer activity[1].

Name: 1-beta-D-Arabinofuranosyluracil Uracil 1-β-D-arabinofuranoside, CAS: 3083-77-0, stock 1.4g, assay 98.9%, MWt: 244.20, Formula: C9H12N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1-beta-D-Arabinofuranosyluracil (Uracil 1-β-D-arabinofuranoside) isolated from the Caribbean sponge Tectitethya crypta, is a methoxyadenosine derivative. 1-beta-D-Arabinofuranosyluracil has demonstrated a diverse bioactivity profile including anti-inflammatory activity, analgesic and vasodilation properties[1]. 1-beta-D-Arabinofuranosyluracil reduces a proliferation of mouse lymphoma cells[2].

Name: 2-Phenylethylamine (hydrochloride), CAS: 156-28-5, stock 6.7g, assay 98.5%, MWt: 157.64, Formula: C8H12ClN, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2-Phenylethanamine hydrochloride is believed to function as a neuromodulator or neurotransmitter.
In Vitro: 2-Phenylethanamine (PEA) is soluble in water, ethanol, and ether. Phenethylamine is a skin irritant and possible sensitizer. 2-Phenylethanamine is believed to function as a neuromodulator or neurotransmitter (a trace amine). It is also found in many foods such as chocolate, especially after microbial fermentation. 2-Phenylethanamine is a precursor to the neurotransmitter phenylethanolamine. High levels of 2-Phenylethanamine have been found in the urine of schizophrenics but it is not significantly elevated in the serum or CSF of schizophrenics[1][2]. Urinary levels of 2-Phenylethanamine are significantly lower in children with attention deficit hyperactivity disorder. 2-Phenylethanamine is useful for scaring off rodent pests[3].

Name: N,N'-Diacetyl-L-cystine DiNAC; (Ac-Cys-OH)2, CAS: 5545-17-5, stock 29.6g, assay 98.2%, MWt: 324.37, Formula: C10H16N2O6S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N,N'-diacetyl-L-cystine (DiNAC) is the disulphide dimer of N-acetylcysteine with immunomodulating properties. N,N'-diacetyl-L-cystine is a potent, orally active modulator of contact sensitivity/delayed type hypersensitivity reactions in rodents. N,N'-diacetyl-L-cystine also has antiatherosclerotic effects in Watanabe-heritable hyperlipidemic rabbit (WHHL) rabbits[1][2].
IC50 & Target: Immunomodulator[1]
In Vivo: N,N'-Diacetyl-L-cystine (DiNAC; 0-973.11 μg/kg; oral administration; daily; for 12 weeks; WHHL rabbits) treatment reduces by 50% thoracic aorta atherosclerosis, without affecting plasma lipid levels[1].

Name: HS-1371, CAS: 2158197-70-5, stock 1.9g, assay 98.9%, MWt: 384.47, Formula: C24H24N4O, Solubility: DMSO : 16.67 mg/mL (43.36 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: RIP kinase, Biological_Activity: HS-1371 is a potent and ATP-competitive receptor-interacting protein kinase 3 (RIP3) inhibitor with an IC50 of 20.8 nM[1].
IC50 & Target: IC50: 20.8 nM (RIP3)[1]
In Vitro: HS-1371 directly binds to RIP3 in an ATP-competitive and time-independent manner. HS-1371 has an inhibitory effect on RIP3 kinase activity in various cell lines[1].
HS-1371 (0.1, 1, 5, 10, 20 μM, 9 h) can block RIP3 S227 phosphorylation[1].
HS-1371 (0.1, 1, 5, 10 μM, 24 h) rescues cells from RIP3-dependent necroptotic cell death but not apoptotic cell death[1].

Name: DDX3-IN-1, CAS: 1919828-83-3, stock 17.2g, assay 98.9%, MWt: 307.35, Formula: C17H17N5O, Solubility: DMSO : 125 mg/mL (406.70 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: HIV;HCV, Biological_Activity: DDX3-IN-1 (Compound 16f) is a DEAD-box polypeptide 3 (DDX3) inhibitor with CC50s of 50 and 36 μM for HIV and HCV, respectively. Antiviral activity[1].

Name: Valnoctamide Valmethamide, CAS: 4171-13-5, stock 5.4g, assay 98.8%, MWt: 143.23, Formula: C8H17NO, Solubility: DMSO : ≥ 100 mg/mL (698.18 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Valnoctamide (Valmethamide), a derivative of valproate, suppresses benzodiazepine-refractory status epilepticus. Valnoctamide (Valmethamide) acts directly on GABAA receptors[1].
IC50 & Target: GABAA receptor[1]

Name: BAY-8002, CAS: 724440-27-1, stock 11.2g, assay 98%, MWt: 415.85, Formula: C20H14ClNO5S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (300.59 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Monocarboxylate Transporter, Biological_Activity: BAY-8002 is a potent, selective, orally active inhibitor of monocarboxylate transporter 1 (MCT1), with an IC50 of 85 nM in the MCT1-expressing DLD-1 cells, displays excellent selectivity against MCT4. Anti-tumor activity[1].
IC50 & Target: IC50: 85 nM (MCT1, in DLD-1 cells)[1]
In Vitro: BAY-8002 is an inhibitor of MCT1, with an IC50 of 85 nM in the MCT1-expressing DLD-1 cells, displays excellent selectivity against MCT4 (IC50 >50 µM in EVSA-T cells)[1].
In Vivo: BAY-8002 (80 and 160 mg/kg, p.o., twice daily, for more than 26 days) significantly inhibits tumor growth in Raji tumor-bearing mice[1].

Name: Glucovanillin, CAS: 494-08-6, stock 9.3g, assay 98.8%, MWt: 314.29, Formula: C14H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Glucovanillin extracted from green pods and simultaneously transformed to vanillin by a combination of enzyme activities involving cell wall degradation and glucovanillin hydrolysis.

Name: L-Eflornithine L-DFMO;L-RMI71782;L-α-difluoromethylornithine, CAS: 66640-93-5, stock 14.6g, assay 98.6%, MWt: 182.17, Formula: C6H12F2N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: L-Eflornithine (L-DFMO) is an enantiomer of Eflornithine. L-Eflornithine is an irreversible ornithine decarboxylase (ODC) inhibitor with a KD of 1.3±0.3 µM, and a Kinact of 0.15±0.03 min-1[1].
IC50 & Target: KD:1.3±0.3 µM (Ornithine decarboxylase, ODC)[1]
In Vitro: Eflornithine (D/L-DFMO) is an inhibitor of ODC, the first enzyme in eukaryotic polyamine biosynthesis. Both enantiomers of Eflornithine (DFMO) irreversibly inactivate ODC. Both Eflornithine enantiomers (L-Eflornithine and D-Eflornithine) suppress ODC activity in a time- and concentration-dependent manner. The inhibitor dissociation constant (KD) values for the formation of enzyme-inhibitor complexes are 28.3±3.4, 1.3±0.3 and 2.2±0.4 µM respectively for D-Eflornithine, L-Eflornithine and Eflornithine. The inhibitor inactivation constants (Kinact) for the irreversible step were 0.25±0.03, 0.15±0.03 and 0.15±0.03 min-1 respectively for D-Eflornithine, L-Eflornithine and Eflornithine. Treatment of human colon tumour-derived HCT116 cells with either L-Eflornithine or D- Eflornithine decreases the cellular polyamine contents in a concentration-dependent manner[1]. The enantiomers display different potencies in vitro, with the L-enantiomer having up to a 20-fold higher affinity for the target enzyme ornithine decarboxylase[2]. 
The L-Eflornithine also appears to be more potent in cultured T.brucei gambiense parasites[2]. 
In Vivo: The more potent L-Eflornithine is present at much lower concentrations in both plasma and cerebrospinal fluid (CSF) than those of the D-Eflornithine. The plasma concentrations of L-Eflornithine are on average 52% of the D-enantiomer concentrations. The typical oral clearances of L-Eflornithine and D-eflornithine are 17.4 and 8.23 liters/h, respectively[2].

Name: Ertugliflozin L-pyroglutamic acid PF-04971729 L-pyroglutamic acid, CAS: 1210344-83-4, stock 40g, assay 98%, MWt: 566.00, Formula: C27H32ClNO10, Solubility: DMSO : ≥ 125 mg/mL (220.85 mM), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel, Target: SGLT, Biological_Activity: Ertugliflozin L-pyroglutamic acid (PF-04971729 L-pyroglutamic acid) is a potent, selective and orally active inhibitor of the sodium-dependent glucose cotransporter 2 (SGLT2), with an IC50 of 0.877 nM for h-SGLT2[1]. A drug for the treatment of type 2 diabetes mellitus[2].
IC50 & Target: IC50: 0.877 nM (h-SGLT2)[1].
In Vitro: Ertugliflozin L-pyroglutamic acid (PF-04971729 L-pyroglutamic acid) demonstrates >2000-fold selectivity for SGLT2 inhibition (relative to SGLT1) in vitro[3].
In Vivo: Ertugliflozin L-pyroglutamic acid (PF-04971729 L-pyroglutamic acid) reveals a concentration-dependent glucosuria after oral administration to rats[3].

Name: OSMI-4, CAS: 2260791-14-6, stock 20.7g, assay 98.7%, MWt: 604.09, Formula: C27H26ClN3O7S2, Solubility: DMSO : 62.5 mg/mL (103.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: OSMI-4 is a low nanomolar O-GlcNAc transferase (OGT) inhibitor, with an EC50 of 3 μM in cells.
IC50 & Target: EC50: 3 μM (OGT)[1].
In Vitro: OSMI-4 (4b) is the best OGT inhibitor reported to date, with a ∼3 μM EC50 in cells, making it especially attractive for probing OGT’s complex biology[1].

Name: DL-alpha-Tocopherol methoxypolyethylene glycol succinate TPGS-750-M, CAS: 1309573-60-1, stock 35.9g, assay 98.3%, MWt: 1000, Formula: (C2H4O)nC34H56O5, Solubility: H2O : ≥ 50 mg/mL, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DL-alpha-Tocopherol methoxypolyethylene glycol succinate solution (TPGS-750-M) is an amphiphile, acts as a surfactant[1].

Name: SRI 31215 (TFA), CAS: 1832686-44-8, stock 32.9g, assay 98.6%, MWt: 533.59, Formula: C27H34F3N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR, Biological_Activity: SRI 31215 (TFA), a triplex inhibitor of matriptase, hepsin and hepatocyte growth factor activator (HGFA) with IC50s of 0.69 μM, 0.65 μM, 0.3 μM, blocks pro-HGF activation and thus mimics the activity of HAI-1/2[1].
IC50 & Target: IC50: 0.69 μM (matriptase), 0.65 μM (hepsin), 0.3 μM (HGFA)[1]

Name: Tafenoquine (Succinate) WR 238605 (Succinate), CAS: 106635-81-8, stock 32.9g, assay 98%, MWt: 581.58, Formula: C28H34F3N3O7, Solubility: DMSO : 125 mg/mL (214.93 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Tafenoquine Succinate (WR 238605 Succinate) is an 8-aminoquinoline. Tafenoquine is an anti-malarial prophylactic agent[1].
IC50 & Target: Anti-malarial[1]
In Vivo: Tafenoquine exhibits no anti-malarial activity in CYP 2D knock-out mice when dosed at their ED100 values (3 mg/kg) established in WT mice. Tafenoquine anti-malarial activity is partially restored in humanized/CYP 2D6 knock-in mice when tested at two times its ED100 (6 mg/kg)[1].

Name: AS-605240, CAS: 648450-29-7, stock 4.7g, assay 98.4%, MWt: 257.27, Formula: C12H7N3O2S, Solubility: DMSO : 5.8 mg/mL (22.54 mM; Need warming), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Autophagy, Target: PI3K;Autophagy, Biological_Activity: AS-605240 is a specific and orally active inhibitor of the PI3Kγ, with an IC50 of 8 nM, and a Ki of 7.8 nM.
IC50 & Target: IC50: 8 nM (PI3Kγ), 60 nM (PI3Kα), 270 nM (PI3Kβ), 300 nM (PI3Kδ)[2] Ki: 7.8 nM (PI3Kγ)[2]
In Vitro: AS-605240 is an isoform-selective inhibitor of PI3Kγ with over 30-fold selectivity for PI3Kδ and β, and 18- and 7.5-fold selectivity over PI3Kα, respectively. AS-605240 shows an inhibitory effect on C5a-mediated PKB phosphorylation in RAW264 mouse macrophages with an IC50 of 0.09 μM. AS-605240 blocks PKB phosphorylation induced by MCP-1 and has little or no effect after stimulation with CSF-1. AS-605240 inhibits MCP-1-mediated phosphorylation of PKB and its downstream substrates GSK3α and β in a concentration-dependent manner. AS605240 suppresses in a dose-dependent manner the proliferation of BDC2.5 CD4+ T cells[2].
In Vivo: AS-605240 (30 mg/kg BW, per os, every 12 h) markedly decreases FoxM1 expression in mouse lungs and fails to restore vascular integrity[1]. AS-605240 reduces RANTES-induced peritoneal neutrophil recruitment, with ED50 of 9.1 mg/kg. In the CCL5 model, AS-605240 shows an ED50 value of 10 mg/kg, in correlation with the percentage of reduction of neutrophil recruitment observed in Pik3cg-/- mice. AS-605240 (50 mg/kg, p.o.) substantially reduces clinical and histological signs of joint inflammation to a similar extent to that of Pik3cg-/- mice[2]. AS605240 (30 mg/kg, i.p.) suppresses intracellular PAkt in splenocytes of NOD mice and delays diabetes onset. AS605240 also prevents autoimmune diabetes in prediabetic NOD mice, and suppresses autoreactive T cells while increasing Tregs in NOD mice. AS605240 (30 mg/kg, i.p.) reverses hyperglycemia in newly hyperglycemic NOD mice, reverses hyperglycemia in early diabetic NOD mice through Tregs and suppresses T-cell infiltration in pancreatic islets while increasing Tregs[3]. AS605240 (25, 50 mg/kg) markedly reduces total cell count and numbers of macrophages, neutrophils and lymphocytes in rats. AS605240 significantly reduces the levels of TNF-α and IL-1β in BALF to 132.7±11.2 pg/mL and 49.2±11.3 pg/mL in 25 mg/kg AS605240 + BLM group and 131.3±10.7 and 49.6±8.8 pg/mL in 50 mg/kg AS605240 + BLM group, respectively. AS605240 inhibits prefibrotic cytokines production in bleomycin-induced pulmonary fibrosis. AS605240 inhibits phosphorylation of Akt of inflammatory cells in bleomycin-induced pulmonary fibrosis model[4].

Name: TAS-114, CAS: 1198221-21-4, stock 14.5g, assay 98.6%, MWt: 451.54, Formula: C21H29N3O6S, Solubility: DMSO : 100 mg/mL (221.46 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: TAS-114 is a dual dUTPase/dihydropyrimidine dehydrogenase (DPD) inhibitor, can improving the therapeutic efficacy of fluoropyrimidine[1].
IC50 & Target: dUTPase, DPD
In Vitro: TAS-114 (1-10 μM; 72 hours) increases the cytotoxicity of 5-Fluorouracil (5-FU) and 5-FU,2′-deoxy-5-fluorouridine (FdUrd) against various cancer cell lines in dose-dependent manner[1]. 
In Vivo: TAS-114 (37.5-1,200 mg/kg/day; orally; 1-14 days) increases the antitumor activity of 5-FU when co-administers with Capecitabine (539 mg/kg/day) in mice[1].

Name: DO34 analog, CAS: 2098969-71-0, stock 10.7g, assay 98.9%, MWt: 531.53, Formula: C26H28F3N5O4, Solubility: DMSO : ≥ 105 mg/mL (197.54 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DO34 analog is a triazole DAGL(α) inhibitor extracted from patent WO2017096315 A1, compound 100.

Name: Eicosatetraynoic acid ETYA, CAS: 1191-85-1, stock 21.5g, assay 98.5%, MWt: 296.40, Formula: C20H24O2, Solubility: Ethanol : < 1 mg/mL (insoluble); DMSO : 2 mg/mL (6.75 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Immunology/Inflammation, Target: PPAR;COX, Biological_Activity: Eicosatetraynoic acid (ETYA) is a nonspecific inhibitor of cyclooxygenase and lipoxygenase (ID50=8 μM and 4 μM, respectively)[1]. Eicosatetraynoic acid (ETYA) activates PPARα and PPARγ chimeras at 10 µM[2].

Name: Kira8 AMG-18, CAS: 1630086-20-2, stock 23.7g, assay 98.9%, MWt: 601.12, Formula: C31H29ClN6O3S, Solubility: DMSO : 65 mg/mL (108.13 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: IRE1, Biological_Activity: Kira8 (AMG-18) is a mono-selective IRE1α inhibitor that allosterically attenuates IRE1α RNase activity with an IC50 of 5.9 nM[1].
IC50 & Target: IRE1α[1] 
IC50: 5.9 nM (IRE1α RNase)[1]
In Vitro: Kira8 blocks IRE1α oligomerization, and potently inhibits IRE1α RNase activity against XBP1 and Ins2 RNAs. Kira8 more potently reduces IRE1α-driven apoptosis in INS-1 cells than KIRA6 and also reverses XBP1 splicing promoted by GNF-2[1].
In Vivo: Male Ins2+/Akita mice are injected i.p. with KIRA8 (50 mg/kg; daily; for 35 days), significant reduction of hyperglycemia become apparent over several weeks[1]. 
One week treatment of pre-diabetic NODs mice with Kira8 (50 mg/kg; i.p.; once a day) leads to significant reductions in islet XBP1 splicing and TXNIP mRNAs, and preserves Ins1/Ins2, BiP and MANF mRNAs[1].

Name: N-Methylnicotinamide, CAS: 114-33-0, stock 39.1g, assay 98.4%, MWt: 136.15, Formula: C7H8N2O, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N-Methylnicotinamide is an endogenous metabolite.

Name: Selpercatinib LOXO-292, CAS: 2152628-33-4, stock 10.9g, assay 98.8%, MWt: 525.60, Formula: C29H31N7O3, Solubility: DMSO : 8.33 mg/mL (15.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: RET, Biological_Activity: Selpercatinib (LOXO-292) is a RET kinase inhibitor extracted from patent WO2018071447A1, Compound Example 163, has an IC50 of 14.0 nM, 24.1 nM, and 530.7 nM for RET (WT), RET (V804M) , and RET (G810R), respectively[1]. Antineoplastic activity[2].
IC50 & Target: IC50: 14.0 nM (RETWT), 24.1 nM (RETV804M), 530.7 nM (RETG810R)[1]

Name: WYC-209, CAS: 2131803-90-0, stock 30.4g, assay 98.9%, MWt: 368.45, Formula: C20H20N2O3S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 83.33 mg/mL (226.16 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Apoptosis;Autophagy, Target: RAR/RXR;Apoptosis;Autophagy, Biological_Activity: WYC-209, a synthetic retinoid, is a retinoic acid receptor (RAR) agonist. WYC-209 induces apoptosis primarily via the caspase 3 pathway (IC50=0.19 μM for inmalignant murine melanoma TRCs), and has long-term effects with little toxicity[1].
IC50 & Target: Retinoic acid receptor[1]
In Vitro: WYC-209 (10 μM; 24 hours) is able to inhibit and block growth of TRCs of human tumor cells in culture with a long-lasting effect[1].
In Vivo: WYC-209 (0.022-0.22 mg/kg; i.v.; once every two days for 25 days) inhibits tumor metastasis in C57BL/6 mice bearing lung metastases[1].

Name: RG7834 RO 7020322, CAS: 2072057-17-9, stock 0.9g, assay 98.1%, MWt: 401.45, Formula: C22H27NO6, Solubility: DMSO : 125 mg/mL (311.37 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Anti-infection, Target: HBV, Biological_Activity: RG7834 (RO 7020322) is a highly selective and orally bioavailable HBV inhibitor, potently inhibits HBV antigens (both HBsAg and HBeAg) and HBV DNA, with IC50s of 2.8, 2.6, and 3.2 nM, respectively, in dHepaRG Cells[1].
IC50 & Target: IC50: 2.8 nM (HBsAg), 2.6 nM (HBeAg), 3.2 nM (HBV DNA)[1]
In Vitro: RG7834 ((S)-(+)-64) is a highly selective and orally bioavailable HBV inhibitor, potently inhibits HBV antigens (both HBsAg and HBeAg) and HBV DNA, with IC50s of 2.8, 2.6, and 3.2 nM, respectively, in dHepaRG Cells[1]. 
RG7834 has no activity against CYP3A4, CYP2D6, CYP2C9 (IC50s >50 μM) or hERG channel[1].
In Vivo: RG7834 (4 mg/kg, twice daily for 21 days) shows anti-HBV efficacy in HBV-infected human liver chimeric uPA-SCID mice[1]. 
RG7834 (2, 14.5 mg/kg, p.o.) exhibits good oral bioavail ability, with a half-life of 4.9 h in mice[1].

Name: AS2717638, CAS: 2148339-28-8, stock 38.8g, assay 98.2%, MWt: 447.48, Formula: C25H25N3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: AS2717638 is an oral active and selective lysophosphatidic acid receptor 5 (LPA5) antagonist, with an IC50 of 38 nM for hLPA5. AS2717638 also significantly improves PGE2-, PGF2α-, and AMPA-induced allodynia[1].
IC50 & Target: IC50: 38 nM (hLPA5)[1].

Name: Radioprotectin-1, CAS: 1622006-09-0, stock 19.8g, assay 98.1%, MWt: 486.92, Formula: C23H19ClN2O6S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (256.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: Radioprotectin-1 is a potent and specific nonlipid agonist of lysophosphatidic acid receptor 2 (LPA2), with an EC50 value of 25 nM for murine LPA2 subtype[1].
IC50 & Target: EC50: 25 nM (murine LPA2 subtype)[1]
In Vitro: Radioprotectin-1 is a potent agonist of LPA2 with an EC50 of 5 pM and functions as a full agonist at the human ortholog of LPA2[1]. 
Radioprotectin-1 (0-3 μM; 15 minutes) effectively reduces apoptosis induced by γ-irradiation and the radiomimetic drug Adriamycin in cells that expressed LPA2 either endogenously or after transfection[1]. 
In Vivo: Radioprotectin-1 is a high-potency specific agonist of the murine LPA2 GPCR [1]. 
Radioprotectin-1 (0.1 mg/kg, 0.3 mg/kg; s.c.; every 12 hours; for 3 days) decreases the mortality of C57BL/6 mice in models of the hematopoietic acute radiation syndromes (HE-ARS) and gastrointestinal acute radiation syndromes (GI-ARS) [1]. 
Radioprotectin-1 exerts its radioprotective and radiomitigative action through specific activation of the upregulated LPA2 GPCR in Lgr5+stem cells[1].

Name: Acetoacetic acid sodium salt, CAS: 623-58-5, stock 2.8g, assay 98.3%, MWt: 124.07, Formula: C4H5NaO3, Solubility: H2O : 50 mg/mL (403.00 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acetoacetic acid sodium salt is a metabolite of non-esterified fatty acids, involved in the development of human diabetes. Acetoacetic acid sodium salt induces oxidative stress to inhibit the assembly of very low density lipoprotein in bovine hepatocytes[1].
In Vitro: Acetoacetic acid sodium salt induces oxidative stress to inhibit the assembly of very low density lipoprotein in bovine hepatocytes[1]. 
Acetoacetic acid (0.6, 2.4, 4.8 mM) increases malondialdehyde (MDA) content in high-dose group (GH) group, decreases mRNA expression of Mn SOD, Cu/Zn SOD, and glutathione peroxidase (GSH-Px) in all groups, lowers catalase (CAT) mRNA expression in medial-dose group (GM), and GH groups. In addition, Acetoacetic acid down-regulates the mRNA expression of apolipoprotein B100 (ApoB100), apolipoprotein E (ApoE), and low density lipoprotein receptor (LDLR). Thus, VLDL assembly is decreased andtriglyceride (TG) accumulation is increased in these bovine hepatocytes[1].

Name: (S)-Mapracorat (S)-ZK-245186; (S)-BOL-303242X, CAS: 887375-15-7, stock 22.9g, assay 98.8%, MWt: 462.48, Formula: C25H26F4N2O2, Solubility: DMSO : ≥ 50.6 mg/mL (109.41 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: (S)-Mapracorat is a selective and less active glucocorticoid receptor agonist.
In Vitro: (S)-Mapracorat concentration dependently inhibited TNFα secretion from activated canine PBMC with IC50 value of approximately 0.2 nM.
In Vivo: Intradermal injection of compound 48/80 (50 μg in 50 μL saline) resulted in a clear wheal and flare reaction over the 60 min observation period. Topical pre-treatment with (S)-Mapracorat (0.1%) leads to significant reduction in the wheal and flare responses compared to vehicle (acetone) treated areas.

Name: GT 949, CAS: 460330-27-2, stock 16.2g, assay 98.3%, MWt: 527.66, Formula: C30H37N7O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: EAAT2, Biological_Activity: GT 949 is a selective excitatory amino acid transporter-2 (EAAT2) positive allosteric modulator with an EC50 of 0.26 nM[1].
IC50 & Target: EC50: 0.26±0.03 nM (EAAT2)[1]
In Vitro: GT 949 (GT949) enhances glutamate transport with an EC50 of 0.26 ± 0.03 nM. GT 949 also demonstrates selectivity to EAAT2 and has no effect on glutamate activity mediated by EAAT1 or EAAT3[1]. 
GT 949 is also tested for its effect on glutamate uptake kinetics in EAAT2-transfected cells. GT 949 enhances glutamate transport in a noncompetitive fashion, with increase in Vmax of about 47%[1].

Name: NVS-ZP7-4, CAS: 2349367-89-9, stock 3.7g, assay 98.7%, MWt: 501.62, Formula: C28H28FN5OS, Solubility: DMSO : ≥ 125 mg/mL (249.19 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NVS-ZP7-4 is a Zinc transporter SLC39A7 (ZIP7) inhibitor that is also the first reported chemical tool to probe the impact of modulating ER zinc levels and investigate ZIP7 as a novel druggable node in the Notch pathway.
IC50 & Target: ZIP7[1].
In Vitro: NVS-ZP7-4 increases ER zinc levels, suggesting functional modulation of ZIP7[1].

Name: (S)-Ketorolac (-)-Ketorolac, CAS: 66635-92-5, stock 5g, assay 98.4%, MWt: 255.27, Formula: C15H13NO3, Solubility: DMSO : 200 mg/mL (783.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: (S)-Ketorolac is a nonsteroidal anti-inflammatory agent. (S)-ketorolac exhibits potent COX1 and COX2 enzyme inhibition[1].
IC50 & Target: COX1, COX2[1]

Name: BAY-293, CAS: 2244904-70-7, stock 4.3g, assay 98.5%, MWt: 448.58, Formula: C25H28N4O2S, Solubility: DMSO : ≥ 125 mg/mL (278.66 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: BAY-293, a valuable chemical probe, blocks RAS activation via disruption of the KRAS-SOS1 interaction with an IC50 of 21 nM. BAY-293 is a potent inhibitor of Son of Sevenless 1 (SOS1). SOS1 is the guanine nucleotide exchange factor (GEF) and activator of RAS[1].
IC50 & Target: IC50: 21 nM (KRAS-SOS1 interaction)[1]
In Vitro: BAY-293 inhibits the activation of RAS in HeLa cells, with IC50 values in the submicromolar range[1]. 
BAY-293 (595 nM-3580 nM; 72 hours) shows efficient antiproliferative activity against wild-type KRAS cell lines (K-562, MOLM-13) and cell lines with KRASG12C mutation (NCI-H358, Calu-1)[1]. 
BAY-293 efficiently inhibits pERK levels in K-562 cells after incubation for 60 min without affecting total protein levels of ERK[1].

Name: TD-106, CAS: 2250288-69-6, stock 15.8g, assay 98.3%, MWt: 273.25, Formula: C12H11N5O3, Solubility: DMSO : ≥ 125 mg/mL (457.46 mM), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for E3 Ligase, Biological_Activity: TD-106 is a cereblon (CRBN) modulator, which can be used for targeted protein degradation. BRD4 PROTACs with TD-106 induce BRD4 degradation[1].
IC50 & Target: CRBN[1]
In Vitro: TD-106 (0.1 nM, 1 nM, 10 nM, 100 nM, 1000 nM, 10 μM, and 100 μM; 72 hours) inhibits the proliferation of NCI-H929 myeloma cell line with an CC50 of 0.039 μM[1]. 
TD-106 (1, 10, 100, and 1000 nM) induces the degradation of IKZF1/3 in NCI-H929 cells[1].
In Vivo: TD-106 (50 mg/kg; intraperitoneally; q.d. for 14 days) possesses anti-myeloma activity in SCID mice with TMD-8 xenograft model.

Name: GB1107, CAS: 1978336-61-6, stock 7g, assay 98%, MWt: 522.32, Formula: C20H16Cl2F3N3O4S, Solubility: DMSO : 50 mg/mL (95.73 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Galectin, Biological_Activity: GB1107 is a potent, selective, orally active inhibitor of Galectin-3 (Gal-3) with a Kd of 37 nM for human Galectin-3. GB1107 reduces human and mouse lung adenocarcinoma growth and blocks metastasis in the syngeneic model[1].
IC50 & Target: Kd: 37 nM (human Gal-3)[1].
In Vitro: Treatment with GB1107 (0-1 μM) increases tumor M1 macrophage polarization and CD8+ T cell infiltration in LLC cells by flow cytometric analysis. GB1107 potentiates the effects of a PD-L1 immune checkpoint inhibitor to increase expression of cytotoxic (IFN-γ, granzyme B, perforin-1, Fas ligand) and apoptotic (cleaved caspase-3) effector molecules[1].
In Vivo: GB1107 (10 mg/kg, p.o., once daily from day 18-30 post implantation) treatment results in significantly reduced tumor growth and final tumor weights[1].

Name: TD-0212, CAS: 1073549-10-6, stock 26.6g, assay 98.3%, MWt: 527.65, Formula: C28H34FN3O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;GPCR/G Protein, Target: Neprilysin;Angiotensin Receptor, Biological_Activity: TD-0212 (compound 35) 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 (compound 35) 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 (compound 35) 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: HDACs/mTOR Inhibitor 1, CAS: 2271413-06-8, stock 25.4g, assay 98.1%, MWt: 566.65, Formula: C28H38N8O5, Solubility: DMSO : 32.5 mg/mL (57.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR;Epigenetics;Cell Cycle/DNA Damage, Target: Apoptosis;mTOR;HDAC;HDAC, Biological_Activity: HDACs/mTOR Inhibitor 1 is a dual Histone Deacetylases (HDACs) and mammalian target of Rapamycin (mTOR) target inhibitor for treating hematologic malignancies, with IC50s of 0.19 nM, 1.8 nM, 1.2 nM and >500 nM for HDAC1, HDAC6, mTOR and PI3Kα, respectively. HDACs/mTOR Inhibitor 1 stimulates cell cycle arrest in G0/G1 phase and induce tumor cell apoptosis with low toxicity in vivo[1].
IC50 & Target: IC50: 0.19 nM (HDAC1),1.8 nM (HDAC6), 1.2 nM (mTOR), >500 nM (PI3Kα)[1].

Name: AWZ1066S, CAS: 2239272-16-1, stock 16.6g, assay 98.9%, MWt: 404.39, Formula: C19H19F3N6O, Solubility: DMSO : 125 mg/mL (309.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: AWZ1066S is a highly specific anti-Wolbachia drug candidate for a short-course treatment of filariasis, with an EC50 of 2.5 nM in cell assay[1].

Name: Omipalisib GSK2126458;GSK458, CAS: 1086062-66-9, stock 33.1g, assay 98.9%, MWt: 505.50, Formula: C25H17F2N5O3S, Solubility: DMSO : 50 mg/mL (98.91 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR;Autophagy, Target: PI3K;mTOR;Autophagy, Biological_Activity: Omipalisib (GSK2126458) is a highly selective and potent inhibitor of PI3K with Kis of 0.019 nM/0.13 nM/0.024 nM/0.06 nM and 0.18 nM/0.3 nM for p110α/β/δ/γ, mTORC1/2, respectively.
IC50 & Target: Ki: 0.019 nM (p110α), 0.13 nM (p110β), 0.024 nM (p110δ), 0.06 nM (p110γ), 0.18 nM (mTORC1), 0.3 nM (mTORC2)
In Vitro: Omipalisib (GSK2126458) potently inhibits the activity of common activating mutants of p110α (E542K, E545K, and H1047R) found in human cancer with Ki of 8 pM, 8 pM and 9 pM, respectively. Omipalisib causes a significant reduction in the levels of pAkt-S473 with remarkable potency in T47D and BT474 cells with IC50 of 0.41 nM and 0.18 nM, respectively. Furthermore, Omipalisib (GSK2126458) leads to a G1 cell cycle arrest and produces the inhibitory effect on cell proliferation in a large panel of cell lines, including T47D and BT474 breast cancer lines with IC50 of 3 nM and 2.4 nM, respectively[1]. The combination of Omipalisib or GSK1120212 with Omipalisib enhances cell growth inhibition and decreases S6 ribosomal protein phosphorylation in drug-resistant clones from the A375 BRAF(V600E) and the YUSIT1 BRAF(V600K) melanoma cell lines[2]. Omipalisib (GSK2126458) potentiates the antiproliferative activity of DDR1-IN-1 in colorectal cancer cell lines[3].
In Vivo: In a BT474 human tumor xenograft model, Omipalisib (GSK2126458) treatment results in a dose-dependent reduction in pAkt-S473 levels, and exhibits dose-dependent tumor growth inhibition at a low dose of 300 μg/kg. Besides, Omipalisib (GSK2126458) shows low blood clearance and good oral bioavailability in four preclinical species (mouse, rat, dog, and monkey)[1].

Name: Amuvatinib hydrochloride MP470 hydrochloride;HPK 56 hydrochloride, CAS: 1055986-67-8, stock 24.8g, assay 98.1%, MWt: 1000, Formula: C23H21N5O3S.xHCl, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;FLT3;PDGFR;RAD51;c-Kit;RET, Biological_Activity: Amuvatinib hydrochloride (MP470 hydrochloride) is an orally bioavailable multi-targeted tyrosine kinase inhibitor with potent activity against mutant c-Kit, PDGFRα, Flt3, c-Met and c-Ret. Amuvatinib hydrochloride (MP470 hydrochloride) 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: Metixene hydrochloride hydrate, CAS: 7081-40-5, stock 32.2g, assay 98.1%, MWt: 363.94, Formula: C20H26ClNOS, Solubility: DMSO : 90 mg/mL (247.29 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Metixene hydrochloride hydrate is an anticholinergic antiparkinsonian agent, potently inhibits binding of quinuclidinyl benzilate (QNB) to the muscarinic receptor in rat brain cortical tissue, with an IC50 of 55 nM and a Kd of 15 nM[1].
IC50 & Target: IC50: 55 nM (mAChR)[1] 
Ki: 15 nM (mAChR)[1]
In Vitro: Metixene hydrochloride hydrate is an anticholinergic antiparkinsonian agent, potently inhibits binding of quinuclidinyl benzilate (QNB) to the muscarinic receptor in rat brain cortical tissue, with an IC50 of 55 nM and a Kd of 15 nM[1].

Name: Burixafor (hydrobromide) TG-0054 (hydrobromide), CAS: 1191450-19-7, stock 14.8g, assay 98.6%, MWt: 769.01, Formula: C27H51N8O3P.5/2HBr, Solubility: H2O : 50 mg/mL (65.02 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: Burixafor hydrobromide (TG-0054 hydrobromide) is an orally bioavailable and potent antagonist of CXCR4 and a well water soluble anti-angiogenic drug that is of potential value in treating choroid neovascularization[1]. Burixafor hydrobromide (TG-0054 hydrobromide) mobilizes mesenchymal stem cells, attenuates inflammation, and preserves cardiac systolic function in a porcine model of myocardial infarction[2].
IC50 & Target: CXCR4[1].

Name: p38α inhibitor 1, CAS: 1034189-82-6, stock 20.1g, assay 98.6%, MWt: 416.46, Formula: C22H26F2N4O2, Solubility: DMSO : ≥ 125 mg/mL (300.15 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: p38α inhibitor 1 is a p38α inhibitor extracted from patent WO 2008076265 A1.

Name: P110δ-IN-1, CAS: 1595129-71-7, stock 35.2g, assay 98.9%, MWt: 604.77, Formula: C31H40N8O3S, Solubility: DMSO : 20.83 mg/mL (34.44 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: P110δ-IN-1 is a potent and selective inhibitor of P110δ extracted from patent WO 2014055647 A1, with an IC50 of 8.4 nM[1].

Name: CB-6644, CAS: 2316817-88-4, stock 26.5g, assay 98%, MWt: 573.06, Formula: C29H34ClFN4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CB-6644 is a selective inhibitor of RUVBL1/2 complex with anti-cancer activity. CB-6644 blocks the ATPase activity of RUVBL1/2 with an IC50 of 15 nM[1].
In Vitro: CB-6644 (20 µM) interacts with the RUVBL1/2 complex in Ramos cells[1]. 
CB-6644 (0.001-10 μM; 72 hours) potently kills 123 cell lines (including HCT116, NCI-1975, and HT29 cells) with an EC50 range of 41 to 785 nM[1]. 
In Vivo: CB-6644 (150 mg/kg, oral administration, 10 days of treatment for SCID-beige mice bearing Ramos xenograft models, 30 days of treatment for SCID-beige mice bearing RPMI8226 xenograft models) has antitumor activity in xenograft tumor models with tumor growth inhibitions (TGIs) of 68 and 81%, respectively in Ramos xenograft models and RPMI8226 xenograft models[1].

Name: Fmoc-Phe-Lys(Boc)-PAB-PNP, CAS: 1646299-50-4, stock 12.9g, assay 98.3%, MWt: 885.96, Formula: C49H51N5O11, Solubility: DMSO : 6 mg/mL (6.77 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Fmoc-Phe-Lys(Boc)-PAB-PNP is a cleavable ADC linker used in the synthesis of antibody-drug conjugates (ADCs).
IC50 & Target: ADC linker

Name: AP1867, CAS: 195514-23-9, stock 35.5g, assay 98.8%, MWt: 693.78, Formula: C38H47NO11, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 125 mg/mL (180.17 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Apoptosis;Autophagy, Target: FKBP;FKBP;FKBP, Biological_Activity: AP1867 is a synthetic FKBP12F36V-directed ligand.
IC50 & Target: FKBP[1]

Name: MRTX-1257, CAS: 2206736-04-9, stock 2g, assay 98.7%, MWt: 565.71, Formula: C33H39N7O2, Solubility: DMSO : 55 mg/mL (97.22 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: MRTX-1257 is a selective, irreversible, covalent and oral active KRAS G12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells[1].
IC50 & Target: IC50: 900 pM (KRAS dependent ERK phosphorylation in H358 cells)[1].
In Vivo: MRTX-1257 (1 mg/kg, 3 mg/kg, 10 mg/kg, 30 mg/kg and 100 mg/kg, orally, daily for 30 days) shows rapid tumor growth inhibition at all dose groups in MIA PaCa-2 G12C Xenograft model in mice[1]. 
MRTX-1257 shows sustained regression at 3,10, 30, and 100 mg/kg dose groups[1]. 
MRTX-1257 dosed of 100 mg/kg daily leads to complete responses that are maintained >70 days after cessation of treatment[1].

Name: LY-2940094, CAS: 1307245-86-8, stock 1.6g, assay 98.9%, MWt: 480.96, Formula: C22H23ClF2N4O2S, Solubility: DMSO : 41.67 mg/mL (86.64 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: LY-2940094 is a potent, selective and orally available nociceptin receptor (NOP receptor) antagonist with high affinity (Ki=0.105 nM) and antagonist potency (Kb=0.166 nM). LY-2940094 reduces ethanol self-administration in animal models[1].
IC50 & Target: Ki: 0.105 nM (NOP receptor)[1] 
Kb: 0.166 nM (NOP receptor)[1]
In Vivo: LY-2940094 (LY2940094; 3, 10, or 30 mg/kg; 2-3 mL/kg; orally daily; for 4 days) dose-dependently reduces homecage ethanol self-administration in Indiana Alcohol-Preferring (P) and Marchigian Sardinian Alcohol-Preferring (msP) rats, without affecting food/water intake or locomotor activity[1].

Name: Plecanatide acetate, CAS: 1075732-84-1, stock 25.8g, assay 98.4%, MWt: 1741.94, Formula: C67H108N18O28S4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: Guanylate Cyclase, Biological_Activity: Plecanatide acetate is a guanylate cyclase-C (GC-C) receptor agonist, with an EC50 of 190 nM in T84 cells. Plecanatide acetate shows anti-inflammatory activity in models of murine colitis[1].
IC50 & Target: EC50: 190 nM (guanylate cyclase-C receptor, T84 cells)[1]
In Vitro: Plecanatide acetate is a GC-C receptor agonist, binds and activates GC-C receptor, with an EC50 of 190 nM in T84 cells[1].
In Vivo: Plecanatide (0.5 and 2.5 mg/kg, p.o.) ameliorates spontaneous and chemically induced colitis after treatment for 7 days in BALB/c mice, and 14 days in TCRα-/- mice[1]. 
Plecanatide (0.005-5 mg/kg, once daily for 7 days) also shows anti-inflammatory activity in dextran sulfate sodium (DSS) and trinitrobenzene sulfonic (TNBS)-induced colitis in BDF-1 mice[1].

Name: Cevipabulin fumarate TTI-237 fumarate, CAS: 849550-67-0, stock 30g, assay 98.5%, MWt: 580.89, Formula: C22H22ClF5N6O5, Solubility: DMSO : 50 mg/mL (86.07 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Cevipabulin fumarate (TTI-237 fumarate) is an oral, microtubule-active, antitumor compound and inhibits the binding of [3H]NSC 49842 to tubulin, with an IC50 of 18-40 nM for cytotoxicity in human tumor cell line[1][2].
IC50 & Target: IC50: 18-40 nM (microtubule in human tumor cells)[1].
In Vitro: Cevipabulin (0-50 nM, 72 hours) shows good activity (between 18 and 40 nM IC50 values) on cell lines from ovarian, breast, prostate, and cervical tumors[1]. 
Flow cytometry experiments reveal that, Cevipabulin (TTI-237) at low concentrations (20-40 nM) produces sub-G1 nuclei and, at concentrations above 50 nM, it causes a strong G2-M block[1].
In Vivo: Cevipabulin (TTI-2370)( 5, 10, 15, and 20 mg/kg, every 4 days for 4 cycles, in mice) is active by i.v. and p.o. administration against human tumor xenografts, showing dose-dependent effects, with good antitumor activity at 20 and 15 mg/kg[1].

Name: INH14, CAS: 200134-22-1, stock 13.5g, assay 98.5%, MWt: 240.30, Formula: C15H16N2O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 125 mg/mL (520.18 mM), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: IKK, Biological_Activity: INH14 is a cell permeable inhibitor of IKKα/IKKβ, with IC50s of 8.97 and 3.59 μM, respectively. INH14 inhibits the IKKα/β-dependent TLR inflammatory response. INH14 also inhibits downstream of TAK1/TAB1 and NF-kB pathways. Anti-inflammatory and anti-cancer activity[1].
IC50 & Target: IC50: 8.97 μM (IKKα), 3.59 μM (IKKβ)[1]
In Vivo: INH14 (5 µg/g, i.p. for 2 hours) reduces lipopeptide-induced inflammation in mice[1].

Name: Zylofuramine, CAS: 3563-92-6, stock 11.2g, assay 98.5%, MWt: 219.32, Formula: C14H21NO, Solubility: DMSO : ≥ 100 mg/mL (455.95 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Zylofuramine is a psychomotor stimulant[1].

Name: Succinyl phosphonate (trisodium salt), CAS: 864167-45-3, stock 4g, assay 98.1%, MWt: 248.01, Formula: C4H4Na3O6P, Solubility: H2O : 125 mg/mL (504.01 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Endogenous Metabolite;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Succinyl phosphonate trisodium salt is an α-ketoglutarate dehydrogenase (KGDHC) inhibitor, effective inhibits (KGDHC) in muscle, bacterial, brain, and cultured human fibroblasts[1][4]. Succinyl phosphonate trisodium salt is an 2-oxoglutarate dehydrogenase (OGDH) inhibitor, impairs viability of cancer cells in a cell-specific metabolism-dependent manner[2]. Succinyl phosphonate trisodium salt inhibits the glutamate-induced ROS production in glutamate-stimulated hippocampal neurons in situ[3].
IC50 & Target: α-ketoglutarate dehydrogenase; 2-oxoglutarate dehydrogenase[1][4]; ROS production[3]

Name: PF-06446846 (hydrochloride), CAS: 1632250-50-0, stock 2.5g, assay 98.4%, MWt: 470.35, Formula: C22H21Cl2N7O, Solubility: DMSO : 250 mg/mL (531.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Ser/Thr Protease, Biological_Activity: PF-06446846 hydrochloride is an orally active and highly selective inhibitor of translation of Proprotein convertase subtilisin/kexin type 9 (PCSK9). PF-06446846 hydrochloride inhibits PCSK9 by inducing the ribosome to stall around codon 34[1].
IC50 & Target: PCSK9[1]
In Vitro: PF-06446846 inhibits the secretion of PCSK9 by Huh7 cells with an IC50 of 0.3 μM[1].
In Vivo: PF-06446846 (oral gavage; 5-50 mg/kg/day for 14 days) lowers plasma PCSK9 in a dose-dependent manner and lowers total cholesterol levels[1].

Name: ORM-10962, CAS: 763926-98-3, stock 34.6g, assay 98.3%, MWt: 459.54, Formula: C27H29N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Na+/Ca2+ Exchanger, Biological_Activity: ORM-10962 is a potent, highly selective sodium-calcium exchanger (NCX) inhibitor, with IC50 values of 67 and 55 nM for the reverse and forward mode inhibition, respectively[1][2].
IC50 & Target: NCX[1][2].

Name: 1V209 TLR7 agonist T7, CAS: 1062444-54-5, stock 19.6g, assay 98.4%, MWt: 359.34, Formula: C16H17N5O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: 1V209 (TLR7 agonist T7) is a Toll-like receptor 7 (TLR7) agonist and has anti-tumor effects. 1V209 can be conjugated with various polysaccharides to improve its water solubility, and enhance its efficacy, and maintain low toxicity[1][2].
In Vitro: 1V209 (0.1-10 μM) treatment significantly stimulates TNFα production in RAW246.7 cells[1]. 
1V209 (18 hours) treatment increases IL-6 production comparain bone marrow derived dendritic cells[1].
In Vivo: The intravenous (IV) administration of the formulation to mice bearing 4T1 breast cancer tumors results in nanoparticle accumulation in tumors, reduction in primary tumor growth, and inhibition of lung metastases, as compared to saline-treated animals. Mice administered 1V209 experience significantly increases plasma levels of proinflammatory cytokines IL-6, IP-10, and MCP-1 at 2 h following IV administration[1].

Name: AZD 6482 KIN-193, CAS: 1173900-33-8, stock 3.2g, assay 98.9%, MWt: 408.45, Formula: C22H24N4O4, Solubility: DMSO : ≥ 100 mg/mL (244.83 mM), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR;Autophagy, Target: PI3K;Autophagy, Biological_Activity: AZD 6482 (KIN-193) is a potent and selective p110β inhibitor with an IC50 of 0.69 nM.
IC50 & Target: IC50: 0.69 nM (p110β)[1]
In Vitro: An in vitrokinase assay demonstrates that AZD 6482 (KIN-193) is highly potent in the inhibition of p110β’s kinase activity (IC50 of 0.69 nM) and has 200, 20, and 70-fold selectivity over p110α, p110δ, and p110γ isoforms, respectively. AZD 6482 also exhibits selectivity of ~80 fold over PI3K-C2β and DNA-PK and more than 1,000-fold over other phosphatidylinositol-3 kinase–related kinases (PIKKs). An inhibitor-kinase interaction profiling of AZD 6482 against a panel of 433 kinases using the KinomeScan approach demonstrates that AZD 6482 is highly selective in its interaction with PI3Ks. To determine whether AZD 6482 selectively targets PTEN-deficient tumors, the effect of AZD 6482 is tested on cell proliferation on a large panel of 422 cancer cell lines using high-throughput tumor cell line profiling. 35% of cell lines with PTEN mutations (20 out of 57) and 16% of cell lines with wild-type PTEN (58 out of 365) are sensitive to AZD 6482 with a threshold of EC50<5 µM[1].
In Vivo: To determine the pharmacodynamics of AZD 6482 (KIN-193) in tumors in vivo, rat fibroblast (Rat1) cells are engineered to express both p53DD, a dominant negative mutant of p53, and a constitutively activated myr-p110β (Rat1-CA-p110β) to enable these cells to form xenograft tumors in mice. For comparison, an isogenic Rat1 cell line expressing p53DD and myr-p110α (Rat1-CA-p110α) is also generated. Rat1-CA-p110α and Rat1-CA-p110β cells are introduced subcutaneously into the contralateral flanks of athymic mice such that tumors driven by activated p110α or p110β would be exposed to identical conditions and that concern about animal-to-animal variability could be eliminated. When tumors reach a volume of ~500 mm3, the tumor-bearing mice receives a single IP injection of AZD 6482 (10 mg/kg). The plasma concentration of AZD 6482 is highest at 1 hour post-injection and declined to undetectable levels by 4h. Concentrations of AZD 6482 in both the CA-p110α- and CA-p110β-driven tumors parallel the plasma concentrations. Analyses of tumor lysates harvested at various time points after AZD 6482 injection reveal that the phosphorylation of AKT is significantly reduced at 1hour after AZD 6482 injection in Rat1-CA-p110β tumors, but remain unchanged in Rat1-CAp110α tumors[1].

Name: RR-11a analog, CAS: 685543-66-2, stock 20.2g, assay 98.8%, MWt: 491.49, Formula: C22H29N5O8, Solubility: DMSO : 125 mg/mL (254.33 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: RR-11a analog is a potent and selective inhibitors of asparaginyl endopeptidases (AE) (Legumain), with IC50 values of 4.5 nM, 4.5 nM and 31 nM for AE1 in Trichomonas Vaginalis, AE in Ixodes ricinus and AE in Schistosoma mansoni, respectively[1].
IC50 & Target: IC50: 4.5 nM (AE1 in Trichomonas Vaginalis), 4.5 nM (AE in Ixodes ricinus), 31 nM (AE in Schistosoma mansoni)[1].

Name: (R)-Citronellol D-Citronellol;(R)-(+)-β-Citronellol, CAS: 1117-61-9, stock 13.7g, assay 98.4%, MWt: 156.27, Formula: C10H20O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (R)-Citronellol (D-Citronellol) is an alcoholic monoterpene found in geranium essential oil. (R)-Citronellol inhibits degranulation of mast cells and does not affect caffeine bitterness perception. (R)-Citronellol can be used in decorative cosmetics, toiletries as well as in non-cosmetic products[1][2][3].
In Vitro: 0.5 mM (R)-Citronellol (D-Citronellol) inhibits degranulation of cultured mast cells (CMCs) by 21.3%[2].

Name: Mutant IDH1-IN-4, CAS: 1416270-18-2, stock 35g, assay 98.8%, MWt: 438.56, Formula: C25H34N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Isocitrate Dehydrogenase (IDH), Biological_Activity: Mutant IDH1-IN-4 (compound 434) is an inhibitor of mutant Isocitrate dehydrogenase 1 (IDH 1), with IC50 values of ≤ 0.5 μM for mutant IDH1 in R132H, HT1080 and U87R132H cells[1].
IC50 & Target: IC50: ≤ 0.5 μM (mutant IDH 1 in cells)[1].

Name: SHP2 IN-1, CAS: 1801764-90-8, stock 34.1g, assay 98.9%, MWt: 441.38, Formula: C18H22Cl2N6OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: SHP2 IN-1 (compound 13) is an allergic inhibitor of SHP2 (PTPN11), with an IC50 of 3 nM.
IC50 & Target: IC50: 3 nM (SHP2)[1].

Name: LMP744 hydrochloride MJ-III65 hydrochloride; NSC706744 hydrochloride, CAS: 308246-57-3, stock 2g, assay 98.5%, MWt: 488.92, Formula: C24H25ClN2O7, Solubility: DMSO : 5.56 mg/mL (11.37 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: Topoisomerase, Biological_Activity: LMP744 hydrochloride (MJ-III65 hydrochloride) is a DNA intercalator and Topoisomerase I (Top1) inhibitor with antitumor activity[1].
IC50 & Target: Top1[1].
In Vitro: The GI50 value of LMP744 (MJ-III-65) for NCI60 cells is 0.1 μM[2]. 
LMP744 (0.1-5 μM, 3 days) induces dose-dependent accumulation of cells in the S and G2 phases of the cell cycle[2].
In Vivo: LMP744 (MJ-III-65) (10-50 mg/kg) administered i.v. push once a week for 4 weeks in nude mice moderately actives against human A253 and FaDu tumor xenografts without significant toxicity[1].

Name: nor-NOHA acetate Nω-hydroxy-nor-Arginine acetate, CAS: 1140844-63-8, stock 34.5g, assay 98.6%, MWt: 296.28, Formula: C9H20N4O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Immunology/Inflammation;Metabolic Enzyme/Protease, Target: Apoptosis;Arginase;Arginase, Biological_Activity: nor-NOHA acetate is a specific and reversible arginase inhibitor, induces apoptosis in ARG2-expressing cells under hypoxia but not normoxia. Anti-leukemic activity, effective in endothelial dysfunction, immunosuppression and metabolism[1].
IC50 & Target: Arginase[1]

Name: 7-Methylguanosine, CAS: 20244-86-4, stock 39.1g, assay 98.9%, MWt: 298.27, Formula: C11H16N5O5+, Solubility: H2O : 83.33 mg/mL (279.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Nucleoside Antimetabolite/Analog, Biological_Activity: 7-Methylguanosine is a novel cNIIIB nucleotidase inhibitor with IC50 value of 87.8 ± 7.5 µM.

Name: GSK547 GSK'547, CAS: 2226735-55-1, stock 27.2g, assay 98.2%, MWt: 396.39, Formula: C20H18F2N6O, Solubility: DMSO : 100 mg/mL (252.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: RIP kinase, Biological_Activity: GSK547 (GSK'547) is a highly selective and potent inhibitor of receptor-interacting serine/threonine protein kinase 1 (RIP1), inhibits macrophage-mediated adaptive immune tolerance in pancreatic cancer[1].
IC50 & Target: RIP1[1]
In Vitro: GSK547 (0.1-100000 nM; 24 hours) pretreats L929 cells with recombinant TNFα and zVAD at various doses for 30 min, then cell death is induced with an IC50 of 32 nM after 24 hours[1]. 
GSK547 up-regulates STAT1 signaling in bone marrow-derived macrophages (BMDM)[1]. 
In Vivo: GSK547 (GSK′547; RIP1i) robustly targets RIP1 in vivo. RIP1 inhibition results in immunogenic macrophage differentiation in pancreatic cancer, leading to adaptive immune activation and tumor protection for pancreatic ductal adenocarcinoma (PDA)[1]. 
GSK547 (100 mg/kg/day; fed via food-based dosing; 15-50 days) reduces tumor burden and extends survival compared with mice treated with controls or Nec-1s[1].

Name: Dulcoside A, CAS: 64432-06-0, stock 5.5g, assay 98.6%, MWt: 788.87, Formula: C38H60O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dulcoside A is isolated from Stevia rebaudiana, it often advertised as a sweetener[1].

Name: BT-13, CAS: 924537-98-4, stock 19.5g, assay 98.5%, MWt: 517.54, Formula: C23H27F4N3O4S, Solubility: DMSO : 25 mg/mL (48.31 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: RET, Biological_Activity: BT-13 is a potent and selective glial cell line-derived neurotrophic factor (GDNF) receptor RET agonist independently of GFLs, promoting neurite growth from sensory neurons in vitro and attenuates experimental neuropathy in the Rat[1].
IC50 & Target: GDNF receptor RET[1].
In Vitro: BT-13 stimulates phosphorylation of RET, as well as RET-dependent intracellular signaling, but activated neither NGF receptor TrkA nor BDNF receptor TrkB nor intracellular signaling in the absence of RET[1].
In Vivo: BT-13 (20 and 25mg/kg in rats induced by ligation of left L5 and L6 spinal nerves) has a slight antinociceptive/antihyperalgesic effect and protected DRG neurons in rats with surgery-induced neuropathy[1].

Name: Pentacosanoic acid, CAS: 506-38-7, stock 23.3g, assay 98.2%, MWt: 382.66, Formula: C25H50O2, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); Ethanol : < 1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Pentacosanoic acid is a 25-carbon long-chain saturated fatty acid. Pentacosanoic is a conjugate acid of a pentacosanoate[1].
In Vivo: The degree of demyelination in adrenoleukodystrophy is related to the Pentacosanoic to Docosanoic acid ratios (C25:0/C22:0 and C26:0/C22:0). Mainly saturated fatty acids of the middle class components (C24:0, C25:0 and C26:0) are found in severely affected areas where the active process is complete. Because a region of high long chain fatty acid content, lacking histopathological change, is detected[1]. 
The area with myelin destruction with axonal preservation is generally most prominent in the frontal edge of the lesion. A bell-shaped distribution of very long chain fatty acids, esterified to cholesterol, are detectable, with the mid-point being formed by Pentacosanoic (C25 : 0) and Hexacosanoic (C26 : 0) acids[1].

Name: Caerulomycin A Cerulomycin;Caerulomycin, CAS: 21802-37-9, stock 17.5g, assay 98.9%, MWt: 229.23, Formula: C12H11N3O2, Solubility: DMSO : 150 mg/mL (654.36 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Caerulomycin A (Cerulomycin; Caerulomycin), an antifungal compound, induces generation of T cells, enhances TGF-β-Smad3 protein signaling via suppressing interferon-γ-induced STAT1 signaling. Antifungal and antibiotic activity, and used in autoimmune diseases[1].
IC50 & Target: Antifungal[1] 
TGF-β-Smad3[1]

Name: dBET57, CAS: 1883863-52-2, stock 4.1g, assay 98.3%, MWt: 699.18, Formula: C34H31ClN8O5S, Solubility: DMSO : 250 mg/mL (357.56 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: dBET57 is a potent and selective degrader of BRD4BD1 based on the PROTAC technology. dBET57 mediates recruitment to the CRL4CRBN E3 ubiquitin ligase, with a DC50/5h of 500 nM for BRD4BD1, and is inactive on BRD4BD2[1].
IC50 & Target: DC50/5h: 500 nM (BRD4BD1)[1]

Name: KPT-6566, CAS: 881487-77-0, stock 21g, assay 98.2%, MWt: 443.54, Formula: C22H21NO5S2, Solubility: DMSO : 120 mg/mL (270.55 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KPT-6566, a potent prolyl isomerase PIN1 inhibitor, covalently binds to the catalytic site of PIN1, selectively inhibits and degrades PIN1. KPT-6566 shows an IC50 of 640 nM and a Ki of 625.2 nM for PIN1 PPIase domain. Anti-cancer activity[1].
IC50 & Target: IC50: 640 nM (PIN1 PPIase)[1] 
Ki: 625.2 nM (PIN1 PPIase)[1]

Name: RPW-24, CAS: 1001625-82-6, stock 34.5g, assay 98.6%, MWt: 284.74, Formula: C15H13ClN4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: RPW-24 protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. RPW-24 has antibacterial activity[1].

Name: RK-287107, CAS: 2171386-10-8, stock 14.4g, assay 98.6%, MWt: 416.46, Formula: C22H26F2N4O2, Solubility: DMSO : 125 mg/mL (300.15 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: RK-287107 is a potent and specific tankyrase inhibitor with IC50s of 14.3 and 10.6 nM for tankyrase-1 and tankyrase-2, respectively. RK-287107 blocks colorectal cancer cell growth[1].
In Vitro: RK-87107 (0.01-10 μM; 12 hours) shows an antiproliferative effect on colorectal cancer cells harboring short adenomatous polyposis coli (APC) mutations. The 50% growth inhibition (GI50) value of RK-287107 on COLO-320DM cells is 0.449 μM[1]. 
RK-287107 (0.03-10 μM; 16 hours) causes accumulation of tankyrase and Axin1/2[1]. 
RK-287107 (0.03-10 μM; 16 hours) also downregulates β-catenin signaling in cultured cells[1].
In Vivo: RK-287107 (100 and 300 mg/kg; i.p. administration; once per day; 5-days on/ 2-days off schedule for 2 weeks) inhibits tumor growth in a mouse xenograft model[1].

Name: HET0016, CAS: 339068-25-6, stock 30g, assay 98.2%, MWt: 206.28, Formula: C12H18N2O, Solubility: DMSO : 5 mg/mL (24.24 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: HET0016 is a potent and selective 20-hydroxyeicosatetraenoic acid (20-HETE) synthase inhibitor, with IC50 values of 17.7 nM, 12.1 nM and 20.6 nM for recombinant CYP4A1-, CYP4A2- and CYP4A3-catalyzed 20-HETE synthesis, respectively. HET0016 also is a selective CYP450 inhibitor, which has been shown to inhibit angiogenesis and tumor growth[1][2].
IC50 & Target: 17.7 nM (CYP4A1), 12.1 nM (CYP4A2), 20.6 nM (CYP4A3)[1], CYP450[2]
In Vitro: HET0016 is a selective, non-competitive and irreversible inhibitor of CYP4A [1]. 
HET0016 (100 μM; 24 hours, 48 hours) decreases migration and invasion of breast cancer metastatic cells [2]. 
In Vivo: HET0016 (10 mg/kg/day; i.v.; for 3 weeks) reduces tumor volume and lung metastasis in an immunocompetent breast cancer mouse model[2]. 
HET0016 reduces the metalloproteinases’ levels in the lungs via PI3K/AKT pathway in mice[2]. 
HET0016 decreases expression of pro-inflammatory and growth factors and granulocytic MDSCs population in lung microenvironment[2]. 
HET0016 protects BBB dysfunction after I/R by regulating the expression of MMP-9 and tight junction proteins[3].

Name: MRS-1191, CAS: 185222-90-6, stock 38g, assay 98%, MWt: 477.55, Formula: C31H27NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: MRS-1191 is a potent and selective A3 adenosine receptor antagonist with a KB value of 92 nM, a Ki value of 31.4 nM for human A3 receptor and an IC50 of 120 nM for CHO cells[1].
IC50 & Target: Ki: 31.4 nM (human A3 adenosine receptor)[1]
In Vitro: The effects of putative A3 adenosine receptor antagonist of MRS-1191 is characterized in receptor binding and functional assays. MRS-1191 is found to be competitive in saturation binding studies using the agonist radioligand [125I]AB-MECA (N6-(4-amino-3-iodobenzyl)adenosine-5'-N-methyluronamide) at cloned human brain A3 receptor expressed in HEK-293 cells. Antagonism is demonstrated in functional assays consisting of agonist-induced inhibition of adenylate cyclase and the stimulation of binding of [35S]guanosine 5'-O-(3-thiotriphosphate) ([35S]GTP-gamma-S) to the associated G-proteins. MRS-1191 with a KB value of 92 nM, proves to be highly selective for human A3 receptor vs human A1 receptor-mediated effects on adenylate cyclase[1].

Name: Taminadenant, CAS: 1337962-47-6, stock 24.3g, assay 99%, MWt: 306.12, Formula: C10H8BrN7, Solubility: DMSO : 125 mg/mL (408.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Taminadenant is an antagonist of adenosine receptor[1].
IC50 & Target: Adenosine receptor[1]

Name: Ziresovir AK0529;RO-0529, CAS: 1422500-60-4, stock 17.5g, assay 99%, MWt: 439.53, Formula: C22H25N5O3S, Solubility: DMSO : 125 mg/mL (284.39 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: RSV, Biological_Activity: Ziresovir (AK0529;RO-0529) is a potent, selective, and orally bioavailable respiratory syncytial virus (RSV) fusion (F) protein (RSV F) protein inhibitor. Ziresovir shows anti-RSV activity (EC50=3 nM) and highlights pharmacokinetics in animal species[1].
IC50 & Target: EC50: 3 nM (RSV F)[1]

Name: Imidazole ketone erastin IKE, CAS: 1801530-11-9, stock 17.7g, assay 98.8%, MWt: 655.14, Formula: C35H35ClN6O5, Solubility: DMSO : ≥ 125 mg/mL (190.80 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Ferroptosis, Biological_Activity: Imidazole ketone erastin (IKE) is a potent, selective, and metabolically stable inhibitor of the cystine-glutamate antiporter, system Xc- and an activator of ferroptosis.
IC50 & Target: System Xc-, ferroptosis[1]

Name: UBCS039, CAS: 358721-70-7, stock 34.2g, assay 98.7%, MWt: 247.29, Formula: C16H13N3, Solubility: DMSO : 125 mg/mL (505.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Autophagy;Epigenetics;Cell Cycle/DNA Damage, Target: Autophagy;Sirtuin;Sirtuin, Biological_Activity: UBCS039 is the first synthetic, specific Sirtuin 6 (SIRT6) activator, inducing autophagy in human tumor cells, with an EC50 of 38 μM[1].
IC50 & Target: EC50: 38 μM (SIRT6)[1].
In Vitro: UBCS039 (75 μM, 48 or 72 hours) induces deacetylation of SIRT6-targeted histone H3 sites in human cancer cells[2]. 
UBCS039 leads to autophagosome accumulation in human cancer cells[2]. 
UBCS039 induces autophagy via AMP-activated protein kinase (AMPK) signaling pathway activation[2].

Name: PP121, CAS: 1092788-83-4, stock 9.2g, assay 98.2%, MWt: 319.36, Formula: C17H17N7, Solubility: DMSO : 20 mg/mL (62.63 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;PI3K/Akt/mTOR, Target: Src;Apoptosis;VEGFR;PDGFR;mTOR, Biological_Activity: PP121 is a multi-targeted kinase inhibitor with IC50s of 10, 60, 12, 14, 2 nM for mTOR, DNK-PK, VEGFR2, Src, PDGFR, respectively.
IC50 & Target: IC50: 10 nM (mTOR), 60 nM (DNK-PK), 12 nM (VEGFR2), 14 nM (Src), 2 nM (PDGFR)[1]
In Vitro: PP121 blocks the PI3K pathway by direct inhibition of PI3K/mTOR in two glioblastoma cell lines, U87 and LN229. PP121 potently inhibits the proliferation of a diverse panel of tumor cell lines containing mutations in the PI3-K pathway components PIK3CA, PTEN, or RAS. PP121 induces a G0G1 arrest in most tumor cells. PP121 directly inhibits Src in cells and reverses its biochemical and morphological effects. PP121 potently inhibits the Ret kinase domain in vitro (IC50<1 nM). PP121 potently blocks VEGF stimulated activation of the PI3-K and MAPK pathways. PP121 inhibits VEGFR2 autophosphorylation at low nanomolar concentrations, confirming that this molecule directly targets VEGFR2 in cells. PP121 inhibits Bcr-Abl induced tyrosine phosphorylation in K562 cells as well as BaF3 cells that express Bcr-Abl[1].
In Vivo: Oral administration of PP121 remarkably inhibits Eca-109 xenograft growth. Mice body weights are not significantly affected by PP121 or the vehicle treatment. PP121 oral administration dramatically inhibits activations of Akt-mTOR and NFkB in xenograft tumors. p-Akt Ser 473 and p-IKKa/b are both inhibited by PP121 administration[2].

Name: MLT-748, CAS: 1832578-30-9, stock 19.7g, assay 98.5%, MWt: 492.32, Formula: C19H19Cl2N9O3, Solubility: DMSO : ≥ 250 mg/mL (507.80 mM), Clinical_Informat: No Development Reported, Pathway: NF-κB;Metabolic Enzyme/Protease, Target: MALT1;MALT1, Biological_Activity: MLT-748 is a potent, selective and allosteric inhibitor of MALT1, binds MALT1 in the allosteric Trp580 pocket, with an IC50 of 5 nM[1].
IC50 & Target: IC50: 5 nM (MALT1)[1] 
Kd: 13 nM (MALT1(329-728)-W580S), 42 nM (MALT1(329-728))[1]
In Vitro: MLT-748 reversibly binds to human mutant MALT1(329-728)-W580S (Kd, 13 nM) with affinity similar to that of the wild type MALT1(329-728) (Kd, 42 nM)[1]. 
MLT-748 (0-2 μM) stabilizes cellular MALT1-W580S, with an EC50 of 69 nM[1]. 
MLT-748 (2 µM, 24 hours) increases the phosphorylation of p65 and IκBα in MALT1mut/mut patient immortalized B cells[1].

Name: IDO1-IN-5, CAS: 2166616-75-5, stock 1.6g, assay 98.8%, MWt: 396.45, Formula: C23H25FN2O3, Solubility: DMSO : ≥ 100 mg/mL (252.24 mM), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Indoleamine 2,3-Dioxygenase (IDO), Biological_Activity: IDO1-IN-5 is a potent, selective and brain penetrated inhibitor of IDO1 activity, binds to apo-IDO1 lacking heme rather than mature heme-bound IDO1[1].
IC50 & Target: IDO1[1]
In Vitro: IDO1-IN-5 (up to 100 µM) shows no obvious agonism of aryl hydrocarbon receptor (AHR)[1].

Name: SW-100, CAS: 2126744-35-0, stock 22.7g, assay 99%, MWt: 316.78, Formula: C17H17ClN2O2, Solubility: DMSO : ≥ 125 mg/mL (394.60 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: SW-100, a selective histone deacetylase 6 (HDAC6) inhibitor with an IC50 of 2.3 nM, shows at least 1000-fold selectivity for HDAC6 relative to all other HDAC isozymes. SW-100 displays a significantly improved ability to cross the blood-brain-barrier[1].
IC50 & Target: IC50: 2.3 nM (Histone deacetylase 6)[1]
In Vitro: SW-100 (0.01-10 µM; 48 hours) shows obvious increase in the acetylated α-tubulin levels in a dose-dependent manner[1].
In Vivo: SW-100 (20 mg/kg; i.p.; twice a day for two days) ameliorates several memory and learning impairments including novel object recognition, temporal ordering, and coordinate and categorical spatial processing in mouse model of Fragile X syndrome[1].

Name: Streptonigrin Bruneomycin, CAS: 3930-19-6, stock 30g, assay 98.9%, MWt: 506.46, Formula: C25H22N4O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Protein Arginine Deiminase, Biological_Activity: Streptonigrin (Bruneomycin), a natural product produced by Streptomyces flocculus, possesses both anti-tumor and anti-bacterial activity. Streptonigrin acts as a pan-PAD inhibitor with IC50s of 48.3±34.2 µM, 26.1±0.3 µM, 0.43±0.03 µM, and 2.5±0.4 µM for PAD1, PAD2, PAD3, and PAD4, respectively[1].
IC50 & Target: Anti-bacterial[1] 
IC50: 48.3±34.2 µM (PAD1), 26.1±0.3 µM, (PAD2), 0.43±0.03 µM (PAD3), 2.5±0.4 µM (PAD4)[1]

Name: PTC299, CAS: 1256565-36-2, stock 25.3g, assay 98.5%, MWt: 467.34, Formula: C25H20Cl2N2O3, Solubility: DMSO : 50 mg/mL (106.99 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK, Target: VEGFR, Biological_Activity: PTC299 is a potent, orally bioavailable VEGFA inhibitor, targets dihydroorotate dehydrogenase (DHODH), resulting in cell growth inhibition and differentiation in leukemias, including acute myeloid leukemia, linking DHODH regulation and stress-induced VEGFA and angiogenesis[1][2][3].
IC50 & Target: VEGF[2]
In Vitro: PTC299 inhibits hypoxia-induced VEGFA protein production in HeLa cells with an EC50 of 1.64 ± 0.83 nM[1]. 
PTC299 is the most potent inhibitor with an IC50 of about 1 nM, over 10 to 1000-fold more potent than Brequinar, Vidofludimus or A 77-1726 in leukemia cells[1].

Name: MT-802, CAS: 2231744-29-7, stock 30.8g, assay 98.5%, MWt: 787.82, Formula: C41H41N9O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;PROTAC, Target: Btk;PROTAC, Biological_Activity: MT-802 is a potent BTK degrader based on PROTAC technology, with a DC50 of 1 nM. MT-802 has potential to treat C481S mutant chronic lymphocytic leukemia (CLL)[1].
IC50 & Target: DC50: 1 nM (BTK)[1].
In Vitro: MT-802 degrades BTK with a DC50 of 9.1 nM with maximal degradation being observed by 250 nM[1].

Name: MPO-IN-28, CAS: 37836-90-1, stock 19.6g, assay 98.8%, MWt: 231.25, Formula: C11H13N5O, Solubility: DMSO : 22.73 mg/mL (98.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glutathione Peroxidase, Biological_Activity: MPO-IN-28 (Compound 28) is a myeloperoxidase (MPO) inhibitor with an IC50 of 44 nM.

Name: BI-3663, CAS: 2341740-84-7, stock 9.7g, assay 98.5%, MWt: 917.84, Formula: C44H42F3N7O12, Solubility: DMSO : 300 mg/mL (326.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;PROTAC, Target: FAK;PROTAC, Biological_Activity: BI-3663 is a highly selective PTK2/FAK PROTAC, with cereblon ligands to hijack E3 ligases for PTK2 degradation. BI-3663 inhibits PTK2 with an IC50 of 18 nM. BI-3663 is a PROTAC that composes of BI-4464 (HY-124625) linked to Pomalidomide (HY-10984) with a linker[1]. Anti-cancer activity[1].
IC50 & Target: IC50: 18 nM (PTK2)[1]
In Vitro: BI-3663 potently degrades PTK2 in Hep3B2.1-7 cells, and A549 cells, with pDC50s of 7.6 and 7.9, respectively[1].

Name: M1001, CAS: 874590-32-6, stock 17.6g, assay 98.3%, MWt: 327.40, Formula: C17H17N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIF/HIF Prolyl-Hydroxylase, Biological_Activity: M1001 is a weak agonist of HIF-2α, directly binds to the HIF-2α PAS-B domain, with a Kd of 667 nM. M1001 enhances the stabilities of HIF-2α-ARNT complex[1].
IC50 & Target: Kd: 667 nM (HIF-2α)[1]

Name: Spastazoline, CAS: 2351882-11-4, stock 28.9g, assay 98.5%, MWt: 382.51, Formula: C20H30N8, Solubility: DMSO : 100 mg/mL (261.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Spastazoline is a potent and selective spastin (a microtubule-severing AAA protein) inhibitor, with an IC50 of 99 nM for Human spastin. Spastazoline shows no effect on ATPase activity of a recombinant human VPS4[1].
IC50 & Target: IC50: 99 nM (spastin)[1]

Name: Bragsin1, CAS: 369631-68-5, stock 21.1g, assay 98.8%, MWt: 273.16, Formula: C11H6F3NO4, Solubility: DMSO : 62.5 mg/mL (228.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bragsin1 is a potent, selective and noncompetitive inhibitor of the ArfGEF BRAG2, inhibits Arf GTPase activation, with an IC50 of 3 μM. Bragsin1 binds to PH domain of BRAG2, and is a noncompetitive interfacial inhibitor. Bragsin1 has no effect on the Sec7 domain of human ArfGEFs. Anti-cancer activity[1].
IC50 & Target: IC50: 3 μM (BRAG2)[1]

Name: FT113, CAS: 1630808-89-7, stock 17.4g, assay 98.9%, MWt: 409.41, Formula: C22H20FN3O4, Solubility: DMSO : 62.5 mg/mL (152.66 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Fatty Acid Synthase (FAS), Biological_Activity: FT113 is a potent and orally active fatty acid synthase (FASN) inhibitor, with an IC50 of 213 nM for full-length recombinant human FASN enzyme. In cell-based assay, FT113 blocks FASN activity in BT474 cells (IC50, 90 nM). FT113 shows anti-proliferative activity, and exhibits anti-cancer activity both in vitro and in vivo[1].
IC50 & Target: IC50: 213 nM (FASN), 90 nM (FASN, in BT474 cell)[1]
In Vitro: FT113 shows anti-proliferative activity against PC3 and MV-411 cells with IC50s of 47 and 26 nM, respectively[1].
In Vivo: FT113 (5 mg/kg, p.o.) exhibits potent oral bioavailability of 95% and 84% in mice and rats, respectively[1]. 
FT113 (5, 25, or 50 mg/kg, p.o., twice daily for 16 days) increases malonyl-CoA concentration in tumors, inhibits tumor growth in a dose-dependent manner in mice[1].

Name: GLP-26, CAS: 2133017-36-2, stock 5.1g, assay 98.9%, MWt: 373.35, Formula: C19H17F2N3O3, Solubility: DMSO : 125 mg/mL (334.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HBV, Biological_Activity: GLP-26 is a HBV capsid assembly modulators (CAM), inhibits HBV DNA replication in Hep AD38 system (IC50=3 nM), and reduces cccDNA by >90% at 1 μM.
GLP-26 disrupts the encapsidation of pre-genomic RNA, causes nucleocapsid disassembly and reduces cccDNA pools[1].
In Vitro: GLP-26 (0.7-1.7 μM; 3 days) reduces secreted HBeAg in HepNTCP-DL cells transfected with HBV
wild type, with EC50 values of 0.7 μM[2].

Name: TAS0728, CAS: 2088323-16-2, stock 31.2g, assay 98%, MWt: 504.58, Formula: C26H32N8O3, Solubility: DMSO : 125 mg/mL (247.73 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: TAS0728 is a potent, selective, oral active, irreversible and covalent-binding HER2 inhibitor, binds to HER2 at C805, inhibits its kinase activity, with an IC50 of 13 nM. TAS0728 shows IC50s of 4.9, 8.5, 31, 65, 33, 25, 86 and 36 nM for BMX, HER4, BLK, EGFR, JAK3, SLK, LOK and human HER2, respectively. TAS0728 also inhibits the phosphorylation of HER2, HER3, and downstream effectors, shows no obvious effect on EGFR. Antitumor activity[1].
IC50 & Target: IC50: 13 nM (HER2), 4.9 nM (BMX), 8.5 nM (HER4), 31 nM (BLK), 65 nM (EGFR), 33 nM (JAK3), 25 nM (SLK), 86 nM (LOK), 36 nM (Human HER2)[1]

Name: GPI-1046, CAS: 186452-09-5, stock 3g, assay 98.6%, MWt: 360.45, Formula: C20H28N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GPI-1046 is a immunophilin ligand without antibiotic action and attenuates ethanol intake in part through the upregulation of glutamate transporter 1 (GLT1) in PFC and NAc-core. GPI-1046 is an analog of FK506, which is an immunophilin ligand that has been shown neuroprotective effects in neurodegenerative disease models[1]. GPI-1046 readily crosses the blood-brain barrier and promotes the regeneration of dopamine (DA) cells in the CNS in association with functional recovery in rodent models[2].
IC50 & Target: GLT1[1]

Name: NNC-0640, CAS: 307986-98-7, stock 34.2g, assay 98%, MWt: 573.67, Formula: C29H31N7O4S, Solubility: DMSO : 250 mg/mL (435.79 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucagon Receptor, Biological_Activity: NNC-0640 is a potent human G-protein-coupled glucagon receptor (GCGR) negative allosteric modulator (NAM) with an IC50 of 69.2 nM[1].
IC50 & Target: Human Glucagon Receptor [1]

Name: BI-4464, CAS: 1227948-02-8, stock 37g, assay 98.3%, MWt: 555.55, Formula: C28H28F3N5O4, Solubility: DMSO : 16.67 mg/mL (30.01 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;PROTAC, Target: FAK;Ligand for Target Protein for PROTAC, Biological_Activity: BI-4464 is a highly selective ATP competitive inhibitor of PTK2/FAK, with an IC50 of 17 nM. A PTK2 ligand for PROTAC[1].
IC50 & Target: IC50: 17 nM (PTK2/FAK)[1].

Name: WJ460, CAS: 1415251-36-3, stock 10.6g, assay 98.6%, MWt: 460.59, Formula: C27H28N2O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: WJ460 is a potent myoferlin (MYOF) inhibitor, which interacts directly with MYOF and exerts anti-metastatic activity in the nanomolar range in breast cancer cells[1].
IC50 & Target: MYOF[1]
In Vitro: WJ460 blocks breast cancer cell invasion with IC50 values of 43.37 ± 3.42 nM in MDA-MB-231 and 36.40 ± 4.51 nM in BT549 cells. WJ460 treatment remarkably inhibits MDA-MB-231 and BT549 cell invasion through Collagen I in a dose-dependent manner[1].
In Vivo: WJ460 inhibits breast tumor growth, angiogenesis, and spontaneous metastasis in a spontaneous metastasis model[1].

Name: PZ-2891, CAS: 2170608-82-7, stock 25g, assay 98.8%, MWt: 349.43, Formula: C20H23N5O, Solubility: DMSO : 75 mg/mL (214.64 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PZ-2891 is an orally bioavailable, brain penetrant pantothenate kinase (PANK) modulator. PZ-2891 act as an orthosteric inhibitor at high concentrations and an allosteric activator at lower sub-saturating concentrations. PZ-2891 inhibits human pantothenate kinases PANK1β, PANK2, and PANK3 with IC50s of 40.2 nM, 0.7 nM and 1.3 nM, respectively[1].
IC50 & Target: IC50: 40.2±4.4 nM (human PANK1β), 0.7±0.08 nM (human PANK2), 1.3±0.2 nM (human PANK3)[1]
In Vitro: PZ-2891 inhibits mouse pantothenate kinases PANK1β, PANK2, and PANK3 with IC50s of 48.7±5.1 nM, 1.0±0.1 nM, and 1.9±0.2 nM, respectively[1].

Name: EN40, CAS: 2094547-67-6, stock 4.8g, assay 98.2%, MWt: 217.26, Formula: C13H15NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aldehyde Dehydrogenase (ALDH), Biological_Activity: EN40 is a potent, selective aldehyde dehydrogenase 3A1 (ALDH3A1) inhibitor as a covalent ligand, exhibits an IC50 value of 2 uM[1]
IC50 & Target: IC50: 2 uM (ALDH3A1)[1]
In Vitro: EN40 (10-1000 μM; 48 hours) shows inhibitory effecton ALDH3A1 activity and impairs A549 cell survival[1].
In Vivo: EN40 (intraperitoneal injection; 50mg/kg; from 14 days; once per day) exerts strong anti-tumorigenic effects in established A549 tumor xenografts, shows good tolerability with no body weight loss in mice[1].

Name: BCI (E)-BCI, CAS: 1245792-51-1, stock 14.1g, assay 98.6%, MWt: 317.42, Formula: C22H23NO, Solubility: DMSO : 125 mg/mL (393.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: BCI is an allosteric inhibitor of dual specificity phosphatase (DUSP). BCI specifically inhibits DUSP6 and DUSP1 with EC50s of 13.3 and 8.0 μM in cells, respectively. BCI does not inhibit DUSP5[1].

Name: HSP27 inhibitor J2 J2, CAS: 2133499-85-9, stock 18g, assay 98.2%, MWt: 264.30, Formula: C13H12O4S, Solubility: DMSO : 25 mg/mL (94.59 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: HSP27 inhibitor J2 (J2) is a HSP27 inhibitor, which significantly induces abnormal HSP27 dimer formation and inhibits a production of HSP27 giant polymers, thereby having an effect of inhibiting a chaperone function of the HSP27 and reducing a cell protection function thereof. HSP27 inhibitor J2 (J2) remarkably enhances the antiproliferative activity of 17-AAG and sensitizes cisplatin-induced lung cancer cell growth inhibition[1][2].
IC50 & Target: HSP27[2]

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2020年3月13日星期五

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