EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2351

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

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Pilot Plant: 20000sq, 40 reactors from 5-200L
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Name: Cauloside F, CAS: 60451-47-0, stock 20.1g, assay 98.5%, MWt: 1237.38, Formula: C59H96O27, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cauloside F is a triterpenoid saponin isolated from Clematis akebioides.

Name: (+)-PD 128907 hydrochloride, CAS: 300576-59-4, stock 26.9g, assay 98.6%, MWt: 285.77, Formula: C14H20ClNO3, Solubility: DMSO : 150 mg/mL (524.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: (+)-PD 128907 hydrochloride is a selective dopamine D2/D3 receptor agonist, with Kis of 1.7, 0.84 nM for human and rat D3 receptors, 179, 770 n M for human and rat D3 receptors, respectively.
IC50 & Target: Ki: 1.7 nM (human D3 receptor), 0.84 nM (rat D3 receptor), 179 nM (human D2 receptor), 770 nM (rat D2 receptor)[1][2].
In Vitro: (+)-PD 128907 displaced [3H]spiperone binding from dopamine D3 receptors (Ki human=1.7 nM and rat=0.84 nM) with >100-fold and 900-fold selectivity over the human (Ki=179 nM) and rat (Ki=770 nM) dopamine D2 receptor[1][2].
In Vivo: (+)-PD 128907 significantly decreases dialysate DA levels in D3 knock out mice. The IC25 values are 61 nM and 1327 nM, respectively, for wild type and D3knock out mice. The ratio of the IC25 values shows that (+)-PD 128907 is 22 times more potent in decreasing dialysate DA levels in wild type as compared to mice lacking the D3 receptor. The D3 agonist evokes a dose related decrease in dialysate DA in wild type mice. Post-hoc analysis shows that all doses tested (0.03, 0.1 and 0.3 mg/kg) significantly inhibit dialysate DA. The IC25 values are 0.05 and 0.44 mg/kg for wild type and knock out mice, respectively, indicating that systemically administered (+)-PD 128907 is 9 times more potent in decreasing dialysate DA in the ventral striatum of wild type as compared to D3 knock out mice. Doses of 1 mg/kg or higher of (+)-PD 128907 markedly inhibits dialysate DA in both wild type and D3 knock out mice[3].

Name: Glycolic acid oxidase inhibitor 1, CAS: 77529-42-1, stock 19.5g, assay 98.3%, MWt: 344.16, Formula: C16H10BrNO3, Solubility: DMSO : ≥ 137 mg/mL (398.07 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Glycolic acid oxidase inhibitor 1 is a glycolate oxidase inhibitor, extracted from patent EP0021228A1, in Table IV.
IC50 & Target: Glycolate oxidase[1]
In Vivo: Glycolic acid oxidase inhibitor 1 inhibits oxalate biosynthesis in isolated perfused rat liver. Glycolate oxidase inhibitors provide a specific approach to the prevention and treatment of calcium oxalate renal lithiasis[1].

Name: 4-IPP 4-Iodo-6-phenylpyrimidine, CAS: 41270-96-6, stock 30.2g, assay 98%, MWt: 282.08, Formula: C10H7IN2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4-IPP (4-Iodo-6-phenylpyrimidine) is a specific suicide substrate and irreversible inhibitor of macrophage migration inhibitory factor (MIF)[1].
IC50 & Target: MIF[1]
In Vitro: 4-IPP is a specific suicide substrate for MIF that binds covalently and irreversibly to MIF to inhibit its biologic activity[1]. 
4-IPP inhibits RANKL-induced p65 phosphorylation and nuclear translocation by preventing the interaction of MIF with thioredoxin-interacting protein-p65 complexes[1]. 
4-IPP can inhibit receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis and potentiate osteoblast-mediated mineralization and bone nodule formation[1]. 
4-IPP (0.5-200μM;24-72 hours) inhibits osteoclastogenesis in a dose-dependent manner[1]. 
4-IPP(5-20μM; 5 days) inhibits RANKL-induced osteoclast differentiation and bone resorption [1]. 
In Vivo: 4-IPP (1 mg/kg, 5 mg/kg; every 2 days; for 8 weeks) ameliorates the bone loss associated with estrogen deficiency by reducing osteoclastic activities and enhancing osteoblastic bone formation[1].

Name: NH2-PEG3-C2-NH-Boc PROTAC Linker 15, CAS: 101187-40-0, stock 22.9g, assay 98.7%, MWt: 292.37, Formula: C13H28N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: NH2-PEG3-C2-NH-Boc is a PROTAC linker, which refers to the PEG composition. NH2-PEG3-C2-NH-Boc can be used in the synthesis of a series of PROTACs. PROTACs contain two different ligands connected by a linker; one is a ligand for an E3 ubiquitin ligase and the other is for the target protein. PROTACs exploit the intracellular ubiquitin-proteasome system to selectively degrade target proteins[1].

Name: TNP, CAS: 519178-28-0, stock 11.6g, assay 98.7%, MWt: 443.38, Formula: C20H16F3N7O2, Solubility: DMSO : ≥ 125 mg/mL (281.93 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TNP is a cell-permeable inhibitor of IP6K1 and IP3K, with IC50 values of 0.55 µM and 10.2 µM for IP3K, respectively. TNP binds to the ATP-binding sites of both enzymes[1].
IC50 & Target: IC50: 0.55 µM (IP6K1), 10.2 μM (IP3K)[1].

Name: CD73-IN-1, CAS: 2132396-40-6, stock 22.9g, assay 98.2%, MWt: 371.41, Formula: C18H17N3O4S, Solubility: DMSO : 150 mg/mL (403.87 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: CD73, Biological_Activity: CD73-IN-1 is an inhibitor of CD73 which can be used in the treatment of cancer extracted from patent WO 2017153952 A1, example 80.
IC50 & Target: CD73[1]

Name: RWJ 50271, CAS: 162112-37-0, stock 34.8g, assay 98.4%, MWt: 410.41, Formula: C18H17F3N4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: RWJ 50271 is an selective inhibitor of lymphocyte function-associated antigen-1/intercellular adhesion molecule-1(LFA-1/ICAM-1) interaction with an IC50 of 5.0 μM (HL60 cells)[1].
IC50 & Target: IC50: 5.0 μM (LFA-1/ICAM-1, HL60 cells)[1]

Name: PTC-028, CAS: 1782970-28-8, stock 13.6g, assay 98.4%, MWt: 405.32, Formula: C19H12F5N5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (308.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: PTC-028 is an orally bioavailable inhibitor of stem cell factor BMI-1 in ovarian cancer. PTC-028 selectively inhibits cancer cells whereas normal cells remain unaffected. Depletion of BMI-1 by PTC-028 induces caspase-mediated apoptosis[1].
IC50 & Target: BMI-1[1]
In Vitro: PTC-028 (25-500 nM; 48 hours) significantly decreases CP20, OVCAR4 and OV90 epithelial ovarian cancer cells viability. However, in normal ovarian surface epithelial cells (OSE) and fallopian tube epithelial cells (FTE) cells, up to 500 nM treatment with PTC-028 for 48 hours has minimal effect (~18-30% decrease)[1]. 
PTC-028 (100 nM; 2-12 hours) increases the phosphorylated BMI-1 species in a time-dependent manner. PTC-028 subsequently reduces BMI-1 in the biochemical functional readout [1]. 
uH2A is observed up to 12 h with PTC-028 (100 nM) in both CP20 and OV90 cells while total H2A levels remain unchanged [1]. 
PTC-028 (100 nM; 48 hours) decreases the expression of XIAP and RIPK1 while LC3B levels remains unchanged compared to that of the control [1]. 
Significant cleavage of Caspase 7, Caspase 9 and PARP is observed in PTC-028 (100 nM; 48 hours)[1].
In Vivo: PTC-028 (15 mg/kg; administered orally twice weekly) causes ~94% (0.169 g) reduction in tumor weight compared to the control (average tumor weight, ~3g) [1]. 
No obvious toxicity is noted in the animals during therapy experiments as assessed by mean body weight[1]. 
PTC-028 (10 mg/kg or 20mg/kg; single oral doses) is administrated to the CD-1 mice. The Cmax is reached at both dose levels 1h post dose after which plasma concentrations slowly reduce[1].

Name: Gardiquimod trifluoroacetate, CAS: 1159840-61-5, stock 24.2g, assay 98.6%, MWt: 541.44, Formula: C21H25F6N5O5, Solubility: H2O : 25 mg/mL (46.17 mM; Need ultrasonic); DMSO : 100 mg/mL (184.69 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Anti-infection, Target: Toll-like Receptor (TLR);HIV, Biological_Activity: Gardiquimod trifluoroacetate is a specific TLR7 agonist which can also inhibit HIV-1 reverse transcriptase.
IC50 & Target: TLR7, HIV-1 reverse transcriptase[1]
In Vitro: Levels of HIV-1 DNA measured by real-time PCR are significantly lower in Gardiquimod trifluoroacetate-treated cells compare to untreated controls on day 9 postinfection. Significantly lower levels of HIV-1 DNA and HIV-1 p24 are observed in Gardiquimod trifluoroacetate-treated and HIV-1-exposed macrophages cocultured with activated PBMCs. Gardiquimod trifluoroacetate significantly increases IFN-α mRNA levels 80-, 20-, and 35-fold above the level of detection at 2, 4, and 6 h posttreatment, respectively[1]. The results show that treatment with Gardiquimod trifluoroacetate results in significant increases in expression of CD69 on T, NK and natural killer T (NKT) cells. It is also found that Gardiquimod trifluoroacetate stimulation increases mRNA expression of IL-12 p40 in RAW264.7 cells. Furthermore, Gardiquimod trifluoroacetate induces augmented secretion of IL-12 p70 into culture supernatant 48 and 72 h after treatment[2].
In Vivo: On day 12, the tumor volume in mice injected with PBS increases to 1770±370 mm3, whereas it is only 230±70 mm3 in mice treated with Gardiquimod trifluoroacetate[2].

Name: TLR7/8 agonist 1 (dihydrochloride), CAS: 1620278-72-9, stock 34.6g, assay 98.8%, MWt: 432.39, Formula: C22H27Cl2N5, Solubility: DMSO : 83.33 mg/mL (192.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: TLR7/8 agonist 1 dihydrochloride is a toll-like receptor (TLR7)/TLR8 dual-agonistic imidazoquinoline.
IC50 & Target: TLR7/TLR8[1]
In Vitro: TLR7/8 agonist 1 (Compound 5d) shows prominent immunostimulatory activities. TLR7/8 agonist 1 serves as a convenient precursor for the covalent attachment of fluorophores without significant loss of activity. TLR7/8 agonist 1 retains TLR7-agonistic activity with an EC50 of 20 nM[1]. TLR7/8 agonist 1 (Compound 1) shows substantially different agonistic potencies in human TLR7 (50 nM) and TLR8 (55 nM) primary screens[2].

Name: (±)-CPSI-1306, CAS: 1309793-47-2, stock 13.3g, assay 98.7%, MWt: 310.30, Formula: C15H16F2N2O3, Solubility: DMSO : 6 mg/mL (19.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (±)-CPSI-1306 is an orally available antagonist of macrophage migration inhibitory factor (MIF).
IC50 & Target: MIF[1].
In Vivo: Mice treated with CPSI-1306 show a significant drop in their blood glucose levels, which is associated with a reduction in serum levels of inflammatory cytokines. As expected, control mice treated with vehicle develop NIDDM as characterized by high serum levels of glucose and inflammatory cytokine. Furthermore, they also show that orally bioavailable CPSI-1306 can be effective in treating this disease[1]. CPSI-1306-induced keratinocyte apoptosis could be appreciated as early as 30 minutes after a single UVB exposure. At 6, 24, and 48 hours following UVB exposure, the CPSI-1306-treated mice show significantly increased expression of cleaved caspase-3 compared with the vehicle-treated mice. CPSI-1306 reduces acute UVB-induced keratinocyte DNA damage and UVB-induced acute inflammation[2].

Name: A-484954, CAS: 142557-61-7, stock 7.7g, assay 98.9%, MWt: 289.29, Formula: C13H15N5O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 20 mg/mL (69.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Autophagy, Target: CaMK;Autophagy, Biological_Activity: A-484954 is a highly selective eukaryotic elongationfactor-2 (eEF2) inhibitor, with an IC50 of 280 nM.
IC50 & Target: IC50: 280 nM (eEF2)[1].
In Vitro: A-484954 is a highly selective eEF2K inhibitor with an IC50 value of 280 nM against eEF2K in the enzymatic assay and little activity against a wide panel of serine/threonine and tyrosine kinases. In enzymatic assay, the IC50 value of A-484954 is increased as the concentration of ATP increased but unaffected by increasing concentrations of calmodulin[1].
In Vivo: A484954 causes relaxation in E (+) and E (-) aorta or mesenteric artery precontracted with NA. Pretreatment with L-NAME but not indomethacin or cimetidine partially inhibits the A484954-induced relaxation in mesenteric artery[2]. Long-term A-484954 treatment inhibits MCT-induced increases PA pressure. It is revealed that A-484954 inhibits MCT-induced PA hypertrophy and fibrosis but not impairment of endothelium-dependent and -independent relaxation. Furthermore, A-484954 inhibits MCT-induced NADPH oxidase-1 expression and ROS generation as well as matrix metalloproteinase-2 activation[3].

Name: ARN272, CAS: 488793-85-7, stock 6.5g, assay 99%, MWt: 432.47, Formula: C27H20N4O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (289.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ARN272 is an anandamide transport inhibitor[1].
IC50 & Target: Anandamide transport[1]

Name: VU0463271 N-Cyclopropyl-N-(4-methyl-2-thiazolyl)-2-[(6-phenyl-3-pyridazinyl)thio]acetamide, CAS: 1391737-01-1, stock 15.6g, assay 98.8%, MWt: 382.50, Formula: C19H18N4OS2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: VU0463271 is a potent KCC2 antagonist, with an IC50 of 61 nM.
IC50 & Target: IC50: 61 nM (KCC2)[1].
In Vitro: VU0463271 is a potent antagonist of the neuronal-specific potassium-chloride cotransporter 2 (KCC2), with an IC50 of 61 nM and >100-fold selectivity versus the closely related Na-K-2Cl cotransporter 1 (NKCC1) and no activity in a larger panel of GPCRs, ion channels and transporters. It is also found rapidly cleared in vitro[1].
In Vivo: VU0463271 is found to be a moderate-to-high clearance compound in rat (CL=57 mL/min/kg) following intravenous administration (1 mg/kg); the low volume of distribution at steady state (Vss 0.4 L/kg), coupled with moderate-to-high clearance produce a relatively short t1/2 (9 min) in vivo[1].

Name: TC-Mps1-12, CAS: 1206170-62-8, stock 31.1g, assay 98.6%, MWt: 324.38, Formula: C17H20N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Mps1;Mps1, Biological_Activity: TC-Mps1-12 is a potent and selective monopolar spindle 1 (Mps1) inhibitor, with an IC50 of 6.4 nM[1].
IC50 & Target: IC50: 6.4 nM (Mps1)[1]
In Vitro: TC-Mps1-12 inhibits the growth of pMps1 cell lines with IC50 values of 131 nM in autophosphorylation assay[1]. 
TC-Mps1-12 (72 hours) inhibits the growth of cells in a dose-dependent manner and with an IC50 values of 0.84 μM[1]. 
In Vivo: TC-Mps1-12 (25-100 mg/kg; p.o.; daily; for 19 days) inhibits the growth of A549 cells in a dose-dependent manner in vivo. At a dose of 100 mg/kg, TC-Mps1-12 exhibits 47% tumor growth inhibition without body weight loss[1]. 
TC-Mps1-12 shows good PK properties with a Cmax of 3542 ng/mL and AUC of 6604 ng h/mL at an oral dose of 25 mg/kg[1].

Name: DSR-6434, CAS: 1059070-10-8, stock 19.9g, assay 98.5%, MWt: 400.48, Formula: C19H28N8O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: DSR-6434 is a potent and selective Toll-like receptor 7 (TLR7) agonist, with EC50s of 7.2 nM and 4.6 nM for human and mice TLR7, respectively. DSR-6434 has a strong antitumor effect[1][2].
In Vitro: To assess the specificity of DSR-6434 toward TLR7, an NF-κB-driven reporter assay is performed in HEK293 cells engineered to express either hTLR7, TLR8 or TLR9. In this assay, successful binding of DSR-6434 to the specific receptor leads to NF-κB activation. DSR-6434 is capable of stimulating reporter gene activity only in HEK293 cells expressing hTLR7 and not in HEK293 cells expressing the structurally similar hTLR8 or hTLR9[2].
In Vivo: DSR-6434 treatment (Compound 20; 0.1-1 mg/kg; intravenous injection; biweekly; for 4 weeks; B6C3F1 mice) suppresses the lung metastasis significantly, 78% inhibition at 0.1 mg/kg dosing (with no tumor metastasis at the 1 mg/kg group)[1].

Name: Fulacimstat BAY1142524, CAS: 1488354-15-9, stock 2.1g, assay 98.5%, MWt: 487.38, Formula: C23H16F3N3O6, Solubility: DMSO : 5 mg/mL (10.26 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Fulacimstat is an orally available chymase inhibitor, with IC50s of 4, 3 nM for human and hamster chymase enzyme, respectively.
IC50 & Target: IC50: 4 nM (human chymase enzyme), 3 nM (hamster chymase enzyme)[1][2].
In Vitro: Fulacimstat inhibits human and hamster chymase enzyme with IC50s of 4 nM and 3 nM, respectively[1][2].
In Vivo: Isoprenaline induces cardiac fibrosis (24.4±1.8%) in hamsters, which is reduced dose dependently by Fulacimstat (16.4±1.2%, 12.4 ± 1.3%, 10.9±1.4% at 1, 3 and 10 mg/kg respectively) and by enalapril (17.7±1.5% at 20 mg/kg). Four weeks after MI, hamster hearts show an increased end diastolic pressure, and reduce contractility and relaxation. Compared to placebo (19.3±2 mmHg), Fulacimstat at 10 mg/kg reduce significantly the end diastolic pressure (13.2±1.4 mmHg) without any effects on blood pressure or heart rate. Moreover, treatment with Fulacimstat reduce the fibrotic area and improve the cardiac response to adrenergic stimulation[1].

Name: PMX 205, CAS: 514814-49-4, stock 6.6g, assay 99%, MWt: 839.04, Formula: C45H62N10O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Complement System, Biological_Activity: PMX 205 is a potent complement C5a receptor (C5aR; CD88) antagonist.
IC50 & Target: C5aR[1]
In Vitro: A complement activation product, C5a, is known to recruit and activate microglia and astrocytes in vitro by activation of a G protein-coupled cell-surface C5aR. In the MTT assay, in 24 h plate, it shows that all groups are significant when compared with negative control group. For PMX 205 (PMX205) group, the value recorded is in between 0.09893 to 0.2465, EP54 group, 0.02724 to 0.1748 and Tamoxifen group, the value recorded in between 0.09880 to 0.2464. For the 48 h plate of incubation time, only two groups show a significant result, which are PMX 205 and Tamoxifen. The values recorded are in between 0.04987 to 0.3273 and 0.5777 to 0.8551 respectively. For the 72 h plate, only one group shows a significant result, PMX 205 (antagonist group) with the value recorded in between 0.02136 to 0.5322[1].
In Vivo: PMX 205 (PMX205) is an orally active, selective C5aR antagonist. Animals treated with PMX 205 (1 mg/kg/day, oral) displays a significant extension of survival time and a reduction in end-stage motor scores, as compared with vehicle-treated rats. PMX 205-treated animals also display reduced levels of astroglial proliferation in the lumbar spinal cord. SOD1G93A rats are orally dosed with PMX 205 (1 mg/kg/day) from two time points (days 28 and 70) before the onset of major clinical symptoms. Both treatment groups have a significant extension in survival time compared with untreated rats (p=0.022, day 28; p=0.015, day 70), with no clear differences in outcomes between the two treatment regimens[2]. Tg2576 mice are treated with PMX 205 (PMX205) at 20 μg/mL in the drinking water (n=17) from 12 to 15 mo of age, the time frame at which there is a rapid accumulation of amyloid deposits in these animals. Untreated Tg2576 animals (n=11) are used as controls. After 3 mo, animals treated with PMX 205 show significantly less fibrillar plaque load (thioflavine reactivity) than do untreated animals. In 3×Tg mice, PMX 205 also significantly reduces hyperphosphorylated tau (69%)[3].

Name: Lazertinib YH25448;GNS-1480, CAS: 1903008-80-9, stock 8.7g, assay 98.9%, MWt: 554.64, Formula: C30H34N8O3, Solubility: DMSO : 9 mg/mL (16.23 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Lazertinib is a potent, highly mutant-selective, blood-brain barrier permeable, orally available and irreversible third-generation EGFR tyrosine kinase inhibitor, and can be used in the research of non-small cell lung cancer.
IC50 & Target: EGFR[1]
In Vitro: Lazertinib (YH25448) is a potent, highly mutant-selective, blood-brain barrier permeable, orally available and irreversible third-generation EGFR tyrosine kinase inhibitor, and can be used in the research of non-small cell lung cancer. Lazertinib targets both T790M mutation and activating EGFR mutations (EGFRm) while sparing wild type[1].

Name: Cot inhibitor-2, CAS: 915363-56-3, stock 9.9g, assay 98.6%, MWt: 539.43, Formula: C26H25Cl2FN8, Solubility: DMSO : ≥ 100 mg/mL (185.38 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MAP3K, Biological_Activity: Cot inhibitor-2 is a COT/Tpl2 inhibitor.

Name: NS19504, CAS: 327062-46-4, stock 39.8g, assay 98.4%, MWt: 269.16, Formula: C10H9BrN2S, Solubility: DMSO : 250 mg/mL (928.82 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: NS19504 is a Ca2+-activated K+ channel (BK channel, KCa1.1 channel) activator (EC50=11.0 µM) with relaxing effect on bladder smooth muscle spontaneous phasic contractions[1].
IC50 & Target: EC50: 11.0 µM (BK channel)[1]
In Vitro: NS19504 increases BK currents in freshly isolated guinea pig bladder smooth muscle cells and whole-cell. NS19504 increases the whole-cell currents response to 127 %, 194 %, 258 %, 561 % of control at a concentration of 0.32 µM, 1.0 µM, 3.2 µM and 10 µM, respectively[1].

Name: LM11A-31 (dihydrochloride), CAS: 1243259-19-9, stock 31.7g, assay 98.9%, MWt: 316.27, Formula: C12H27Cl2N3O2, Solubility: H2O : 125 mg/mL (395.23 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LM11A-31 dihydrochloride, a p75NTR (neurotrophin receptor p75) Ligand, is a potent proNGF (nerve growth factor) antagonist. LM11A-31 dihydrochloride is a water-soluble, non-peptide with high blood-brain barrier permeability[1][2].
IC50 & Target: proNGF[1]
In Vivo: LM11A-31 (oral gavage; 50 mg kg/day for 4 weeks) significantly mitigates proNGF accumulation and preserves BRB integrity[1]. 
LM11A-31 (orally; 50 or 75 mg/kg) administered for 3 months starting at 6-8 months of age prevents and/or reverses atrophy of basal forebrain cholinergic neurites and cortical dystrophic neurites in mid-stage male APPL/S mice[2].

Name: Pozanicline (dihydrochloride) ABT-089 (dihydrochloride), CAS: 161416-61-1, stock 1.2g, assay 98%, MWt: 265.18, Formula: C11H18Cl2N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Pozanicline dihydrochloride (ABT-089 dihydrochloride) is an orally bioavailable nicotinic acetylcholine receptor (nAChR) agonist with a Ki of 16.7 nM for binding to [3H]cytisine sites[1]. Pozanicline is an α4β2-selective nAChR agonist, which binds to rat brain α4β2 nAChR with a Ki of 17 nM while binding to α7 nAChR is insignificant[2].
In Vitro: Pozanicline (ABT-089) is a partial agonist at α4β2 nAChR. Moreover, one α6β2 nAChR subtype is particularly sensitive to Pozanicline with an EC50 of 0.11 μM[2]. 
Pozanicline (ABT-089) shows high selectivity for α6β2 and α4α5β2 nAChR subtypes[3].
In Vivo: Pozanicline (ABT-089; 0.3 mg/kg and 0.6 mg/kg) reverses nicotine withdrawal-induced deficits in contextual fear conditioning[3].

Name: AdipoRon hydrochloride, CAS: 1781835-20-8, stock 16.9g, assay 98%, MWt: 464.98, Formula: C27H29ClN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adiponectin Receptor, Biological_Activity: AdipoRon hydrochloride is an orally active and specific AdipoR agonist, binding to AdipoR1 and AdipoR2, with Kds of 1.8 and 3.1 μM, respectively.
IC50 & Target: Kd: 1.8 μM (AdipoR1), 3.1 μM (AdipoR2)[1]
In Vitro: AdipoRon hydrochloride is an orally active and specific AdipoR agonist, binds to AdipoR1 and AdipoR2, with Kds of 1.8 and 3.1 μM. AdipoRon (50 nM-50 μM) increases AMPK phosphorylation via AdipoR1[1]. AdipoRon (50 μM) dose-dependently attenuates the expression of TNF-α and TGF-β1 in the L02 cells. AdipoRon exhibits significant and dosage-dependent growth suppression on macrophages[2]. AdipoRon treatment significantly improves cardiac functional recovery after reperfusion, and inhibits post-MI apoptosis[3]. AdipoRon exerts vasodilation by mechanisms distinct to adiponectin and induces vasorelaxation without a marked decrease in VSMC [Ca2+]i[4].
In Vivo: AdipoRon (50 mg/kg, i.v.) cuases significant phosphorylation of AMPK in skeletal muscle and liver of wild-type mice but not Adipor1−/− Adipor2−/− double-knockout mice[1]. AdipoRon (0.02, 0.1, and 0.5 mg/kg, i.g.) alleviates D-GalN induced hepatotoxicity in mice, and prevents hepatic architecture distortion against D-GalN challenge. The hepatoprotective potential of AdipoRon is particularly evident in higher dosages (0.1 and 0.5 mg/kg)[2]. Enhanced cardiomyocyte apoptosis in APN-deficient mice is rescued by AdipoRon (50 mg/kg, p.o.) administration. Antiapoptotic effect of AdipoRon is attenuated but not lost in AMPK-DN mice[3].

Name: PD 90780, CAS: 77422-99-2, stock 38.8g, assay 98.1%, MWt: 362.34, Formula: C19H14N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PD 90780 is a non peptide antagonist of nerve growth factor (NGF) binding to the P75 NGF receptor, inhibits NGF-p75 NTR interaction with IC50s values of 23.1 µM and 1.8 µM in PC12 cells and PC12 nnr5 cells, respectively [1] .
IC50 & Target: IC50: 23.1 µM (NGF, PC12 cells), 1.8 µM (NGF, PC12 nnr5 cells)

Name: Neuronostatin-13 (human), CAS: 1096485-24-3, stock 8.1g, assay 98.7%, MWt: 1415.68, Formula: C64H110N20O16, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Neuronostatin-13 human is a 13-amino acid peptide hormone encoded by the somatostatin gene and plays an important role in the regulation of hormonal and cardiac function.
In Vitro: Neuronostatin-13 human is a 13-amino acid peptide hormone encoded by the somatostatin gene and plays an important role in the regulation of hormonal and cardiac function. Treatment with Neuronostatin-13 human (1,000 nM) enhances low-glucose-induced glucagon release compare with islets treated with control medium alone. Treatment with Neuronostatin-13 human for 1 h leads to a significant increase in the accumulation of glucagon mRNA compare with vehicle-treated control cells. In αTC1-9 α-cells, treatment with 100 nM Neuronostatin-13 human leads to an increase in phosphorylated PKA at 30 and 40 min[1].
In Vivo: Infusion with Neuronostatin-13 human delays glucose clearance in the rat model, such that blood glucose levels in Neuronostatin-13 human-treated animals are significantly higher at 1 and 10 min following intra-arterial injection of a glucose bolus[1]. Chocardiographic measurement reveals a remarkable drop in heart rate after 3-, 6- and 12-hr of Neuronostatin-13 human challenge. In addition, Neuronostatin-13 human treatment significantly decreases left ventricular end-systolic diameter (LVESD) and fractional shortening without affecting left ventricular end-diastolic diameter (LVEDD) between 6 and 12 hrs following Neuronostatin-13 human challenge, the effect of which returns to basal level 18-hr after Neuronostatin-13 human treatment[2].

Name: ASP2535, CAS: 374886-51-8, stock 18.4g, assay 98.8%, MWt: 382.42, Formula: C22H18N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GlyT;GlyT, Biological_Activity: ASP2535 is a potent, orally bioavailable, selective, brain permeable and centrally-active glycine transporter-1 (GlyT1) inhibitor. ASP2535 can improve cognitive impairment in animal models of schizophrenia and Alzheimer's disease[1].
IC50 & Target: GlyT1[1]
In Vitro: ASP2535 potently inhibits rat GlyT1 (IC50=92 nM) with 50-fold selectivity over rat glycine transporter-2 (GlyT2) in vitro[1]. 
In Vivo: ASP2535 (0.3-3 mg/kg; p.o) attenuates working memory deficit in MK-801-treated mice and visual learning deficit in neonatally phencyclidine (PCP)-treated mice[1]. 
ASP2535 (1-3 mg/kg, p.o.) also improves the PCP-induced deficit in prepulse inhibition in rats[1].

Name: Pregnenolone monosulfate (sodium salt) 3β-Hydroxy-5-pregnen-20-one monosulfate (sodium salt), CAS: 1852-38-6, stock 27.5g, assay 98.4%, MWt: 418.52, Formula: C21H31NaO5S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Autophagy;GPCR/G Protein;Metabolic Enzyme/Protease;Neuronal Signaling, Target: Autophagy;Cannabinoid Receptor;Endogenous Metabolite;Cannabinoid Receptor, Biological_Activity: Pregnenolone monosulfate sodium salt (3β-Hydroxy-5-pregnen-20-one monosulfate sodium salt) is a powerful neurosteroid, the main precursor of various steroid hormones including steroid ketones. Pregnenolone monosulfate sodium salt acts as a signaling-specific inhibitor of cannabinoid CB1 receptor, inhibits the effects of tetrahydrocannabinol (THC) that are mediated by the CB1 receptors. Pregnenolone monosulfate sodium salt can protect the brain from cannabis intoxication[1][2].
IC50 & Target: Cannabinoid CB1 receptor[1]
In Vitro: CB1 receptor stimulation increases brain Pregnenolone levels, which in turn exerts a negative feedback on the activity of the CB1 receptor antagonizing most of the known behavioral and somatic effects of THC. Pregnenolone likely acts as a signaling-specific negative allosteric modulator binding to a site distinct from that occupied by orthosteric ligands. Pregnenolone does not modify agonist binding but only agonist efficacy[1]. 
The effect of THC is significantly attenuated when slices are pre-treated with Pregnenolone 100 nM (15.1±1.8 % of inhibition). These effects are likely due to a pre-synaptic action of Pregnenolone. Thus, Pregnenolone blocks the increase in paired-pulse ratio (PPR) induced by THC but does not modify either the amplitude or the decay time of miniature EPSC (mEPSC)[1].
In Vivo: Pregnenolone administration (2-6 mg/kg) blocks THC-induced food-intake in Wistar rats and in C57BL/6N mice, and blunts the memory impairment induced by THC in mice, but it does not modify these behaviors per se. Injections of Pregnenolone (2 and 4mg/kg) before each self-administration session reduce the intake of WIN 55,212-2 and reduce the break-point in a progressive ratio schedule[1].

Name: ML 297 VU 0456810;CID 56642816, CAS: 1443246-62-5, stock 20.1g, assay 98.4%, MWt: 328.32, Formula: C17H14F2N4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: ML 297 (VU 0456810) is a potent and selective GIRK1/2 activator, with an EC50 of 0.16 μM. ML 297 is potential for the treatment of epilepsy[1][2].
IC50 & Target: EC50: 0.16 μM (GIRK1/2), 18 μM (GIRK1/4)[1]
In Vitro: ML 297 is completely inactive for GIRK2/3[1]. 
ML297 shows concentration-dependent efficacy in expressing GIRK1/2 cells and with an EC50 of 162 nM[2]. 
ML297 shows a complete inability to modulate the activity of HEK-293 cells expressing GIRK2 alone and GIRKGIRK2/3[2]. 
In Vivo: ML297 (60 mg/kg; i.p.) shows a highly significant ability to both prevent convulsions and prevent fatality of the PTZ treatment[2].

Name: SPP-86, CAS: 1357349-91-7, stock 14.6g, assay 98.3%, MWt: 277.32, Formula: C16H15N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: RET, Biological_Activity: SPP-86 is a potent and selective cell permeable inhibitor of RET tyrosine kinase, with an IC50 of 8 nM. SPP-86 inhibits RET-induced phosphatidylinositide 3-kinases (PI3K)/Akt and MAPK signaling, also inhibits RET-induced estrogen receptorα (ERα) phosphorylation in MCF7 cells[1].
IC50 & Target: IC50: 8 nM (RET)[1].
In Vitro: SPP86 (0-10 μM) inhibits MAPK signaling and proliferation in RET/PTC1 expressing TPC1 but not 8505C or C643 cells[1]. 
SPP86 (0-10 μM) inhibits RET- induced phosphatidylinositide 3-kinases (PI3K)/Akt and MAPK signaling and estrogen receptorα (ERα) phosphorylation in MCF7 cells[1].

Name: Smurf1-IN-A01 A01, CAS: 1007647-73-5, stock 33.3g, assay 98.3%, MWt: 512.93, Formula: C22H20ClF3N4O3S, Solubility: DMSO : 62.5 mg/mL (121.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Smurf1-IN-A01 (A01) is an ubiquitin ligase Smad ubiquitination regulatory factor-1 (Smurf1) inhibitor with a kd of 3.664 nM, which increases BMP-2 responsiveness by inhibiting Smurf1-mediated Smad1/5 degradation[1].
IC50 & Target: Kd: 3.664 nM (Smurf1)[1]

Name: TC-I 2014, CAS: 1221349-53-6, stock 15.9g, assay 98.4%, MWt: 467.41, Formula: C23H19F6N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: TC-I 2014 (compound 5) is a potent and orally active Benzimidazole-containing transient receptor potential melastatin 8 (TRPM8) antagonist, with IC50 values of 0.8 nM, 3.0 nM and 4.4 nM for canine, human and rat channels respectively. TC-I 2014 exhibits antiallodynic properties in pain models[1].
IC50 & Target: TRPM8[1].
In Vitro: TC-I 2014 (compound 5) potently inhibits cold-induced TRPM8 currents in HEK293 cells stably expressing canine or human TRPM8, with IC50 values of 0.413 and 1 nM, respectively[1].
In Vivo: TC-I 2014 (10 mg/kg, Orally once) completely prevents icilin-induced WDS[1].

Name: R-7050 TNF-α Antagonist III, CAS: 303997-35-5, stock 11.5g, assay 98.1%, MWt: 380.77, Formula: C16H8ClF3N4S, Solubility: DMSO : 25 mg/mL (65.66 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: TNF Receptor, Biological_Activity: R-7050 (TNF-α Antagonist III) is a tumor necrosis factor receptor (TNFR) antagonist with greater selectivity toward TNFα.
IC50 & Target: TNFα[1]
In Vitro: R-7050 (TNF-α Antagonist III) is a potent and fully reversible hit with greater selectivity toward TNFα. In TNFα-induced intercellular adhesion molecule 1 (ICAM-1) expression, R-7050 inhibition potency (EC50=0.63 μM) is 2- to 3-fold greater than EC50 for IL-1β-induced ICAM-1 expression (EC50=1.45 2 μM). R-7050 inhibits phosphorylation of both the JNK pathway (MKK4, JNKs, and ATF2) and p38 pathway (MKK3/6, p38, and MAPKAP2)[1]. R-7050 is a cell-permeable triazoloquinoxaline compound that selectively inhibits TNF-α induced cellular signaling. Unlike biologic TNF inhibitors (e.g. Infliximab, Etanercept, Adalimumab) that directly bind TNF-α and function as decoy receptors, R-7050 does not affect binding of TNF-α to TNFR. In contrast, R-7050 selectively inhibits the association of TNFR with intracellular adaptor molecules (e.g. TRADD, RIP), limits receptor internalization, and prevents subsequent cellular responses after TNF-α binding[2].
In Vivo: R-7050 (TNF-α Antagonist III) (6 mg/kg) reduces Evans blue extravasation to 28.7±5.9 μg and 30.3±1.9 μg Evans blue/g brain tissue when administered at 0.5 h or 2 h post-ICH, respectively (p<0.05 and p<0.01 vs ICH, respectively; not significantly different from sham). Brain water content, a measure of brain edema, increases from 75.6±0.3% in sham-operated mice to 81.5±0.5% at 24h post-ICH (p<0.05 vs. sham). 6, 12, or 18 mg/kg R-7050 reduces brain water content to 78.5±0.3%, 78.3±0.3%, or 79.3±0.5%, respectively (all treatments p<0.05 vs. ICH; treatments not significantly different from each other). Notably, mice treated with 18 mg/kg exhibit a reduction in general activity/locomotion. As is observed with Evans blue extravasation, R-7050 (6 mg/kg) significantly reduces brain water content after ICH. Administration of R-7050 at 0.5h or 2h post-ICH attenuates brain water content to levels observed in sham-operated mice (p<0.05 vs ICH, not significantly different from sham)[2].

Name: Dianicline (dihydrochloride), CAS: 292634-27-6, stock 9g, assay 98.8%, MWt: 289.20, Formula: C13H18Cl2N2O, Solubility: DMSO : 25 mg/mL (86.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Dianicline dihydrochloride is a α4β2 nicotinic acetylcholine receptor partial agonist, a class of drugs that includes varenicline and cytisine for smoking cessation. Dianicline dihydrochloride increases cessation rates in a dose-dependent manner[1].

Name: TRAF-STOP inhibitor 6877002, CAS: 433249-94-6, stock 9.9g, assay 98.9%, MWt: 251.32, Formula: C17H17NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;NF-κB, Target: TNF Receptor;NF-κB, Biological_Activity: TRAF-STOP inhibitor 6877002, is a selective inhibitor of CD40-TRAF6 interaction, compound VII, shows inhibition of NF-κB activation in RAW cells, extracted from patent WO2014033122A1[1]. TRAF-STOP 6877002 prevents the progression of established atherosclerosis in mice, reduces leukocyte recruitment and reduces macrophage activation; reduces macrophage proliferation in atherosclerotic plaques[2].
IC50 & Target: CD40-TRAF6 interaction; NF-κB

Name: CINPA1, CAS: 102636-74-8, stock 20.3g, assay 98.5%, MWt: 395.49, Formula: C23H29N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CINPA1 is a potent and specific inhibitor of constitutive androstane receptor (CAR) that does not activate pregnane X receptor (PXR). CINPA1 reduces CAR-mediated transcription with an IC50 of ~70 nM. CINPA1 can be used as a molecular tool for understanding CAR function[1].
IC50 & Target: IC50: ~70 nM (CAR)[1]
In Vitro: CINPA1 (1μM ; 24 hours) inhibits CAR-mediated transactivation without activating PXR in HepG2 cells[1]. 
CINPA1 is a specific xenobiotic receptor inhibitor and has no cytotoxic effects up to 30 μM[1]. 
CINPA1 inhibits CAR-mediated gene expression in primary human hepatocytes, where CAR is endogenously expressed[1]. 
CINPA1 does not alter the protein levels or subcellular localization of CAR[1]. 
CINPA1 increases corepressor and reduces coactivator interaction with the CAR ligand-binding domain in mammalian two-hybrid assays[1]. 
CINPA1 disrupts CAR binding to the promoter regions of target genes in chromatin immunoprecipitation assays[1]. 
CINPA1 efficiently inhibits CAR-LBD interaction with the coactivator peptide that suggesting that CINPA1 is a ligand of CAR[1].

Name: DFHBI, CAS: 1241390-29-3, stock 7.9g, assay 98.6%, MWt: 252.22, Formula: C12H10F2N2O2, Solubility: DMSO : ≥ 83.33 mg/mL (330.39 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DFHBI is a small molecule that resembles the chromophore of green fluorescent protein (GFP). Spinach and DFHBI are essentially nonfluorescent when unbound, whereas the Spinach-DFHBI complex is brightly fluorescent both in vitro and in living cells.
In Vitro: These RNAs interact with DFHBI to produce a bluish-green fluorescence emission (501 nm) after excitation at 447 nm. Spinach and Spinach2 are RNA aptamers that can be used for the genetic encoding of fluorescent RNA. Spinach2 binds and activates the fluorescence of DFHBI, allowing the dynamic localizations of Spinach2-tagged RNAs to be imaged in live cells. The spectral properties of Spinach2 are limited by DFHBI, which produces fluorescence that is bluish-green and is not optimized for filters commonly used in fluorescence microscopes. Spinach and Spinach2 bind to DFHBI have fluorescence excitation maxima of 447 nm and peak fluorescence emission of 501 nm[1]. Broccoli-tagged RNAs are selectively detected in total cellular RNA by gel electrophoresis followed by staining of gels with DFHBI, the Broccoli-binding fluorophore. Spinach is a 98-nt-long RNA aptamer that binds to and switches on the fluorescence of DFHBI. Both Spinach and DFHBI are essentially nonfluorescent when unbound, whereas the Spinach-DFHBI complex is brightly fluorescent both in vitro and in living cells. DFHBI should be shielded from light. All stock solutions of DFHBI should be maintained in dark tubes or wrapped in foil. Plates containing cultures incubated with DFHBI should be kept in the dark by using a foil overwrap[2].

Name: AZD 9272, CAS: 327056-26-8, stock 16.9g, assay 98.2%, MWt: 284.22, Formula: C14H6F2N4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: AZD 9272 is a brain penetrant mGluR5 antagonist.
IC50 & Target: mGluR5[1]
In Vitro: AZD 9272 causes a concentration dependent decrease in the magnitude of the intracellular Ca2+ response to 1.5 μM of the mGluR group I selective agonist DHPG in both the human and the rat mGluR5 expressing cell lines. The maximal inhibition is 100%. The mean IC50 (±SD) value at the human mGluR5 is 7.6±1.1 nM (n=13) for AZD9272. The mean IC50 value at the rat mGluR5 is 2.6±0.3 nM (n=3) for AZD9272. In contrast, 10 μM of AZD9272 does not diminish the response to 10 μM ATP in the background GHEK cells. Increasing concentrations of AZD9272 causes a decrease in the potency and the maximal response of DHPG. AZD9272 completely reverses the glutamate-stimulated (EC80, 80 μM) phosphatidyl inositol hydrolysis in human mGluR5-GHEK cells in a concentration-dependent manner, with IC50 of 26±3 nM (n=21)[1].
In Vivo: The clearance of AZD 9272 is low following a single intravenous dose at 3 μmol/kg and AZD 9272 is eliminated from plasma with terminal half-lives between 2 and 6 h. The terminal half-lives following oral dosing are similar to the half-lives following intravenous dosing. The volume of distribution at steady state is intermediate for AZD9272[1]. AZD9272 causes no cocaine-appropriate responding and causes a non-dose-dependent reduction in response rates at higher doses. AZD9272 at 2.84 mg/kg causes greater than 80% and typically more than 99% MTEP-appropriate responding up to 20 hours after dose, with a decline to approximately 20% at 24 hours after dose, yielding a t1/2 of 21.93 hours, and causes no systematic effects on response rates. The first time point at which AZD9272 causes >90% MTEP-appropriate responding is at 30 minutes after dose[2].

Name: AZD 2066, CAS: 934282-55-0, stock 13.5g, assay 98.7%, MWt: 381.82, Formula: C19H16ClN5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: AZD 2066 is a selective, orally active and brain-penetrant mGluR5 antagonist, with analgesia activity[1].

Name: N-Acetylcysteine amide, CAS: 38520-57-9, stock 16.7g, assay 98.8%, MWt: 162.21, Formula: C5H10N2O2S, Solubility: H2O : 200 mg/mL (1232.97 mM; Need ultrasonic); DMSO : ≥ 100 mg/mL (616.48 mM), 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: N-Acetylcysteine amide is a cell membranes and blood brain barrier permeant thiol antioxidant and neuroprotective agent, reduces ROS production.
In Vitro: N-Acetylcysteine amide shows no obvious effect on the viability of H9c2 cells treated with doxorubicin (DOX) at < 1 mM, but causes significant cytotoxicity at 10-20 mM. N-Acetylcysteine amide (750 μM) reduces the ROS levle and lipid peroxidation induced by DOX, and restores GSH/GSSG ratio and activities of antioxidant enzymes, such as catalase (CAT), gluthathione peroxidase (GPx), gluthathione reductase (GR)[1]. N-Acetylcysteine amide (1 mM) protects the human brain microvascular endothelial (HBMVEC) from methamphetamine (METH)- induced cell death[3].
In Vivo: N-Acetylcysteine amide has increased CNS bioavailability. N-Acetylcysteine amide (150 mg/kg, i.p.) improves cortical sparing and functional outcome, reduces oxidative stress, improves mitochondrial bioenergetics, and maintains mitochondrial glutathione content following traumatic brain injury (TBI) in rats[2].

Name: ML334 LH601A, CAS: 1432500-66-7, stock 0.1g, assay 98.8%, MWt: 446.50, Formula: C26H26N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: Keap1-Nrf2, Biological_Activity: ML334 is a potent, cell permeable activator of NRF2 by inhibition of Keap1-NRF2 protein-protein interaction. ML334 binds to Keap1 Kelch domain with a Kd of 1 μM. ML334 stimulates NRF2 expression and nuclear translocation and induces antioxidant response elements (ARE) activity[1][2].
IC50 & Target: Ki: 1 μM (Keap1)[2]
In Vitro: ML334 (LH601A; 50-100 µM; 6-16 hours; HEK293 cells) treatment increases NQO1 and TRX1 mRNAs between 2- and 3-fold at both 6 and 16 h. And also enhances HO-1 mRNA expression between 4- and 7-fold at 6 h, with lesser fold-changes at 16 h[1]. 
ML334 (LH601A; 50-100 µM; 16 hours; HEK293 cells) treatment induces HO-1 and TRX1 proteins in HEK293 cells[1]. 
ML334 (LH601A) stimulates NRF2 expression and nuclear translocation in HEK293 cells[1].

Name: HFI-142, CAS: 332164-34-8, stock 33.3g, assay 98.3%, MWt: 312.32, Formula: C17H16N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aminopeptidase, Biological_Activity: HFI-142 is an insulin-regulated aminopeptidase (IRAP) inhibitor with a Ki of 2.01 μM[1].
IC50 & Target: Ki: 2.01 μM (Insulin-regulated aminopeptidase)[1]

Name: EML 425, CAS: 1675821-32-5, stock 29.8g, assay 98.6%, MWt: 440.49, Formula: C27H24N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Epigenetic Reader Domain;Histone Acetyltransferase, Biological_Activity: EML425 is a potent and selective CREB binding protein (CBP)/p300 inhibitor with IC50s of 2.9 and 1.1 μM, respectively.
IC50 & Target: IC50: 1.1 μM (p300), 2.9 μM (CBP)[1]
In Vitro: EML 425 (EML425, Compound 7h) is a potent and selective reversible inhibitor of CBP/p300, noncompetitive versus both acetyl-CoA and a histone H3 peptide, and endows with good cell permeability. EML 425 inhibits both p300 and CBP (IC50 values of 2.9 and 1.1 μM, respectively) while being practically inactive against the enzymes general control non derepressible-5 (GCN5) and p300/CBP-associated factor (PCAF). EML 425 induces a marked and time-dependent reduction in the acetylation of lysine H4K5 and H3K9 in U937 cells. EML 425 is shown to be a reversible inhibitor, noncompetitive versus both acetyl-CoA and a histone H3 peptide, and able to bind both the free enzyme and the enzyme-substrate complex, even with unequal affinity constants. The best scoring docking poses suggest that the binding site for EML 425 is an alternative pocket lying near the substrate lysine binding groove and close to the acetylation site[1].

Name: GN44028, CAS: 1421448-26-1, stock 8.1g, assay 98.1%, MWt: 305.33, Formula: C18H15N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIF/HIF Prolyl-Hydroxylase, Biological_Activity: GN44028 is a hypoxia inducible factor (HIF)-1 inhibitor, with an IC50 of 14 nM. GN44028 inhibits hypoxia-induced HIF-1α transcriptional activity without suppressing HIF-1α mRNA expression, HIF-1α protein accumulation, or HIF-1α/HIF-1β heterodimerization[1].
IC50 & Target: IC50: 14 nM (HIF-1)[1].

Name: S 2101, CAS: 1239262-36-2, stock 5.9g, assay 98.1%, MWt: 311.75, Formula: C16H16ClF2NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: S 2101 is a lysine-specific demethylase 1 (LSD1) inhibitor with an IC50 of 0.99 μM, Ki of 0.61 μM and Kinact/Ki of 4560 M/s.
IC50 & Target: IC50: 0.99 μM (LSD1)[1] 
Ki: 0.61 μM (LSD1)[1]
In Vitro: S 2101 is a lysine-specific demethylase 1 (LSD1) inhibitor with an IC50 of 0.99 μM, Ki of 0.61 μM and Kinact/Ki of 4560 M/s. S 2101 also displays much lower inhibition activity toward MAO-B (Ki=17 µM, Kinact/Ki=18 M/s) and MAO-A (Ki=110 µM, Kinact/Ki=60 M/s). The treatment of HEK293T cells with S 2101 results in a dose-dependent increase in the level of H3K4me2, which must have accumulated by the inactivation of LSD1. During the course of S 2101 treatment, the amounts of histone H3 and LSD1 in the nuclear extracts remain essentially unaffected. Because the treatment with 1 μM S 2101 generates a level of H3K4me2 similar to that elicited by 50 μM 2-PCPA, S 2101 is assumed to have approximately 50-fold stronger LSD1 inhibition activity than 2-PCPA in human cells[1].

Name: Ogerin, CAS: 1309198-71-7, stock 11.8g, assay 98.3%, MWt: 307.35, Formula: C17H17N5O, Solubility: DMSO : 250 mg/mL (813.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ogerin is a selective GPR68 positive allosteric modulator, with a pEC50 of 6.83. Ogerin shows inverse agonist and antagonist activity (Ki, 220 nM) at A2A receptoor and weak antagonist activity (Ki, 736 nM) at 5-HT2B receptor. Ogerin blocks recall in fear conditioning in mice[1].
IC50 & Target: pEC50: 6.83 (GPR68)[1] 
Ki: 220 nM (A2A receptoor), 736 nM (5-HT2B receptor)[1]

Name: Aphidicolin, CAS: 38966-21-1, stock 37.9g, assay 98.2%, MWt: 338.48, Formula: C20H34O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Anti-infection;Cell Cycle/DNA Damage, Target: Apoptosis;HSV;DNA/RNA Synthesis, Biological_Activity: Aphidicolin is an inhibitor of DNA polymerase α and δ, prevents mitotic cell division by interfering with the activity of DNA polymerase[1].
Aphidicolin is an antibiotic produced by the mold Cephalosporium aphidicola. Aphidicolin is a potent inhibitor of cellular deoxyribonucleic acid synthesis and inhibits the growth of herpes simplex virus[2].
Aphidicolin potentiates apoptosis induced by arabinosyl nucleosides in a human promyelocytic leukemia cell line[3].

Name: BAM 15, CAS: 210302-17-3, stock 38.2g, assay 98%, MWt: 340.29, Formula: C16H10F2N6O, Solubility: DMSO : 75 mg/mL (220.40 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BAM 15 is a novel mitochondrial protonophore uncoupler.
In Vitro: BAM 15 is able to increase O2 consumption across a broad dosing range without increasing ROS. BAM 15 and FCCP are structurally unrelated and it is observed that low doses of BAM 15 from 100 nM to 1 μM increase cellular O2 consumption rate (OCR) to a similar degree as FCCP, but higher concentrations from 1 μM to 50 μM reveal that BAM 15 is able to maintain uncoupled respiration at a high rate in a range of cell lines. BAM 15 is fully capable of increasing mitochondrial respiration in the presence of oligomycin and does so across a broader concentration range than FCCP in both myoblasts and hepatocytes. BAM 15 induces mitochondrial swelling, demonstrating that BAM 15 is a protonophore. BAM15-treated cells are more viable than FCCP-treated cells when administered across a broad dosing range up to 50 μM[1].
In Vivo: Compare to vehicle-treated mice, animals that receive BAM 15 are protected from kidney injury as indicated by lower plasma creatinine levels at 24 and 48 h post-ischemia, reduced tubular necrosis, less depletion of brush border villi, less obstruction of proximal tubules, and less immune cell infiltration[1].

Name: FTI 276 (TFA), CAS: 1217471-51-6, stock 16.6g, assay 98.6%, MWt: 547.61, Formula: C23H28F3N3O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Farnesyl Transferase, Biological_Activity: FTI-276 is a protein farnesyl transferase (PFT) inhibitor with IC50s of 0.9 nM and 0.5 nM for Plasmodium falciparum and human, respectively[1].
IC50 & Target: IC50: 0.9 nM (PFT, Plasmodium falciparum), 0.5 nM (PFT, human)[1].

Name: Amyloid β-peptide (1-40) (rat), CAS: 144409-98-3, stock 25.6g, assay 98.3%, MWt: 4233.76, Formula: C190H291N51O57S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Amyloid β-peptide (1-40) (rat) is the prone-to-aggregation product of amyloid precursor protein proteolytic cleavage, and is the major constituent of senile plaques observed in the brain of Alzheimer’s disease.
IC50 & Target: The Amyloid β-peptide (1-40) (rat)-treated rats require longer to find the platform hidden under the water. In the visible platform test, the latency for each group is similar (20.56±11.31 s in control and 14.68±9.97 s in Amyloid β-peptide (1-40) (rat) group, p=0.304). Among these tested proteins, 6 ones are significantly up-regulated and 7 ones significantly down-regulated in Amyloid β-peptide (1-40) (rat) group comparing with the control. Tubulin β chain is significantly down-regulated in Amyloid β-peptide (1-40) (rat) group (p=0.014) when compare with control. Similar changes are also observed for ATP synthase β subunit (p=0.010) and synapsin Ib between Amyloid β-peptide (1-40) (rat) and control groups, but not significantly for synapsin Ib (p=0.295)[1].

Name: β-Amyloid (1-42), rat Amyloid β-peptide (1-42) (rat), CAS: 166090-74-0, stock 21.5g, assay 98.4%, MWt: 4418.02, Formula: C199H307N53O59S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (1-42), rat is a 42-aa peptide, shows cytotoxic effect on acute hippocampal slices, and used in the research of Alzheimer's disease.
IC50 & Target: Amyloid-β[1]
In Vitro: β-Amyloid (1-42), rat shows cytotoxic effect on the hippocampal slices at 20 μM[1]. β-Amyloid (1-42), rat causes morphological changes in NGF-induced PC12 cells, induces formed cell processes to retract in differentiated cells and affect the expression of exons 2/3 in both undifferentiated and differentiated cells[2].

Name: Liarozole (dihydrochloride) R75251 (dihydrochloride), CAS: 1883548-96-6, stock 21g, assay 98.9%, MWt: 381.69, Formula: C17H15Cl3N4, Solubility: H2O : ≥ 50 mg/mL (131.00 mM); DMSO : 50 mg/mL (131.00 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Liarozole dihydrochloride (R75251; R85246) is a cytochrome P450 (CYP450) dependent inhibitor, orally active, it also a potent inhibitor of estrogen (via inhibition of aromatase) and testicular androgen synthesis (inhibition of 17 ,20-lyase). Liarozole dihydrochloride prevents the catabolism of retinoic acid via inhibition of 4-hydroxylase and exhibits retinoid sparing and retinoid-mimetic effects in vivo. Liarozole dihydrochloride is an imidazole derivative; it is being investigated as a non-hormonal agent in prostate cancer and in the treatment of various other cancers and skin disorders[1].
In Vitro: Liarozole inhibits the metabolism of retinoic acid to more polar metabolites in hamster liver microsomes (IC50=2.2 μM), rat liver homogenate (IC50=0.14 μM), dunning prostate cancer homogenate (IC50=0.26 μM) and MCF-7 human breast cancer cells (almost complete block at 10μM) [1].
Liarozole inhibits 17a-hydroxylase activity in bovine adrenal microsomes (IC50=0.15 μM) [1].
Liarozole has modest inhibitory activity on cholesterol synthesis in human hepatoma cells(IC50=5 μM)[1].

Name: VUF11207 (fumarate), CAS: 1785665-61-3, stock 5.4g, assay 98.4%, MWt: 586.65, Formula: C31H39FN2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: VUF11207 fumarate (Compound 29) is a CXCR7 agonist and a high-potency CXCR7 (pKi of 8.1) ligand that induces recruitment of β-arrestin2 (pEC50 of 8.8) and subsequent internalization (pEC50 of 7.9) of CXCR7[1].

Name: KHS101 hydrochloride, CAS: 1784282-12-7, stock 20.9g, assay 98.7%, MWt: 375.92, Formula: C18H22ClN5S, Solubility: DMSO : 160 mg/mL (425.62 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KHS101 hydrochloride could selectively induce a neuronal differentiation phenotype and interacts with transforming acidic coiled-coil-containing protein 3 (TACC3).
IC50 & Target: TACC3[1]
In Vitro: KHS101 increases neuronal differentiation of adherently cultured rat NPCs in a dose-dependent fashion (EC50 ~1 μM). KHS101-induced neuron formation (40-60% TuJ1+ cells at 1.5–5 μM KHS101) is also observed under neurosphere-forming conditions in secondary neurospheres derived from both the hippocampus and the subventricular zone (SVZ) of adult rats. Moreover, hippocampal NPCs treated with KHS101 and cultured adherently on microelectrode arrays for 12 d exhibit neuronal morphologies as well as spontaneous spiking activity, hence indicating the presence of functional, maturing neurons[1]. KHS101 markedly attenuates tumor cell growth as compared to the cells treated with the vehicle [dimethyl sulfoxide (DMSO)]. TACC3 is a known target of KHS101 in rodent neural progenitor cells. KHS101 has been shown to cause cellular destabilization of TACC3, hence reducing endogenous TACC3 protein levels over time [2].
In Vivo: Tumor cell proliferation is markedly reduced in KHS101-treated tumors (about twofold). KHS101-treated tumors show signs of elevated cell death (reduced cellularity/increased pyknosis) compared with tumors treated with vehicle control. KHS101 treatment markedly reduces both frontal-to-caudal tumor expansion and corpus callosum invasion of vimentin-positive GBM1 cells. It is also found that the survival of animals carrying GBMX1 tumors (established 2 or 6 weeks before treatment) is markedly increased by the KHS101 treatment regimen for 10 weeks. None of the mice have to be removed from the study because of adverse side effects of the treatment. An additional experiment using a continuous KHS101 treatment regimen until the experimental endpoints also shows a marked increase in the survival of GBMX1-bearing animals. Histological endpoint analysis of KHS101- and vehicle-treated animals confirms a significantly decreased tumor size in KHS101-treated mice[2].

Name: GsMTx4, CAS: 1209500-46-8, stock 38.6g, assay 98.8%, MWt: 4101.89, Formula: C185H279N49O45S6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GsMTx4 is a spider venom peptide that selectively inhibits cation-permeable mechanosensitive channels (MSCs) belonging to the Piezo and TRP channel families. GsMTx4 is an important pharmacological tool for identifying the role of these excitatory MSCs in normal physiology and pathology[1]. GsMTx4 significantly attenuates bladder hyperactivity[2].
IC50 & Target: MSCs[1]

Name: MS023 (dihydrochloride), CAS: 1992047-64-9, stock 10.9g, assay 98.3%, MWt: 360.32, Formula: C17H27Cl2N3O, Solubility: DMSO : ≥ 150 mg/mL (416.30 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: MS023 dihydrochloride is a potent, selective, and cell-active inhibitor of human type I protein arginine methyltransferases (PRMTs) inhibitor, with IC50s of 30, 119, 83, 4 and 5 nM for PRMT1, PRMT3, PRMT4, PRMT6, and PRMT8, respectively[1].
IC50 & Target: IC50: 30 nM (PRMT1), 119 nM (PRMT3), 83 nM (PRMT4), 4 nM (PRMT6), 5 nM (PRMT8)[1]
In Vitro: MS023 (1-1000 nM; 48 hours) inhibits PRMT1 methyltransferase activity in MCF7 cells[1]. 
MS023(1-1000 nM; 20 hours) inhibits PRMT6 methyltransferase activity in HEK293 cells[1].

Name: LY2562175, CAS: 1103500-20-4, stock 0.9g, assay 98.5%, MWt: 540.44, Formula: C28H27Cl2N3O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (115.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: FXR;Autophagy, Biological_Activity: LY2562175 is a potent and selective FXR agonist with an EC50 of 193 nM.
IC50 & Target: EC50: 193 nM (FXR)
In Vitro: LY2562175 promotes transcriptional activation of human FXR in a cell-based co-transfection assay with an EC50 of 193 nM. LY2562175 promotes recruitment of a peptide from the nuclear receptor interaction domain of the coactivator SRC-1 with a relative EC50 of 121 nM and 93.5% efficacy as compare to GW4064[1].
In Vivo: LY2562175 causes a dose-dependent decrease in serum cholesterol and serum triglycerides. At a dose of 10 mg/kg, the decrease in cholesterol with LY2562175 is 80% below vehicle-treated animals, and the decrease in serum triglycerides is 76% from control group. The ED50 for serum cholesterol is determined to be 2 and 3.4 mg/kg for serum triglycerides. Treatment of female ZDF rats with LY2562175 results in a dose dependent lowering of plasma triglycerides in the fasted and nonfasted states. When administered as a fixed dose combination with BRL49653, LY2562175 further lowers fasted and nonfasted plasma triglycerides. FPLC fractionation of the lipoproteins reveals that LY2562175 treatment results in a reduction in vLDL-C and a dramatic increase in HDL-c in this animal model[1].

Name: iCRT3, CAS: 901751-47-1, stock 39g, assay 98.1%, MWt: 394.53, Formula: C23H26N2O2S, Solubility: DMSO : 150 mg/mL (380.20 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Stem Cell/Wnt, Target: Apoptosis;Wnt, Biological_Activity: iCRT3 is an inhibitor of both Wnt and β-catenin-responsive transcription.
IC50 & Target: Wnt[1], β-catenin-responsive transcription[2]
In Vitro: iCRT3 is an inhibitor of both Wnt and β-catenin-responsive transcription. iCRT3 significantly decreases TOP Flash activity and reduces the level of NTSR1. The anti-apoptotic effects of Neurotensin (NTS) and Wnt3a can be largely abrogated by iCRT3[1]. Cells maintained long term with iCRT3 show enhanced expression of classic pluripotency genes compare with the DMSO control, whereas expression of differentiation markers and T-cell factor (TCF) target genes is concomitantly reduced[2]. Treatment with iCRT3 at doses of 12.5, 25, 50, and 75 μM decreases TNF-α levels by 14.7%, 18.5%, 44.9% and 61.3%, respectively. With iCRT3 treatment, IκB levels are increased in a dose-dependent manner compare to the vehicle[3].
In Vivo: The tumor growth rates are markedly retarded by iCRT3 treatment. Consistently, the tumor-suppressive role of iCRT3 is accompanied with a reduction in Ki67 index, a proliferation marker[1]. The IL-6 levels in the 10 mg/kg iCRT3 treatment group are 82.9% lower than those in the vehicle group. IL-1β levels are undetectable in the sham but reach 371 pg/mL in septic mice and are down by 30.2% and 53.2%, respectively, with 5 and 10 mg/kg iCRT3. With iCRT3 treatment at doses of 5 and 10 mg/kg, AST levels in these septic mice are 15.4% and 44.2% lower, respectively, than those in the vehicle-treated mice. After treatment with 10 mg/kg iCRT3, lung morphology is improved with much reduced microscopic deterioration, compare to the vehicle group. The number of apoptotic cells in the lung tissues of the iCRT3-treated mice is significantly reduced by 92.7% in comparison with the vehicle group[3].

Name: ROC-325, CAS: 1859141-26-6, stock 1.6g, assay 98.7%, MWt: 503.06, Formula: C28H27ClN4OS, Solubility: DMSO : 32 mg/mL (63.61 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: ROC-325 is a novel inhibitor of autophagy.
IC50 & Target: Autophagy[1]
In Vitro: ROC-325 is a novel inhibitor of autophagy. Treatment with ROC-325 results in a significant loss of acridine orange fluorescence. ROC-325 triggers a highly significant increase in cathepsin D (CTSD) levels. ROC-325 treatment yields pharmacodynamic effects that are consistent with inhibition of autophagy. Treatment with 5 μM ROC-325 for 24 hours leads to the formation of LC3B punctae and a robust increase in LC3B levels in both A498 and 786-0 RCC cells. Immunoblotting analysis conducted in both A498 and 786-0 cells demonstrates that ROC-325 promotes a dose-dependent increase in LC3B expression in a manner that correlated with a corresponding increase in the levels of p62 and cathepsin D[1].
In Vivo: ROC-325 treatment leads to significant, dose-dependent inhibition of disease progression. ROC-325 is well tolerated and no notable toxicities are observed other than a very modest, nonsignificant reduction in mean body weight at the highest dose. Immunohistochemical analysis of specimens collected from animals treated with ROC-325 demonstrates significant, dose-dependent increases in the autophagic markers LC3B and p62 and increases apoptosis[1].

Name: Parsaclisib INCB050465, CAS: 1426698-88-5, stock 33.7g, assay 98.6%, MWt: 432.88, Formula: C20H22ClFN6O2, Solubility: DMSO : 125 mg/mL (288.76 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: Parsaclisib is a potent and selective PI3Kδ inhibitor, with an IC50 of 1 nM at 1 mM ATP, and shows appr 20,000-fold selectivity for PI3Kα, PI3Kβ, PI3Kγ and 57 other kinases.
IC50 & Target: IC50: 1 nM (PI3Kδ, 1 mM ATP)[1]
In Vitro: Parsaclisib (INCB050465) is a potent and selective PI3Kδ with an IC50 of 1 nM at 1 mM ATP, and shows appr 20,000-fold selectivity for PI3Kα, PI3Kβ, PI3Kγ and 57 other kinases. Parsaclisib displays significant activity with IC50 values ranging from 0.2 to 2 nM in B and T cell proliferation aaasys. Parsaclisib inhibits proliferation of several DLBCL and MCL cell lines in vitro (EC50 < 10 nM)[1].

Name: Petesicatib, CAS: 1252637-35-6, stock 8.1g, assay 98.4%, MWt: 603.54, Formula: C25H23F6N5O4S, Solubility: DMSO : 125 mg/mL (207.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cathepsin, Biological_Activity: Petesicatib is a cathepsin S inhibitor, used in research of immune diseases[1].
IC50 & Target: Cathepsin S[1]
In Vitro: Petesicatib (Example 238) is a cathepsin S inhibitor, used in research of immune diseases[1].

Name: TMRM Perchlorate T668, CAS: 115532-50-8, stock 34.5g, assay 98.4%, MWt: 500.93, Formula: C25H25ClN2O7, Solubility: DMSO : 41.67 mg/mL (83.19 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TMRM Perchlorate is a cell-permeant cationic lipophilic red fluorescent dye (λex=530 nm, λem=592 nm).
In Vitro: TMRM Perchlorate is a fluorescent probe (excitation, 530±21 nm; emission, 592±22 nm). The fluorescence signal in the presence of TMRM Perchlorate shows a slight decrease after the addition of glutamate, indicative of increased polarization of the mitochondrial inner membrane. In the presence of TMRM Perchlorate (2 μM) the coupled respiration with Complex I substrates or upon the addition of Complex II substrate is decreased by 27%[1]. Exposure of hippocampal cultures to low concentrations of TMRM Perchlorate (50 to 500 nM) for 1 to 3 hours results in selective staining of mitochondria in both neurons and the underlying glial cells. Exposure of hippocampal cultures to high concentrations of TMRM Perchlorate (1 to 25 µM) stains mitochondria selectively and quickly, reaching a plateau after 5 to 10 min. Low concentrations of TMRM Perchlorate (50 to 200 nM) do not induce apoptosis, whereas higher concentrations (0.5 and 2.5 µM) enhance apoptosis (KD = 500 nM)[2].

Name: BMS-813160, CAS: 1286279-29-5, stock 22.2g, assay 99%, MWt: 484.64, Formula: C25H40N8O2, Solubility: DMSO : 25 mg/mL (51.58 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: BMS-813160 is the first dual CCR2/CCR5 antagonist to enter clinical development for cardiovascular.
IC50 & Target: CCR2/CCR5[1]

Name: SAR405 R enantiomer, CAS: 1946010-79-2, stock 26.4g, assay 98.1%, MWt: 443.85, Formula: C19H21ClF3N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SAR405 R enantiomer is the less active enantiomer of SAR405. SAR405 is a PIK3C3/Vps34 inhibitor.

Name: Rovazolac, CAS: 1454288-88-0, stock 37g, assay 98.8%, MWt: 452.45, Formula: C21H19F3N2O4S, Solubility: Ethanol : 25 mg/mL (55.25 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: LXR, Biological_Activity: Rovazolac is a liver x receptor (LXR) modulator extracted from patent WO2013130892A1.
IC50 & Target: Target: LXR[1]
In Vitro: Rovazolac is an anti-inflammatory drug candidate[1].

Name: Vecabrutinib SNS-062, CAS: 1510829-06-7, stock 38.9g, assay 98.2%, MWt: 529.92, Formula: C22H24ClF4N7O2, Solubility: DMSO : 125 mg/mL (235.88 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Itk;Btk, Biological_Activity: Vecabrutinib is a potent, noncovalent BTK and ITK inhibitor, with Kd of 0.3 nM and 2.2 nM, respectively; Vecabrutinib shows an IC50 of 24 nM for ITK.
IC50 & Target: IC50: 24 nM (ITK)[2] 
Kd: 0.3 nM (BTK), 2.2 nM (ITK)[1]
In Vitro: Vecabrutinib inhibits pBTK in human whole blood with an average IC50 of 50 nM. Vecabrutinib inhibits WT and C481S BTK with similar IC50s (pBTK IC50s: WT BTK 2.9 nM, C481S BTK 4.4 nM)[1]. In a recombinant kinase assay, IC50s of Vecabrutinib against WT BTK and C481S BTK are 4.6 nM and 1.1 nM. Vecabrutinib retains activity against the mutated BTK variant. Vecabrutinib is six times more potent than PCI-32765 and greater than 640 times more potent than acalabrutinib against C481S BTK. Vecabrutinib demonstrates dose-dependent inhibition of BTK in primary patient CLL cells comparable to PCI-32765 via immunoblot for BTK phosphorylation. Vecabrutinib decreases viability of primary CLL cells in the presence of HS5 stromal protection by 5.5%[2].
In Vivo: Vecabrutinib has good oral bioavailability in rat and dog (%F ≥ 40%) and a terminal half-life of 5 to 6 hours. Vecabrutinib is well tolerated with continuous drug levels and at exposures much greater than those achieved for PCI-32765[1].

Name: CBL0137 hydrochloride Curaxin-137 hydrochloride;CBL-C137 hydrochloride, CAS: 1197397-89-9, stock 15.9g, assay 98.2%, MWt: 372.89, Formula: C21H25ClN2O2, Solubility: H2O : 10 mg/mL (26.82 mM; Need ultrasonic); DMSO : 25 mg/mL (67.04 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis;NF-κB, Target: MDM-2/p53;NF-κB, Biological_Activity: CBL0137 hydrochloride is an inhibitor of the histone chaperone, FACT. CBL0137 hydrochloride can also activate p53 and inhibits NF-κB with EC50s of 0.37 and 0.47 µM, respectively.
IC50 & Target: FACT[1] 
EC50: 0.37 µM (p53), 0.47 µM (NF-Κb)[2]
In Vitro: Treatment with CBL0137 hydrochloride leads to complete absence of living cells at concentrations above 2.5 μM. CBL0137 hydrochloride causes a greater reduction in the number of colonies formed of not only MiaPaCa-2 cells when combines with gemcitabine, but also gemcitabine-resistant PANC-1 cells. Treatment of human pancreatic cancer cells with CBL0137 hydrochloride results in a dose dependent reduction of protein and mRNA levels of RRM1 and RRM2[1].
In Vivo: The CBL0137 hydrochloride monotherapy group and the CBL0137 hydrochloride-gemcitabine combination group samples show large necrotic fields, numerous apoptotic bodies and loss of tumor cells. Sub-optimal doses of 50 to 60 mg/kg CBL0137 hydrochloride causes similar enhancement of gemcitabine antitumor activity as that produced by the maximum tolerated dose (MTD) of 90 mg/kg as indicated by the lack of statistically significant differences among the combination groups. CBL0137 hydrochloride inhibits FACT function through depletion of the pool of active FACT involved in transcription elongation[1]. CBL0137 hydrochloride, given by oral gavage at a nontoxic dose of 30 mg/kg per day on a 5 days on/2 days off schedule, suppresses tumor growth in xenografts of colon (DLD-1), renal cell carcinoma (Caki-1), and melanoma (Mel-7) tumor cell lines and transplanted surgical samples from patients with pancreatic ductal adenocarcinoma[2].

Name: D4-abiraterone Δ4-Abiraterone;CB-7627;Abiraterone D4A metabolite, CAS: 154229-21-7, stock 25.1g, assay 98.3%, MWt: 347.49, Formula: C24H29NO, Solubility: DMSO : 50 mg/mL (143.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others;Metabolic Enzyme/Protease, Target: Androgen Receptor;Cytochrome P450, Biological_Activity: D4-abiraterone is a major metabolite of abiraterone. D4-abiraterone is an inhibitor of CYP17A1, 3b-hydroxysteroid dehydrogenase (3βHSD) and steroid-5a-reductase (SRD5A) and also an antagonist of androgen receptor.
IC50 & Target: CYP17A1, 3βHSD, SRD5A, androgen receptor[1]
In Vitro: D4-abiraterone (D4A ) (10 mM) nearly completely blocks conversion from D4-androstenedione (AD) to 5α-androstanedione and other 5α-reduced androgens. The affinity of D4-abiraterone for mutant (expressed in LNCaP, half-maximum inhibitory concentration (IC50=5.3 nM)) and wild type (expressed in LAPC4, IC50=7.9 nM) androgen receptor (AR) is greater than that of abiraterone (Abi) (IC50=418 and >500 nM, respectively). Compare with Abi, D4-abiraterone clearly better suppresses PSA, TMPRSS2 and FKBP5 expression in LNCAP, LAPC4 and C4-2 cell lines. D4-abiraterone also inhibits AR target gene expression in a dose-dependent manner[1].
In Vivo: D4-abiraterone (D4A) is tenfold more potent than abiraterone (Abi) in blocking conversion from dehydroepiandrosterone (DHEA) by 3β-hydroxysteroid dehydrogenase (3βHSD) to D4-androstenedione (AD) in LNCaP and VCaP xenografts. 0.1 μM D4-abiraterone is equivalent to 1 μM Abi for blocking AD accumulation at 48 h in both LNCaP and VCaP xenografts. Progression is significantly delayed in the D4-abiraterone group compare with the Abi acetate group (P=0.011). D4-abiraterone treatment increases progression-free survival compare with Abi acetate[1].

Name: (-)-GSK598809 1S,5R-GSK598809, CAS: 863680-46-0, stock 20.6g, assay 98.9%, MWt: 481.51, Formula: C22H23F4N5OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (-)-GSK598809 is an isomer of GSK598809. GSK598809 is a potent and selective dopamine D3 Receptor (DRD3) antagonist.

Name: Ensulizole, CAS: 27503-81-7, stock 35.2g, assay 98.5%, MWt: 274.30, Formula: C13H10N2O3S, Solubility: 0.1 M NaOH : 10 mg/mL (36.46 mM; ultrasonic and adjust pH to 8 with NaOH), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK, Target: ROS, Biological_Activity: Ensulizole is a sulfonated UV absorber and can intense UVB and partial UVA absorption. Ensulizole can damage the DNA through the generation of reactive oxygen species (ROS) upon UV or sunlight irradiation. Ensulizole is a water soluble sunscreen ingredient[1].
In Vitro: At 4.0 mM [H2O2]0, a complete removal of 40.0 μM parent PBSA and 25% decrease in TOC are achieved with 190 min of UV irradiation[1].

Name: Ethylhexyl triazone Octyl triazone, CAS: 88122-99-0, stock 33.9g, assay 98.5%, MWt: 823.07, Formula: C48H66N6O6, Solubility: DMSO : 30 mg/mL (36.45 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ethylhexyl triazone is an approved ultraviolet-B (UV-B) chemical filter for commercial sunscreens.
In Vitro: One property of Ethylhexyl triazone (EHT) is its large molecular weight (823.07 g/mol); such filters are unlikely to penetrate the skin, thereby reducing effects associated with such skin penetration. It displays a broad absorption profile across the UV-B region, with a maximum absorption at ~311 and ~313 nm for Ethylhexyl triazone-dioxane and Ethylhexyl triazone-methanol, respectively[1].

Name: Diethylamino hydroxybenzoyl hexyl benzoate DHHB, CAS: 302776-68-7, stock 23.6g, assay 99%, MWt: 397.51, Formula: C24H31NO4, Solubility: DMSO : ≥ 50 mg/mL (125.78 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diethylamino hydroxybenzoyl hexyl benzoate is a photostable UV-A absorber.
In Vitro: Diethylamino hydroxybenzoyl hexyl benzoate (DHHB) absorbs UV-A radiation with a peak at 354 nm. The molar absorption coefficient of Diethylamino hydroxybenzoyl hexyl benzoate in EtOH at 25°C is obtained to be 39 000 mol/dm3/cm at 354 nm. The emission spectrum of Diethylamino hydroxybenzoyl hexyl benzoate in EtOH is dependent on the excitation wavelength[1].

Name: JFD00244, CAS: 96969-83-4, stock 3.1g, assay 98.9%, MWt: 478.54, Formula: C30H26N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: JFD00244 is a sirtuin 2 (SIRT2) inhibitor. Anti-tumor effect[1].

Name: Nezukone C2-deoxyhinokitiol;4-Isopropyltropone, CAS: 13656-81-0, stock 15.8g, assay 98%, MWt: 148.20, Formula: C10H12O, Solubility: DMSO : ≥ 100 mg/mL (674.76 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nezukone is a derivative of hinokitiol. Hinokitiol can restore iron transports, however, Nezukone cannot bind or transport iron.

Name: 2,2,5,7,8-Pentamethyl-6-Chromanol PMC, CAS: 950-99-2, stock 24g, assay 98.4%, MWt: 220.31, Formula: C14H20O2, Solubility: DMSO : 250 mg/mL (1134.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: 2,2,5,7,8-Pentamethyl-6-Chromanol (PMC) is the anti-oxidant moiety of vitamin E (α-tocopherol). 2,2,5,7,8-Pentamethyl-6-Chromanol has potent androgen receptor (AR) signaling modulation and anti-cancer activity against prostate cancer cell lines[1].

Name: KU-57788 NU7441, CAS: 503468-95-9, stock 17.9g, assay 98.4%, MWt: 413.49, Formula: C25H19NO3S, Solubility: DMSO : 14.29 mg/mL (34.56 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage;Cell Cycle/DNA Damage, Target: DNA-PK;DNA-PK;CRISPR/Cas9, Biological_Activity: KU-57788 is a potent and selective inhibitor of DNA-PK with an IC50 of 13 nM, with selectivity over a range of kinases including mTOR, PI 3-K, ATM and ATR.
IC50 & Target: IC50: 13 nM (DNA-PK)[3], 1 μM (BRD4), 3.5 μM (BRDT)[4]
In Vitro: NU7441 at non-toxic concentration of 0.3 μM induces radio-sensitization in non-small cell lung cancer cells irradiated with low-LET and high-LET radiation, and does not show double strand break-repair inhibition in irradiated cells. NU7441 (3 μM) shows significantly increased persistent γ-H2AX signals. NU7441 (0.3 μM) causes significant G2/M arrest and a remarkable increase of DNA fragmentation and enhances cellular senescence in irradiated H1299 cells[1]. NU7441 (0.5 to 10 µM) inhibits the growth of liver cancer HepG2 cells dose- and time-dependently. NU7441 reduces pDNA-PKcs (S2056) protein expression in liver cancer cells. Furthermore, double treatment of NU7441 and 60Coγ IR affects DNA damage repair[2]. NU7441 is solvent-exposed in BRD4, this inhibitor can be classified as a Type I BRD inhibitor[4]. NU7441 reduces the frequency of NHEJ while increasing the rate of HDR following Cas9-mediated DNA cleavage[5].
In Vivo: lung cancer cells irradiated with low-LET and high-LET radiation, and does not show double strand break-repair inhibition in irradiated cells. KU-57788 (3 μM) shows significantly increased persistent γ-H2AX signals. KU-57788 (0.3 μM) causes significant G2/M arrest and a remarkable increase of DNA fragmentation and enhances cellular senescence in irradiated H1299 cells[1]. KU-57788 (0.5 to 10 µM) inhibits the growth of liver cancer HepG2 cells dose- and time-dependently. KU-57788 reduces pDNA-PKcs (S2056) protein expression in liver cancer cells. Furthermore, double treatment of KU-57788 and 60Coγ IR affects DNA damage repair[2]. KU-57788 weakly inhibits BRD4 and BRDT with IC50s of 1 μM and 3.5 μM, respectively. KU-57788 is solvent-exposed in BRD4, this inhibitor can be classified as a Type I BRD inhibitor[4]. KU-57788 reduces the frequency of NHEJ while increasing the rate of HDR following Cas9-mediated DNA cleavage[5].

Name: CORM-401, CAS: 1001015-18-4, stock 23.7g, assay 98.5%, MWt: 333.22, Formula: C8H8MnNO6S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CORM-401 is an oxidant-sensitive CO-releasing molecule, can be used in the research of inflammatory and oxidative stress-mediated pathologies.

Name: Corin, CAS: 1808113-09-8, stock 19.9g, assay 98.2%, MWt: 428.53, Formula: C26H28N4O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (233.36 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics;Cell Cycle/DNA Damage, Target: Histone Demethylase;HDAC;HDAC, Biological_Activity: Corin is a dual inhibitor of histone lysine specific demethylase (LSD1) and histone deacetylase (HDAC), with a Ki(inact) of 110 nM for LSD1 and an IC50 of 147 nM for HDAC1.
IC50 & Target: IC50: 147 nM (HDAC1), Ki(inact): 110 nM (LSD1)[1].
In Vitro: Corin is able to inhibit the deacetylation of semisynthetic, reconstituted nucleosomes by the CoREST ternary complex. Corin shows irreversible inhibition of HDAC1 activity. In Comparison to MS-275, corin appears to more potently (Corin EC50 95 nM vs. MS-275 EC50 420 nM) and efficaciously induce cellular H3K9 acetylation. Interestingly, Corin (1 μM) is non-toxic to primary human melanocytes in contrast to MS-275 (1 μM)[1].

Name: JNJ-38877618, CAS: 943540-74-7, stock 35.1g, assay 98.9%, MWt: 374.35, Formula: C20H12F2N6, Solubility: DMSO : 5 mg/mL (13.36 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR, Biological_Activity: JNJ-38877618 is a potent, highly selective, orally bioavailable Met kinase inhibitor with IC50s of 2 and 3 nM for wild type and mutant Met, respectively.
IC50 & Target: IC50: 2 nM (wt Met), 2 nM (mutant Met)[1]
In Vitro: OMO-1 (formerly JNJ-38877618), is a potent, highly selective, orally bioavailable Met kinase inhibitor with nM binding affinity (Kd=1.4 nM) and enzyme inhibitory activity against wt and M1268T mutant Met (2 and 3 nM IC50). Met inhibitory effects are assessed in proliferation, colony formation and motility assays. JNJ-38877618 displays nM potency against Met Ampl/mutant and therapy resistant models[1].
In Vivo: JNJ-38877618 induces complete inhibition of tumor growth in 3 models: the SNU5 Met amp gastric, U87-MG HGF autocrine glioblastoma and Hs746T Met exon 14 skipping mutant gastric cancer. JNJ-38877618 induces regression of large Met amplified EBC-1 SqNSCLC where JNJ-38877618 leads to dose- and time-dependent inhibition of Met kinase activation, with the duration of target shut down considerably exceeding plasma exposure times. Combination treatments are well tolerated and improved EGFR targeted therapy[1].

Name: BIP-135, CAS: 941575-71-9, stock 30.6g, assay 98.1%, MWt: 421.24, Formula: C21H13BrN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR, Target: GSK-3;GSK-3, Biological_Activity: BIP-135 is a potent and selective ATP-competitive GSK-3 inhibitor, with IC50s of 16 nM and 21 nM for GSK-3α and GSK-3β, respectively. BIP 135 exhibits neuroprotective effect[1].
IC50 & Target: IC50: 16 nM (GSK-3α), 21 nM (GSK-3β)[1]
In Vitro: BIP-135 (20-30 μM; 72 hours) increases the survival motor neuron (SMN) protein levels at a dose of 25 μM in human SMA fibroblasts. And the typical bell-shaped dose-response curve is observed due to some toxicity at higher concentrations[1]. 
BIP-135 (20 μM; 48 hours) is a superior neuroprotective agent in the model of oxidative stress[1]. 
In Vivo: BIP-135 does not appear to be toxic and was well-tolerated by the animals (no decrease in body weight)[1]. 
BIP-135 (75 mg/kg; i.p.; daily; from postnatal day 0 to 21) prolongs the median survival time of Δ7 SMA KO mouse model of spinal muscular atrophy[1].

Name: Sterigmatocystine, CAS: 10048-13-2, stock 3.1g, assay 98.6%, MWt: 324.28, Formula: C18H12O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;DNA/RNA Synthesis, Biological_Activity: Sterigmatocystine is a precursor of aflatoxins and a mycotoxin produced by common mold strains from Aspergillus versicolor[1][2]. Sterigmatocystine, a inhibitor of G1 Phase and DNA synthesis, is used to inhibit p21 activity. Sterigmatocystine has teratogenic, and carcinogenic effects in animals[3].
In Vitro: Sterigmatocystine-induced DNA damage activates the ATM/53-dependent signaling pathway, which contributes to the induction of G2 arrest in GES-1 cells[4].
In Vivo: Sterigmatocystine (ip; 3 mg/kg once daily for 14 days) inhibits p21WAF1/CIP1[3].

Name: PLGA poly(lactic-co-glycolic acid), CAS: 34346-01-5, stock 28.7g, assay 98.7%, MWt: 10000-20000, Formula: N/A, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PLGA is a copolymer of poly lactic acid (PLA) and poly glycolic acid (PGA) which can be used to fabricate devices for drug delivery and tissue engineering applications.

Name: D-(-)-Lactic acid (R)-2-Hydroxypropionic acid, CAS: 10326-41-7, stock 19g, assay 99%, MWt: 90.08, Formula: C3H6O3, Solubility: DMSO : ≥ 125 mg/mL (1387.66 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-(-)-Lactic acid is a normal intermediate in the fermentation (oxidation, metabolism) of sugar. D-(-)-Lactic acid is identified to be a competitive inhibitor of ProDH (proline dehydrogenase) in plants.

Name: GLPG1837 ABBV-974, CAS: 1654725-02-6, stock 23.6g, assay 98.3%, MWt: 348.42, Formula: C16H20N4O3S, Solubility: DMSO : ≥ 250 mg/mL (717.52 mM), Clinical_Informat: Phase 2, Pathway: Autophagy;Membrane Transporter/Ion Channel, Target: Autophagy;CFTR, Biological_Activity: GLPG1837 is a potent and reversible CFTR potentiator, with EC50s of 3 nM and 339 nM for F508del and G551D CFTR, respectively.
IC50 & Target: EC50: 3 nM (F508del CFTR), 339 nM (G551D CFTR)[1]
In Vitro: GLPG1837 is a potent CFTR potentiator, with EC50s of 3 nM and 339 nM for F508del and G551D CFTR, respectively. GLPG1837 increases the conductivity of the G551D CFTR channel with obtained potency of 181 nM[1]. GLPG1837 is reversible CFTR potentiator, with a the apparent affinity within a range of 0.2∼2 µM[2].

Name: AZ1495, CAS: 2196204-23-4, stock 26g, assay 98.8%, MWt: 385.50, Formula: C21H31N5O2, Solubility: DMSO : 10 mg/mL (25.94 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Protein Tyrosine Kinase/RTK, Target: IRAK;IRAK, Biological_Activity: AZ1495 (compound 28) is an oral active inhibitor of Interleukin-1 receptor associated kinase 4 (IRAK4), with IC50 values of 5 nM and 23 nM for IRAK4 and IRAK1, respectively. Shows activity in treatment of mutant MYD88L265P diffuse large B-cell lymphoma (DLBCL)[1].
IC50 & Target: IC50: 5 nM (IRAK4), 23 nM (IRAK1)[1].

Name: FL-411 BRD4-IN-1, CAS: 2118944-88-8, stock 9.2g, assay 98%, MWt: 341.43, Formula: C18H19N3O2S, Solubility: DMSO : 5.4 mg/mL (15.82 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: FL-411 is a potent and selective BRD4 inhibitor with an IC50 of 0.43±0.09 μM for BRD4(1).
IC50 & Target: IC50: 0.43±0.09 μM (BRD4(1))[1]
In Vitro: FL-411 is a selective BRD4 inhibitor. Binding affinities of FL-411 are measured by TR-FRET against the first and second bromodomains of BRD2(1), BRD4(1), and BRD4(2) with IC50s of 24.60±0.70 μM, 0.47±0.02 μM, 0.93±0.05 μM, respectively. FL-411 possesses a good BRD4(1) inhibition activity (IC50=0.43±0.09 μM), antiproliferative activity (MCF-7, IC50=1.62±0.06 μM; MDA-MB-231, IC50=3.27±0.14 μM), and autophagic activity (42.29% in MCF-7 cells), as well as displays a low toxicity against MCF10A cells). FL-411 induces ATG5-dependent autophagy-associated cell death (ACD) by blocking BRD4-AMPK interaction and thus activating AMPK-mTOR-ULK1-modulated autophagic pathway in breast cancer cells[1].
In Vivo: To evaluate the antitumor activity of FL-411 in vivo, two breast tumor xenograft models, namely, MCF-7 and MDA-MB-231 cell lines models, are used. The in vivo study is conducted using three different doses of FL-411: 25 mg/kg, 50 mg/kg, and 100 mg/kg. In all the models, FL-411 shows significant tumor growth inhibition in a dose-dependent manner as determined by 80% and 76% tumor growth inhibition ratio in MCF-7 and MDA-MB-231 cell models, respectively. A remarkable loss of tumor weights is observed in all dose groups (p<0.001). FL-411 displays no obvious effects on the body weight of all the treatment groups. To examine whether FL-411-mediated inhibition of tumor growth in vivo is associated with reduced cell proliferation and the increased autophagy-associated cell death, tumor tissues from control and FL-411-treated mice are processed for the immunohistochemical analysis of Ki-67 and LC3. FL-411 treatment obviously reduces the number of Ki-67 (p<0.001) positive cells as well as increases autophagy levels, which is determined by increased LC3 expression (p<0.001)[1].

Name: LDH-IN-1, CAS: 1964515-43-2, stock 19.5g, assay 98.1%, MWt: 570.68, Formula: C30H26N4O4S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 52 mg/mL (91.12 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Lactate Dehydrogenase, Biological_Activity: LDH-IN-1 is a novel pyrazole-based inhibitor of human lactate dehydrogenase (LDH) with IC50s of 32 and 27 nM for LDHA and LDHB, respectively.
IC50 & Target: IC50: 32 nM (LDHA), 27 nM (LDHB)[1]
In Vitro: LDH-IN-1 exhibits low nM inhibition of both LDHA and LDHB (IC50=32, 27 nM, respectively), submicromolar inhibition of lactate production, and inhibition of lactate in MiaPaCa2 pancreatic cancer and A673 sarcoma cells (IC50=0.517, 0.854μM, respectively). LDH-IN-1 inhibits the growth of MiaPaCa2 pancreatic cancer and A673 sarcoma cells with IC50s of 2.23 and 1.21 μM). Dose−response treatment of MiaPaCa-2 cells with LDH-IN-1 shows effects on cellular proliferation at concentrations as low as 250 nM and with nearly complete arrest of cell growth at 20 μM[1].
In Vivo: LDH-IN-1 shows clearance values that far exceed hepatic blood flow (HBF) in mouse species (90 mL/min/kg), with in vivo clearances of 227 mL/min/kg[1].

Name: EZM 2302, CAS: 1628830-21-6, stock 15.9g, assay 98.3%, MWt: 585.09, Formula: C29H37ClN6O5, Solubility: DMSO : ≥ 125 mg/mL (213.64 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: EZM 2302 is an inhibitor of coactivator-associated arginine methyltransferase 1 (CARM1) with an IC50 of 6 nM.
IC50 & Target: IC50: 6 nM (CARM1)[1]
In Vitro: EZM 2302 binds to CARM1 and is a selective inhibitor of CARM1 activity (IC50=6 nM) with broad selectivity against other histone methyltransferases. Treatment of MM cell lines with EZM 2302 leads to inhibition of PABP1 and SMB methylation and cell stasis with IC50 values in the nanomolar range (9, 31 nM, respectively). EZM 2302 inhibits the in vitro proliferation of multiple hematopoietic cell lines, with day 14 IC50 values of less than 100 nM in 9 of 15 cell lines[1].
In Vivo: EZM 2302 is stable in human hepatocytes (CL<3 mL/min/kg), and moderately binds to human, mouse and rat plasma proteins with a mean fraction unbound of 0.66, 0.46 and 0.74, respectively. In mouse and rat, the plasma clearance (CL) is 43 and 91 mL/min/kg, respectively. EZM 2302 shows dose-dependent exposure and tumor growth inhibition (TGI) after 21 days in the RPMI-8226 xenograft model. Tumors in all EZM 2302 dose groups measured on day 21 show significant decreases in tumor growth compared to vehicle[1].

Name: 3-Methyltoxoflavin, CAS: 32502-62-8, stock 24.5g, assay 98.3%, MWt: 207.19, Formula: C8H9N5O2, Solubility: DMSO : 150 mg/mL (723.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Methyltoxoflavin is a potent Protein disulfide isomerase (PDI) inhibitor, with an IC50 of 170 nM.
IC50 & Target: IC50: 170 nM (PDI)[1].
In Vitro: 3-Methyltoxoflavin is a potent Protein disulfide isomerase (PDI) inhibitor, with an IC50 of 170 nM. 3-Methyltoxoflavin is toxic in a panel of human glioblastoma cell lines. From the screen, 3-Methyltoxoflavin emerges as the most cytotoxic inhibitor of PDI. Bromouridine labeling and sequencing (Bru-seq) of nascent RNA reveals that 3-Methyltoxoflavin induces Nrf2 antioxidant response, ER stress response, and autophagy. Specifically, 3-Methyltoxoflavin upregulates heme oxygenase 1 and SLC7A11 transcription and protein expression and represses PDI target genes such as TXNIP and EGR1. Interestingly, 3-Methyltoxoflavin-induced cell death does not proceed via apoptosis or necrosis, but by a mixture of autophagy and ferroptosis[1].

Name: Astragaloside VI, CAS: 84687-45-6, stock 33.8g, assay 98.5%, MWt: 947.11, Formula: C47H78O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Astragaloside VI could activate EGFR/ERK signalling pathway to improve wound healing.
In Vitro: Pretreatment with Astragaloside VI (AS-VI) at 1 μM increases EGFR activation in HaCaT cells. Astragaloside VI, a major intestinal metabolite of astragalosides, exerts the strongest EGFR activation. In HaCaT cells, the positive control, EGF expectedly results in 1.5±0.03-fold increase in cell proliferation, compared to the control. Astragaloside VI at the indicated concentrations also significantly promots cell proliferation in both HaCaT and HDF cells[1]. Astragaloside VI promotes neural stem cell proliferation and enhances neurological function recovery in transient cerebral ischemic injury via activating EGFR/MAPK signaling cascades[2].
In Vivo: Astragaloside VI improves wound healing, compared to the control. In the simple noninfected wound model, wound healing in mice is accelerated by Astragaloside VI, where in the time required for wound closure is shortened by approximately 2-4 days, compared to that in the control group. Topical treatment with Astragaloside VI reduces the volume of pus produced, compared to the control group. Astragaloside VI treated wounds show an accelerated rate of healing, compared to the control and vaseline groups. By day 22, the Astragaloside VI -treated wounds fully close, whereas the blank and vaseline-treated wounds do not fully close until day 26. Angiogenesis is a crucial step in the formation of granulation tissue and wound healing. Astragaloside VI increases blood vessel formation in both the non-infected and infected wound models[1]. Astragaloside VI could effectively activate EGFR/MAPK signaling cascades, promote NSCs proliferation and neurogenesis in transient cerebral ischemic brains, and improve the repair of neurological functions in post-ischemic stroke rats[2].

Name: Saikogenin A, CAS: 5092-09-1, stock 23.8g, assay 98.4%, MWt: 472.70, Formula: C30H48O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Dipeptidyl Peptidase, Biological_Activity: Saikogenin A, extracted from a Chinese herbal plant called Tsai-Fu, is a dipeptidyl peptidase-IV (DPP-IV) inhibitor.
IC50 & Target: DPP-IV[1]
In Vitro: Saikogenin A has certain inhibitory effect on the enzyme DPP-IV. At a concentration of 20 μg/mL DPP-IV inhibition is 47.6%. DPP-IV is a non-classical serine aminopeptidase from its amino terminus of polypeptides and proteins (N-terminus) removing Xaa-Pro dipeptide[1].
In Vivo: Saikogenin A, an anti-inflammatory drug, is present in the crude extract of a Chinese herbal plant called Tsai-Fu. Saikogenin A is less effective in adrenalectomized rats than in normal rats in reducing the carrageenin-induced edema. The anti-inflammatory action of Saikogenin A are due to an increase in corticosterone caused by the release of arenocorticotropic hormone (ACTH) and a direct effect on the process of inflammation[2].

Name: Cholera toxin choleragen, CAS: 9012-63-9, stock 19.6g, assay 98.9%, MWt: 1000, Formula: N/A, Solubility: H2O, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Cholera toxin is a multifunctional protein produced by Vibrio cholera. Cholera toxin is not just another enterotoxin that causes cholera but also able to influence the immune system in many ways.

Name: 7-Hydroxy-4H-chromen-4-one 7-Hydroxychromone, CAS: 59887-89-7, stock 17.2g, assay 98.9%, MWt: 162.14, Formula: C9H6O3, Solubility: DMSO : 150 mg/mL (925.13 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Src, Biological_Activity: 7-Hydroxychromone is a Src kinase inhibitor with an IC50 of <300 μM.
IC50 & Target: IC50: <300 μM (Src)[1]
In Vitro: 7-Hydroxychromone (compound 8) is a 4-oxo-4H-1-benzopyran derivative which can inhibit Src kinase with an IC50 of <300 μM[1].

Name: JT010, CAS: 917562-33-5, stock 24.4g, assay 98.4%, MWt: 354.85, Formula: C16H19ClN2O3S, Solubility: DMSO : ≥ 120 mg/mL (338.17 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: JT010 is a potent agonist of TRPA1 with an EC50 of 0.65 nM.
IC50 & Target: EC50: 0.65 nM (TRPA1)[1]

Name: D-Glucuronic acid, CAS: 6556-12-3, stock 14.1g, assay 98.1%, MWt: 194.14, Formula: C6H10O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-Glucuronic acid is an important intermediate isolated from many gums. D-Glucuronic acid and its derivative glucuronolactone are as a liver antidote in the prophylaxis of human health. D-Glucuronic acid has an anti-inflammatory effect for the skin[1].

Name: Aflatoxin B1, CAS: 1162-65-8, stock 23.5g, assay 98.6%, MWt: 312.27, Formula: C17H12O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aflatoxin B1 (AFB1) is a Class 1A carcinogen, which is a secondary metabolite of Aspergillus flavus and A. parasiticus. Aflatoxin B1 (AFB1) mainly induces the transversion of G-->T in the third position of codon 249 of the p53 tumor suppressor gene, resulting in mutation[1][2].

Name: CZC-8004 CZC-00008004, CAS: 916603-07-1, stock 38g, assay 98.7%, MWt: 309.34, Formula: C17H16FN5, Solubility: DMSO : 77.5 mg/mL (250.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Bcr-Abl, Biological_Activity: CZC-8004 is a pan-kinase inhibitor and binds a range of tyrosine kinases, including ABL kinase.

Name: MS417 GTPL7512, CAS: 916489-36-6, stock 8.3g, assay 98.9%, MWt: 414.91, Formula: C20H19ClN4O2S, Solubility: Ethanol : 50 mg/mL (120.51 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Anti-infection, Target: Epigenetic Reader Domain;HIV, Biological_Activity: MS417 is a BET-specific BRD4 inhibitor, binds to BRD4-BD1 and BRD4-BD2 with IC50s of 30, 46 nM and Kds of 36.1, 25.4 nM, respectively, with weak selectivity at CBP BRD (IC50, 32.7 μM).
IC50 & Target: IC50: 30 nM (BRD4-BD1), 46 nM (BRD4-BD2), 32.7 μM (CBP BRD)[1] 
Kd: 36.1 nM (BRD4-BD1), 25.4 nM (BRD4-BD2)[1]
In Vitro: MS417 is a BET-specific BRD4 inhibitor, binds to BRD4-BD1 and BRD4-BD2 with IC50s of 30, 46 nM and Kds of 36.1, 25.4 nM, respectively, with less selectivity at CBP BrD (IC50, 32.7 μM). MS417 effectively blocks BRD4 binding to NF-κB, almost completely suppresses TNFα-induced NF-κB transcription activation in human embryonic kidney 293T cells at 1 μM and also reduces NF-κB p65 acetylation in the HIV-infected RTECs. MS417 (1 μM) modulation of gene transcription in HIV-infected human primary renal tubular epithelial cells. In addition, MS417 suppresses NF-κB-targeted cytokines and chemokines[1].
In Vivo: MS417 (0.08 mg/kg) markedly improves renal function, reduces proteinuria and decreases glomerulosclerosis, tubular injury, and infiltration of inflammatory cells in the kidney of Tg26 mice[1].

Name: BGT226 NVP-BGT226, CAS: 915020-55-2, stock 9.5g, assay 98.6%, MWt: 534.53, Formula: C28H25F3N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR;Autophagy, Target: PI3K;mTOR;Autophagy, Biological_Activity: BGT226 (NVP-BGT226) is a PI3K (with IC50s of 4 nM, 63 nM and 38 nM for PI3Kα, PI3Kβ and PI3Kγ)/mTOR dual inhibitor which displays potent growth-inhibitory activity against human head and neck cancer cells[1][2].
IC50 & Target: IC50: 4 nM (PI3Kα), 63 nM (PI3Kβ), 38 nM(PI3Kγ)[1].
In Vitro: BGT226 shows significant growth inhibition or signal blockage profiles compared with LY294002 and Rapamycin. BGT226 (10-10000 nM) inhibits FaDu and OECM1 cells growth with IC50s of 23.1±7.4 and 12.5±5.1 nM, respectively[2]. 
The expression levels of p-mTOR Ser2481 are decreased in BGT226-treated cell lines (200 nM; 24 hours) and both p-AKT Ser473 and p-mTOR Ser2448 are also decreased in BGT226-treated cell lines[2].
In Vivo: BGT226 (2.5 and 5 mg/kg; oral administration for 21 days in male athymic mice) causes 34.7% and 76.1% reduction of the tumor growth on day 21 compared with control[2].

Name: PS372424, CAS: 914291-61-5, stock 39.8g, assay 98.3%, MWt: 588.74, Formula: C33H44N6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: PS372424, a three amino-acid fragment of CXCL10, is a specific human CXCR3 agonist with anti-inflammatory activity[1][2].
IC50 & Target: Human CXCR3[2]
In Vitro: PS372424 (10-200 nM; 30 min) causes a concentration-dependent phosphorylation of CCR5 on CXCR3+ T cells not in CXCR3- T cells[1].

Name: AR-9281 APAU, CAS: 913548-29-5, stock 14.9g, assay 98.6%, MWt: 319.44, Formula: C18H29N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AR9281 is a potent and selective inhibitor of soluble epoxide hydrolase (s-EH), with potential for the treatment of hypertension and type 2 diabetes[1].
IC50 & Target: s-EH[1]

Name: Ac-Leu-Arg-AMC, CAS: 929621-79-4, stock 36.1g, assay 98.9%, MWt: 486.56, Formula: C24H34N6O5, Solubility: DMSO : 300 mg/mL (616.57 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ac-Leu-Arg-AMC is a fluorogenic peptide substrate.

Name: ELN484228, CAS: 312-63-0, stock 20g, assay 98.7%, MWt: 251.28, Formula: C12H10FNO2S, Solubility: DMSO : ≥ 50 mg/mL (198.98 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ELN484228 is a blocker of α-synuclein which is a key protein in Parkinson’s disease.
IC50 & Target: α-synuclein[1]

Name: IBR2, CAS: 313526-24-8, stock 13.4g, assay 98.8%, MWt: 400.49, Formula: C24H20N2O2S, Solubility: DMSO : ≥ 150 mg/mL (374.54 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: RAD51, Biological_Activity: IBR2 is a specific RAD51 inhibitor.
IC50 & Target: RAD51[1]
In Vitro: IBR2 shows interesting RAD51 inhibition activities. RAD51 is rapidly degraded in IBR2-treated cancer cells, and the homologous recombination repair is impaired, subsequently leading to cell death. The IC50 values of the original IBR2 are in the range of 12-20 µM for most tested cancer cell lines. IBR2 can inhibit the growth of triple-negative human breast cancer cell line MBA-MD-468 with an IC50 of 14.8 µM[1].

Name: Penicillic acid, CAS: 90-65-3, stock 28.1g, assay 98.5%, MWt: 170.16, Formula: C8H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;Caspase, Biological_Activity: Penicillic acid is a polyketide mycotoxin produced by several species of Aspergillus and Penicillium, which exhibits cytotoxicity in rat alveolar macrophages (AM) in vitro. Penicillic acid inhibits Fas ligand-induced apoptosis by blocking self-processing of caspase-8[1][2].

Name: IDO-IN-12, CAS: 1888341-29-4, stock 6.5g, assay 98.3%, MWt: 416.23, Formula: C13H11BrFN5O3S, Solubility: DMSO : ≥ 50 mg/mL (120.13 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Indoleamine 2,3-Dioxygenase (IDO), Biological_Activity: IDO-IN-12 is an indoleamine 2,3-dioxygenase (IDO) inhibitor extracted from patent WO 2017181849 A1.
IC50 & Target: IDO[1]

Name: Vabicaserin hydrochloride SCA 136, CAS: 887258-94-8, stock 0.5g, assay 98.6%, MWt: 264.79, Formula: C15H21ClN2, Solubility: H2O : 4 mg/mL (15.11 mM; Need ultrasonic); DMSO : 75 mg/mL (283.24 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Vabicaserin hydrochloride is a 5-hydroxytryptamine 2C (5-HT2C) receptor-selective agonist with an EC50 of 8 nM.
IC50 & Target: EC50: 8 nM (5-HT2C Receptor)[1]
In Vitro: Vabicaserin displaces 125I-(2,5-dimethoxy)phenylisopropylamine binding from human 5-HT2C receptor sites in Chinese hamster ovary cell membranes with a Ki value of 3 nM and is >50-fold selective over a number of serotonergic, noradrenergic, and dopaminergic receptors. Binding affinity determined for the human 5-HT2B receptor subtype using [3H]5HT is 14 nM. Vabicaserin is a potent and full agonist (EC50, 8 nM; Emax, 100%) in stimulating 5-HT2C receptor-coupled calcium mobilization and exhibits 5-HT2A receptor antagonism and 5-HT2B antagonist or partial agonist activity in transfected cells, depending on the level of receptor expression. Vabicaserin exhibits lower affinity at the 5-HT2C antagonist binding site (22 nM) labeled with [3H]mesulergine. Additional binding studies indicate that Vabicaserin possesses affinity for the 5-HT2B and 5-HT1A receptors with Ki values of 14 and 112 nM, respectively[1].
In Vivo: After a single oral dose of [14C]Vabicaserin at 50, 5, and 15 mg/kg, unchanged drug represents less than 19, 20, and 35% of total plasma radioactivity at all the time points examined in mice, rats, and dogs, respectively. The carbamoyl glucuronide (CG) represents approximately 7 to 36% of plasma radioactivity in mice and 2 to 28% of plasma radioactivity in dogs but is not detected in rat plasma after the single [14C]Vabicaserin dose. However, the CG is observed in rat plasma after multiple-dose administration of Vabicaserin at higher doses, and the CG is approximately 20 times less than Vabicaserin based on steady-state AUC0-24 values. The estimated plasma AUC0-24 ratios of CG to the parent drug are 1.5 and 1.7 in mice and dogs after the single [14C]Vabicaserin dose, respectively. The plasma AUC0-24 ratios for the CG to Vabicaserin at steady state with doses used for safety assessment are less for mice (0.2-0.6) and slightly higher for dogs (1.8-4.0) compared with the single dose values. The CG is detected in dog urine in similar amounts to the parent drug, although it is not detected in mouse or rat urine after the single [14C]Vabicaserin dose. Radioactivity in a 0- to 24-h bile collection from rats receiving a 5 mg/kg [14C]Vabicaserin dose accounts for 19 and 24% of the administered dose in males and females, respectively. Although the CG is not detected in urine or feces of rats after a single oral administration, it represents an average of up to 30% of biliary radioactivity in male rats and 15% in female rats. In monkeys after a single oral 25-mg/kg dose of Vabicaserin, the plasma concentrations of the CG exceeded those of Vabicaserin at all the time points (2-24 h) postdose, although the amount of CG relative to Vabicaserin decreased by 24 h postdose, with ratios of 17.5 at 2 h and 1.7 at 24 h. The CG to Vabicaserin AUC0-24 ratio of 12:1 indicates that the CG is a major metabolite in monkeys[2].

Name: Pyributicarb TSH-888, CAS: 88678-67-5, stock 22.1g, assay 98.2%, MWt: 330.44, Formula: C18H22N2O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (302.63 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Pyributicarb, a carbamate-type herbicide, is a potent activator of both CYP3A4 gene and human pregnane X receptor (hPXR).
IC50 & Target: CYP3A4[1], hPXR[2]
In Vitro: Pyributicarb, a carbamate-type herbicide, is a potent activator of both CYP3A4 gene and human pregnane X receptor (hPXR). Pyributicarb is found to increase the CYP3A4 reporter activity at 0.1 to 1 μM more strongly than typical CYP3A4 inducer rifampicin. Expression of hPXR-siRNA clearly diminishes the Pyributicarb-stimulated CYP3A4 reporter activity in 3-1-10 cells and decreases the endogenous CYP3A4 mRNA levels in HepG2 cells[1]. Pyributicarb induces luciferase transcription via hPXR at low concentrations in the order of 10 nM. The relative potency of Pyributicarb for hPXR is 8.6-fold that of rifampicin (RIF)[2].
In Vivo: Pyributicarb causes enhancement of CYP3A4-derived reporter activity in mouse livers introduced with hPXR by adenovirus[1].

Name: Pitofenone hydrochloride, CAS: 1248-42-6, stock 27g, assay 98.6%, MWt: 403.90, Formula: C22H26ClNO4, Solubility: DMSO : 103.3 mg/mL (255.76 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Pitofenone hydrochloride, a spasmolytic compound, inhibits the acetylcholinesterase (AChE) activity from bovine erythrocytes and from electric eel with Kis of 36 and 45 μM, respectively.
IC50 & Target: Ki: 36 μM (AChE, bovine erythrocytes), 45 μM (AChE, electric eel)

Name: GR148672X, CAS: 263890-70-6, stock 24.6g, assay 98.7%, MWt: 340.32, Formula: C15H11F3N2O2S, Solubility: DMSO : 310 mg/mL (910.91 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GR148672X is a triacyglycerol hydrolase (TGH) inhibitor with an IC50 of 4 nM extracted from patent WO 2001016358 A2.
IC50 & Target: IC50: 4 nM (TGH)[1]

Name: SPD304, CAS: 869998-49-2, stock 34.1g, assay 99%, MWt: 547.61, Formula: C32H32F3N3O2, Solubility: H2O : 20 mg/mL (36.52 mM; Need ultrasonic); DMSO : 25 mg/mL (45.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: TNF Receptor, Biological_Activity: SPD304 is a selective TNF-α inhibitor, which promotes dissociation of TNF trimers and therefore blocks the interaction of TNF and its receptor. SPD304 has an IC50 of 22 µM for inhibiting in vitro TNF receptor 1 (TNFR1) binding to TNF-α[1][2]. SPD304 cannot be used in vivo due to its high toxicity[3].
IC50 & Target: IC50: 22 µM (TNFα)[1].
In Vitro: SPD304 (2 μM) significantly rescues the survivability of aHSCs, reduces the production of lipid hydroxides, and increased intracellular GSH. The co-treatment of GA (75 μM) and SPD304 (2 μM), down-regulate TRADD almost 2-fold (w/o inhibitor vs. w/ inhibitor) and p−RIP3 1.4−fold compared to GA alone, and promotes caspase 8 activation[4].

Name: Aftin-4, CAS: 866893-90-5, stock 14.2g, assay 98.9%, MWt: 368.48, Formula: C20H28N6O, Solubility: DMSO : ≥ 250 mg/mL (678.46 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Aftin-4 is an Amyloid-β42 (Aβ42) inducer.
IC50 & Target: Amyloid-β[1]
In Vitro: Aftin-4 selectively and potently increases Aβ1-42 in N2a cells, primary neurons, and brain lysates, with an EC50 value around 30 μM[1].
In Vivo: Aftin-4 increases Aβ1-42 levels in vivo in mice and provokes rapidly a sustained toxicity highly reminiscent of Alzheimer’s disease (AD). Aftin-4 is administered at increasing doses, between 3 and 20 nmol/mouse, into the lateral ventricle and animals are sacrificed at various time points, between 3 to 14 days after injection. The hippocampus is dissected out the contents in Aβ1-40 or Aβ1-42 is determined using a mouse ELISA assay. Aftin-4 dose-dependently and significantly increases Aβ1-42 content, up to +216% at the highest dose tested[1].

Name: L 888607, CAS: 860033-06-3, stock 24.1g, assay 98.1%, MWt: 375.84, Formula: C19H15ClFNO2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 150 mg/mL (399.11 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: L 888607 is a potent, and selective CRTH2 (also known as DP2) agonist with a Ki of 0.8 nM.
IC50 & Target: Ki: 0.8±0.4 nM (CRTH2), 283±52 nM (TP), 1260±211 nM (EP3-III), 2331±947 nM (DP), 8748±2571 nM (EP2), 4634±1903 nM (EP4), 10018±2907 nM (FP), 14434±5405 nM (IP)[1][2].

Name: HAMNO NSC111847, CAS: 138736-73-9, stock 3.4g, assay 98.3%, MWt: 263.29, Formula: C17H13NO2, Solubility: DMSO : 155 mg/mL (588.70 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: HAMNO is a novel protein interaction inhibitor of replication protein A (RPA).
IC50 & Target: RPA[1]
In Vitro: HAMNO is a novel protein interaction inhibitor of replication protein A (RPA). RPA is involved in the ATR/Chk1 pathway. HAMNO alone inhibits colony formation in both HNSCC cell lines in the low micromolar range. HAMNO combined with etoposide significantly inhibits colony formation to a greater degree than HAMNO alone. After UMSCC38 cells are exposed to HAMNO, increased pan-nuclear γ-H2AX staining occurs in a dose dependent manner. Cancer derived UMSCC38 cells, as well as another cancer cell line, UMSCC11B, have prominent γ-H2AX staining, particularly after incubation with 20 μM HAMNO. Both UMSCC38 and OKF4 cells present increased γ-H2AX staining after addition of HAMNO, with the greatest increase in signal occurring in S-phase[1].
In Vivo: In mice, HAMNO slows the progression of UMSCC11B tumors. Ser33 of RPA32, an ATR substrate, is highly phosphorylated after two hours of treatment with 20 μM of etoposide, which is reduced with the addition of 2 μM HAMNO, and is nearly absent at higher concentrations, demonstrating an in vivo effect of HAMNO as an inhibitor of RPA32 phosphorylation by ATR[1].

Name: Synta66, CAS: 835904-51-3, stock 6.3g, assay 98.8%, MWt: 352.36, Formula: C20H17FN2O3, Solubility: DMSO : 77.5 mg/mL (219.95 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: CRAC Channel, Biological_Activity: Synta66 is an inhibitor of store-operated calcium entry channel Orai, which forms the pore of the CRAC channel, and used for the research of neurological disease.
IC50 & Target: Orai[1]
In Vitro: Synta66 is an inhibitor of Orai, which forms the pore of the CRAC channel. Synta66 (10 μM) attenuates peak SOCE in Müller glia. Synta66 (10 μM) prevents orai channels mediating the residual SOC current in Trpc1−/− Müller cells[1]. Synta66 (10 μM) nearly completely blocks the Ca2+ entry signal evoked by CaCl2 addition, whereas it moderately reduces Ca2+ mobilization from stores with 10% to 30% in platelet. Synta66 (10 μM) suppresses human platelet activation in plasma and whole-blood thrombus formation. Synta66 (10 μM) also inhibits murine platelet responses and thrombus formation[2]. Synta66 (10 μM) inhibits LAD2 human mast cell line. Synta66 (10 μM) significantly inhibits FcεRI stimulated histamine and TNFα secretion, and has differential effects on FcεRI stimulated prostaglandin D2 and cytokine release in human lung mast cells (HLMCs)[3].

Name: Neratinib HKI-272, CAS: 698387-09-6, stock 38g, assay 98.3%, MWt: 557.04, Formula: C30H29ClN6O3, Solubility: DMSO : 6.4 mg/mL (11.49 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Neratinib is an orally available, irreversible tyrosine kinase inhibitor with IC50s of 59 nM and 92 nM for HER2 and EGFR, respectively.
IC50 & Target: IC50: 59 nM (HER2), 92 nM (EGFR)
In Vitro: Neratinib has inhibition of tyrosine kinases KDR and Src with IC50 of 0.8 μM and 1.4 μM, respectively, being 14- and 24-fold less active compared with HER2. Neratinib displays no activity against other serine-threonine kinases such as Akt, cyclin D1/cdk4, cyclin E/cdk2, cyclin B1/cdk1, IKK-2, MK-2, PDK1, c-Raf, and Tpl-2, as well as the tyrosine kinase c-Met. Neratinib selectively inhibits the proliferation of 3T3 cells transfected with the HER2 (3T3/neu), as well as two other HER-2-overexpressing SK-Br-3 and BT474 cells with IC50 values of 2-3 nM, displaying > 230-fold potency compared with non-transfected 3T3 cells as well as MDA-MB-435 and SW620 which are EGFR- and HER2-negative. Neratinib also inhibits the proliferation of EGFR-dependent A431 cells with an IC50 of 81 nM. Neratinib reduces HER2 receptor autophosphorylation in BT474 cells with an IC50 of 5 nM, and EGF-dependent phosphorylation of EGFR in A431 cells with IC50 of 3 nM. Blocking of HER-2 by Neratinib results in inhibition of downstream MAPK and Akt pathways with IC50 of 2 nM. Neratinib inhibits the cyclin D1 expression and the phosphorylation of the Rb-susceptibility gene production in BT474 cells with IC50 of 9 nM, leading to G1-S arrest and ultimately decreased cell proliferation[1].
In Vivo: Orally treated neratinib significantly inhibits the growth of 3T3/neu xenografts, with inhibition of 34%, 53%, 98%, and 98% at dose of 10, 20, 40, and 80 mg/kg/day, respectively. Consistent with the inhibition of HER-2 phosphorylation by 84% within 1 hour of administration at 40 mg/kg/day, Neratinib inhibits the growth of BT474 xenografts by 70-82%, 67%, and 93% at dose of 5, 10, and 40 mg/kg/day, respectively. Neratinib is also effective against SK-OV-3 xenografts with inhibition of 31% and 85% at 5 and 60 mg/kg/day, respectively. Neratinib is less potent against EGFR-dependent A431 xenografts than HER-2-dependent tumors, with 32% and 44% inhibition at 5 and 20 mg/kg/day, respectively. Neratinib displays little activity against MCF-7 and MX-1 xenografts expressing low levels of HER-2 and EGFR, with only 28% inhibition at 80 mg/kg/day, suggesting that Neratinib has selective activity for cells expressing HER-2 or EGFR[1].

Name: ARS-1323, CAS: 1698024-73-5, stock 24.8g, assay 98.4%, MWt: 430.84, Formula: C21H17ClF2N4O2, Solubility: DMSO : ≥ 125 mg/mL (290.13 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: ARS-1323, the racemate of ARS-1620, is a novel inhibitor of mutant K-ras G12C extracted from patent WO 2015054572 A1.
IC50 & Target: K-Ras G12C[1]

Name: AZD5904, CAS: 618913-30-7, stock 13.6g, assay 98.5%, MWt: 252.29, Formula: C10H12N4O2S, Solubility: DMSO : 125 mg/mL (495.46 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glutathione Peroxidase, Biological_Activity: AZD5904 is a potent and irreversible inhibitor of human Myeloperoxidase (MPO) with an IC50 of 140 nM and has similar potency in mouse and rat.
IC50 & Target: IC50: 140 nM (human MPO)[1]
In Vitro: AZD5904 is a potent and irreversible inhibitor of human Myeloperoxidase (MPO) with an IC50 of 140 nM and has similar potency in mouse and rat. It is 10 to 19-fold selective compare to the closely related lactoperoxidase and thyroid peroxidase; >70-fold to a broad panel of other enzymes, ion channels, and receptors. In isolated human neutrophils, 1 µM AZD5904 inhibits PMA stimulated HOCl by >90%[1].

Name: HDAC8-IN-1, CAS: 1417997-93-3, stock 30.6g, assay 98.3%, MWt: 345.39, Formula: C22H19NO3, Solubility: DMSO : 150 mg/mL (434.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: HDAC8-IN-1 is a HDAC8 inhibitor with an IC50 of 27.2 nM.
IC50 & Target: IC50: 27.2 nM (HDAC8)
In Vitro: HDAC8-IN-1 is a HDAC8 inhibitor with an IC50 of 27.2 nM in cancer cell lines. HDAC8-IN-1 (compound 22 d) shows antiproliferative effects toward several human lung cancer cell lines (A549, H1299, and CL1-5); HDAC8-IN-1 exhibits cytotoxicity against human lung CL1-5 cells without significant cytotoxicity for normal IMR-90 cells[1].

Name: ARS-1630, CAS: 1698055-86-5, stock 33.8g, assay 98.7%, MWt: 430.84, Formula: C21H17ClF2N4O2, Solubility: DMSO : ≥ 69 mg/mL (160.15 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: ARS-1630, a less active enantiomer of ARS-1620, is a novel inhibitor of mutant K-ras G12C extracted from patent WO 2015054572 A1.
IC50 & Target: K-Ras G12C[1]
In Vitro: KRASG12C is recently identified to be potentially druggable by allele-specific covalent targeting of Cys-12 in vicinity to an inducible allosteric switch II pocket (S-IIP). Success of this approach requires active cycling of KRASG12C between its active-GTP and inactive-GDP conformations as accessibility of the S-IIP is restricted only to the GDP-bound state. This strategy proves feasible for inhibiting mutant KRAS in vitro[2].

Name: ONC212, CAS: 1807861-48-8, stock 27.5g, assay 98.9%, MWt: 440.46, Formula: C24H23F3N4O, Solubility: DMSO : 50 mg/mL (113.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;GPCR/G Protein, Target: Apoptosis;GHSR, Biological_Activity: ONC212, a fluorinated-ONC201 analogue, is a promising anti-cancer drug and also a selective agonist of GPR132.
IC50 & Target: GPR132[1]
In Vitro: Cell proliferation assay reveals that at least a ten-fold lower concentration of ONC212 is needed to achieve 50% growth inhibition in comparison to ONC201. ONC212 shows GI50 values in the range of 0.1 to 0.4 μM, while the corresponding ONC201 GI50 values are in the range of 4 to 9 μM for the seven pancreatic cancer cell lines tested. Long-term cell proliferation assay shows that both ONC201 and ONC212 are comparable in inhibiting colony formation at a 20 µM dose. However, at a 5 µM dose, ONC212 is about 50-times more potent than ONC201 in preventing colony formation in four out of the seven pancreatic cancer cell lines tested. Induction of apoptosis by ONC212 is an earlier event than ONC201. Treatment with ONC201 and ONC212 reduces the expression of anti-apoptotic markers such as XIAP and MCL-1. Western blot analysis shows that in the HPAF-II cell line, ATF4 and phosphorylated EIF2α are upregulated as early as 6 to 12 hours post ONC201 or ONC212 treatment[2].
In Vivo: Biweekly oral administration of 50 mg/kg ONC212 markedly inhibits Acute myeloid leukemia (AML) expansion and prolongs overall survival (p=0.0003). Median survival increases from 43 d in controls to 49 d in the ONC212-treated group (+14%)[1]. ONC212 treatment exhibits significantly greater growth inhibition in comparison to ONC201. A dose of 50 mg/kg of ONC212 administered three-times a week is sufficient to lead to significant growth inhibition of tumors compare to the control group for these two models. Results demonstrate that ONC212 treated tumors show reduced proliferation in the HPAF-II model[2]. In vivo toxicity assessment experiments show that ONC212 is well tolerated up to 250 mg/kg. 300 mg/kg of ONC212 causes splenic damage and elevates liver enzymes. ONC212 has a slightly shorter half-life than ONC201, with a clearance from the blood at 12 hours, T1/2 of 4.3 hours, and Cmax of 1.4 µg/mL[3].

Name: ARS-1620, CAS: 1698055-85-4, stock 23.7g, assay 98.8%, MWt: 430.84, Formula: C21H17ClF2N4O2, Solubility: DMSO : ≥ 53 mg/mL (123.02 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: ARS-1620 is an atropisomeric selective KRASG12C inhibitor with desirable pharmacokinetics.
IC50 & Target: KRASG12C[1]
In Vitro: ARS-1620 is an atropisomeric selective KRASG12C inhibitor with desirable pharmacokinetics. ARS-1620 exhibits complete growth suppression of p.G12C cell lines (IC50=150 nM) with relatively benign effects on control cell lines. It is found that ARS-1620 significantly reduces expression of the gene set in p.G12C mutant cells in a time-dependent manner but not in the p.G12S mutant cells. Following a 5-day treatment period, only a minority of G12C mutant cell lines are sensitive to ARS-1620 under monolayer culture conditions, whereas in 3D-spheroid conditions, ARS-1620 elicits a robust response (p=0.0140)[1].
In Vivo: Following a single oral dose or 5 consecutive daily doses, ARS-1620 yields average peak tumor concentrations of 1.5 μM (50 mg/kg) and 5.5 μM (200 mg/kg), respectively, that enables significant KRASG12C target occupancy (>=70% G12C-TE at 200 mg/kg) for >24 hr. In MIAPaCa2 xenografts (p.G12C), ARS-1620 significantly inhibits tumor growth (p<0.001) in a dose-dependent manner with marked regression at a dose of 200 mg/kg, given once daily. Across all tumor models employed, ARS-1620 is well tolerated over the entire 3-week treatment period. Moreover, there are no observed clinical signs or toxicity of ARS-1620 in CD-1 mice even at oral doses up to 1,000 mg/kg administered daily over a 7-day period.

Name: Opioid receptor modulator 1, CAS: 77514-44-4, stock 3.9g, assay 98.5%, MWt: 285.38, Formula: C18H23NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Opioid receptor modulator 1 is a opioid receptor modulator extracted from patent WO2014072809A2, Compound RA11 in EXAMPLE 7.
IC50 & Target: Opioid receptor[1]

Name: K-756, CAS: 130017-40-2, stock 35.8g, assay 98.7%, MWt: 433.50, Formula: C24H27N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: K-756 is a direct and selective tankyrase (TNKS) inhibitor, which inhibits the ADP-ribosylation activity of TNKS1 and TNKS2 with IC50s of 31 and 36 nM, respectively.
IC50 & Target: IC50: 31 nM (TNKS1), 36 nM (TNKS2)[1]
In Vitro: K-756 is a novel and selective Wnt/β-catenin pathway inhibitor targeting tankyrase (TNKS). TNKS is one of the members of the PARP family (it is also known as PARP5). K-756 binds to the induced pocket of TNKS and inhibits its enzyme activity. To study the isoform selectivity of K-756, the PARP family enzyme inhibitory activity at 10 μM is evaluated. K-756 inhibits TNKS1 and TNKS2 by 97% and 100%, respectively. In contrast, the inhibitory activity of K-756 against PARP1, PARP2, PARP3, PARP6, PARP7, and PARP11 is less than 13%. K-756 inhibits the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. K-756 strongly inhibits the reporter activity in DLD-1/TCF-Luc cells with an IC50 of 110 nM, but does not inhibit DLD-1/mtTCF-Luc cells, even at 1,000 nM. APC-mutant colorectal cancer cell line COLO 320DM and SW403 cells are treated with K-756 and after 144 hours, cell growth inhibition is measured by an XTT assay. The application of K-756 inhibits the cell growth of COLO 320DM with a GI50 of 780 nM. K-756 also inhibits SW403 with a GI50 of 270 nM[1].
In Vivo: DLD-1/TCF-Luc cell xenografts are created in SCID mice. Vehicle (0.5% MC400) or K-756 is administered orally once a day for 3 days at 100, 200, and 400 mg/kg. The Wnt/β-catenin signal inhibition in the tumor is detected by measuring FGF20 and LGR5 and luciferase activity. The expression of FGF20 and reporter activity are significantly decreased at doses of 100 mg/kg and above at 3-day administration. The expression of LGR5 is significantly decreased at doses of 200 mg/kg and above at 3-day administration. The maximum inhibitory activity is reached with the administration of K-756 at a dose of 400 mg/kg at 3-day administration. The Wnt/β-catenin signal inhibition at a dose of 400 mg/kg is observed from 1-day administration[1].

Name: CRTH2-IN-1 Ramatroban analog, CAS: 926661-54-3, stock 2.1g, assay 98.5%, MWt: 416.47, Formula: C21H21FN2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: CRTH2-IN-1 (Ramatroban analog) is a selective prostaglandin D2 receptor DP2 (CRTH2) antagonist with an IC50 of 6 nM in a human DP2 binding assay.
IC50 & Target: IC50: 6 nM (hDP2, CRTH2), 1 μM (hDP1)[1]
In Vitro: CRTH2-IN-1 (Ramatroban analog, Compound 5) is a novel prostaglandin D2 receptor DP2 (CRTH2) antagonist with an IC50 of 7 nM in a human whole blood eosinophil shape change assay (hESC). CRTH2-IN-1 (Ramatroban analog) is a novel tricyclic antagonist of the prostaglandin D2 receptor DP2 (CRTH2) with efficacy in a murine model of allergic rhinitis. Human prostaglandin D1 receptor (hDP1) binding is performed using 3H-PGD2 and human platelet membranes. Human thromboxane receptor (hTP) binding performed using human platelet membranes and 3H-SQ-29,548. Human prostacyclin receptor (hIP) binding perfomed using hIP/293 membranes and 3Hiloprost. CRTH2-IN-1 inhibits hDP1 binding with an IC50 of 1μM. CRTH2-IN-1 inhibits hTP and hIP binding with IC50s of >100 μM. CRTH2-IN-1 inhibits human CYP isoforms CYP3A4, CYP 2C9 and CYP2D6 with IC50s of 7, 5 and >30 μM, respectively[1].

Name: Chol-5-en-24-al-3β-ol Vitamin D3 derivative, CAS: 27460-33-9, stock 27.2g, assay 98.9%, MWt: 358.56, Formula: C24H38O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Vitamin D Related, Target: VD/VDR, Biological_Activity: Chol-5-en-24-al-3β-ol is a steroid compound (Vitamin D3 derivative) extracted from patent US 4354972 A, Compound IX.
In Vitro: Chol-5-en-24-al-3β-ol is a steroid 24-aldehyde, which is useful for their biological activity or which may be converted to steroids which have such activity[1]. Chol-5-en-24-al-3β-ol is a Vitamin D3 derivative[2].

Name: Parbendazole SKF 29044, CAS: 14255-87-9, stock 33.7g, assay 98.6%, MWt: 247.29, Formula: C13H17N3O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 4 mg/mL (16.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Anti-infection, Target: Microtubule/Tubulin;Microtubule/Tubulin;Parasite, Biological_Activity: Parbendazole is a potent inhibitor of microtubule assembly, destabilizes tubulin, with an EC50 of 8.79 nM, and exhibits a broad-spectrum anthelmintic activity.
IC50 & Target: EC50: 8.79 nM (tubulin)[1]
In Vitro: Parbendazole is a tubulin destabilizer, with an EC50 of 8.79 nM, and can induce DNA damage[1]. Parbendazole (2-10 μM) inhibits the assembly of microtubules dose-dependently, with an IC50 of 3 μM. Parbendazole (2-20 μM)-treated cells show an complete absence of microtubules in Vero cells[2]. Parbendazole (up to 10 μM) inhibits the growth of CLd-AXE myxamoebae. Parbendazole (2-5 μM) potently inhibits tubulin purified from the wild-type myxamoebae[3].

Name: (3β,20E)-24-Norchola-5,20(22)-diene-3,23-diol, CAS: 53495-21-9, stock 17.8g, assay 98.2%, MWt: 344.53, Formula: C23H36O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (3β,20E)-24-Norchola-5,20(22)-diene-3,23-diol is a steroid-based allylic alcohol.

Name: Pyrotinib Racemate SHR-1258 Racemate, CAS: 1246089-97-3, stock 2.4g, assay 98.5%, MWt: 583.08, Formula: C32H31ClN6O3, Solubility: DMSO : 1.81 mg/mL (3.10 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Pyrotinib Racemate is the racemate of Pyrotinib. Pyrotinib is a potent and selective EGFR/HER2 dual inhibitor.

Name: 1-Linoleoyl Glycerol 1-Linoleoyl-rac-glycerol;1-Monolinolein, CAS: 2277-28-3, stock 33.1g, assay 98.3%, MWt: 354.52, Formula: C21H38O4, Solubility: DMSO : ≥ 100 mg/mL (282.07 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phospholipase, Biological_Activity: 1-Linoleoyl Glycerol is a fatty acid glycerol that has been isolated from S. chinensis roots.
IC50 & Target: The (R)-1-Linoleoyl Glycerol and (S)-1-Linoleoyl Glycerol exhibit Lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitory activities with IC50 values of 45.0 and 52.0 μM, respectively[1].

Name: PROTAC ERRα ligand 1, CAS: 1264754-13-3, stock 16.3g, assay 98.6%, MWt: 420.36, Formula: C19H11F3N2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: PROTAC ERRα ligand 1 is an estrogen-related receptor α (ERRα) antagonist with IC50s of 0.04 and 2.8 μM for ERRα and ERRγ, respectively[1].
IC50 & Target: Ligand for E3 Ligase[1]

Name: BF738735, CAS: 1436383-95-7, stock 1.2g, assay 98.3%, MWt: 426.46, Formula: C21H19FN4O3S, Solubility: DMSO : 125 mg/mL (293.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;PI3K/Akt/mTOR, Target: Reverse Transcriptase;PI4K, Biological_Activity: BF738735 is a phosphatidylinositol 4-kinase III beta (PI4KIIIβ) inhibitor with an IC50 of 5.7 nM.
IC50 & Target: IC50: 5.7 nM (PI4KIIIβ), 1.7 μM (PI4KIIIα)[1]
In Vitro: BF738735 (Compound 1) strongly inhibits PI4KIIIβ activity in vitro, with an IC50 of 5.7 nM. BF738735 also impairs PI4KIIIα, but only at an ~300-fold-higher concentration (IC50 of 1.7 μM). In addition, the activity of BF738735 is analyzed on a set of 150 cellular kinases, including 13 lipid kinases at a concentration of 10 μM. For all kinases, the inhibition is less than 10%, indicating that BF738735 specifically inhibits PI4KIIIβ in vitro. BF738735 exhibits a broad spectrum of antiviral activity, as it inhibits all tested species of enteroviruses and rhinoviruses, with 50% effective concentrations ranging between 4 and 71 nM. BF738735 potently inhibits all viruses tested, with EC50s ranging between 4 and 71 nM. The cytotoxicity of BF738735, determined in parallel with the EC50 and using the same culture conditions for 3 to 4 days, is low, with CC50 values ranging from 11 to 65 μM, resulting in high selectivity indices. Low concentrations of BF738735 reduce the amount of luciferase to GuaHCl-treated levels, suggesting that the BF738735 blocks viral RNA replication. The EC50 of BF738735 in this assay is 77 nM, which is comparable to the inhibition observed in the multicycle assay for coxsackievirus serotype B3 (CVB3)[1].
In Vivo: BF738735 is well tolerated by specimens with good plasma levels of the antiviral in circulation and a complete inhibition with 25 mg/kg and some inhibition with 5 mg/kg dose is observed[2].

Name: PDE2/PDE10-IN-1, CAS: 1426833-08-0, stock 9.1g, assay 99%, MWt: 295.73, Formula: C15H10ClN5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: PDE2/PDE10-IN-1 is a phosphodiesterase 2 (PDE2) and PDE10 inhibitor with IC50s of 29 and 480 nM, respectively.
IC50 & Target: IC50: 29 nM (hPDE2A), 480 nM (rPDE10A), 5890 nM (hPDE4D), 6920 nM (hPDE11A), >10000 nM (hPDE1A, hPDE3B, hPDE5A, hPDE6AB, hPDE7A and hPDE9A)[1]
In Vitro: PDE2/PDE10-IN-1 (Compound 6) inhibits PDE2 and PDE10, respectively, with an IC50 value of 29 and 480 nM. PDE2/PDE10-IN-1 also inhibits PDE11A and PDE4D with IC50s of 6920 nM and 5890 nM, respectively. In addition PDE2/PDE10-IN-1 does not show significant inhibition of a panel of CYP450 enzymes (CYP1A2, 2C9, 2D6, 2C19, and 3A4). PDE2/PDE10-IN-1 is also inactive up to a concentration of 125 μg/mL in a bacterial mutagenicity assay[1].
In Vivo: The PK properties of PDE2/PDE10-IN-1 are studied in rats after 2.5 mg/kg i.v. and 10 mg/kg p.o. administration. After i.v. administration, a rapid clearance is observed (t1/2=0.47 h), which is not expected based on the in vitro metabolic stability in rat liver microsomes (rLMs). Interestingly, PDE2/PDE10-IN-1 shows much slower clearance after p.o. administration (t1/2=2.36 h), resulting in good bioavailability and a maximum plasma concentration (Cmax) of 997 ng/mL. PDE2/PDE10-IN-1 is assessed for its potential to cross the blood–brain barrier in rats after 10 mg/kg s.c. administration. PDE2/PDE10-IN-1 shows good formulatability with 10 to 20% HPβCD at pH>3.5. The brain concentration for PDE2/PDE10-IN-1 after 1 h administration is in the range of 370-895 ng/g with high brain free fractions and brain/plasma ratios. More specifically, PDE2/PDE10-IN-1, which is orally bioavailable, occupies PDE2 with an ED50 of 21 mg/kg[1].

Name: GNE 220, CAS: 1199590-75-4, stock 11.7g, assay 98.5%, MWt: 438.53, Formula: C25H26N8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MAP4K, Biological_Activity: GNE-220 is a potent and selective inhibitor of MAP4K4 with an IC50 of 7 nM.
IC50 & Target: IC50: 7 nM (MAP4K4), 9 nM (MINK/MAP4K6), 476 nM (DMPK), 1.06 μM (MELK), 1.1 μM (KHS1/MAP4K5), 1.13 μM (TBK1), 2.02 μM (Flt3), 2.06 μM (Rse)[1]
In Vitro: GNE-220 also inhibits a few other kinases with IC50s of 9 nM, 476 nM and 1.1 μM for MINK (MAP4K6), DMPK and KHS1 (MAP4K5), respectively. GNE-220 alters human umbilical vein endothelial cells (HUVEC) sprout morphology. GNE-220 also reduces pERM+ retraction fibres in a dose-dependent manner. GNE-220 also dose-dependently increased the number of active-INTβ1+ long focal adhesions (FAs)[1].

Name: NOT Receptor Modulator 1, CAS: 1015231-98-7, stock 1g, assay 98.8%, MWt: 362.85, Formula: C22H19ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NOT Receptor Modulator 1 is a nuclear receptor NOT modulator extracted from patent WO 2008034974 A1, Example 39 in table1.
IC50 & Target: Nuclear receptor NOT[1]

Name: MGAT2-IN-2, CAS: 1710630-11-7, stock 4.4g, assay 98.4%, MWt: 580.53, Formula: C26H21F5N4O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: MGAT2-IN-2 is a potent and selective acyl CoA:monoacylglycerol acyltransferase 2 (MGAT2) inhibitor with an IC50 of 3.4 nM.
IC50 & Target: IC50: 3.4 nM (MGAT2)[1]
In Vitro: MGAT2-IN-2 (Compound 24d) exhibits potent MGAT2 inhibitory activity with an IC50 value of 3.4 nM and a ligand lipophilicity efficiency (LLE) value of 5.4[1]. MGAT2-IN-2 (Compound 2) exhibits time-dependent inhibition (TDI) of cytochrome P450 3A4 (CYP3A4). Preincubation of MGAT2-IN-2 with microsomes leads to a significant loss of the activity of CYP3A4 relative to that under a condition without preincubation[2].
In Vivo: Effect of MGAT2-IN-2 on plasma TG is elevated during the oral fat tolerance test in C57BL/6J mice. MGAT2-IN-2 (3, 10 and 30 mg/kg) is orally administered 6 h prior to oil challenge. Pharmacokinetic studies reveal that MGAT2-IN-2 displays a high plasma concentration (AUC0-8h=842 ng•h/mL) and favorable oral bioavailability (F=52%), which are probably driven by the improved stability against oxidative metabolism and hydrolysis. For evaluating the in vivo efficacy, MGAT2-IN-2 is examined for its effect on hypertriglyceridemia during oral fat tolerance test (OFTT) using C57BL/6J mice. To inhibit the hydrolysis of plasma triacylglycerol (TG) by lipoprotein lipase (LPL), mice are pretreated with an LPL inhibitor, Pluronic F127, permitting measurement of the accumulation of plasma TG following olive oil administration. MGAT2-IN-2 and vehicle are administered 6 h before the oral olive oil load, and plasma chylomicron TG concentrations are monitored for 4 h. MGAT2-IN-2 effectively and dose-dependently suppresses plasma TG elevation after olive oil challenge. The TG-lowering effect of MGAT2-IN-2 is significant (p<0.025) at doses of 10 and 30 mg/kg. A similar effect of reducing the rate of fat entrance into the circulation is observed in MGAT2 gene knockout mice[1].

Name: CCG 203769, CAS: 410074-60-1, stock 10.7g, assay 99%, MWt: 202.27, Formula: C8H14N2O2S, Solubility: DMSO : 62.5 mg/mL (308.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: RGS Protein, Biological_Activity: CCG 203769 is a selective G protein signaling (RGS4) inhibitor, which blocks the RGS4-Gαo protein-protein interaction in vitro with an IC50 of 17 nM.
IC50 & Target: IC50: 17 nM (RGS4), 140 nM (RGS19), 6 μM (RGS16), 79 μM (RGS8), 5.4 μM (GSK3β), >100 μM (RGS7)[1]
In Vitro: CCG 203769 also displays dramatic selectivity (8- to >5000-fold) for RGS4 over other RGS proteins. CCG 203769 inhibits RGS19 with an IC50 of 140 nM (8-fold selective for RGS4) and 6 μM for RGS16 (350-fold selective for RGS4). The closely related RGS8 is very weakly inhibited (IC50>60 μM) providing >4500-fold selectivity for RGS4. CCG 203769 inhibits GSK-3β with an IC50 value of 5 μM. CCG 203769 does not inhibit the cysteine protease papain at 100 μM. CCG 203769 does not inhibit RGS7, which lacks cysteines in the RGS domain. CCG 203769 inhibits RGS/Gαo binding in an RGS-selective manner. CCG 203769 enhances Gαq-dependent cellular Ca2+ signaling in an RGS4-dependent manner. CCG 203769 also blocks the GTPase accelerating protein (GAP) activity of RGS4. In single-turnover and steady-state GTPase experiments with Gαo and Gαi1, the rate of GTP hydrolysis is strongly stimulated by RGS4, and this effect is inhibited by CCG 203769 with an IC50<1 μM[1].
In Vivo: To determine whether this genetic disruption of RGS4 function can be replicated pharmacologically, CCG 203769 is tested for effects on Carbamoylcholine chloride-mediated bradycardia in conscious, unrestrained rats. Carbamoylcholine chloride (0.1 mg/kg, IP) produces a modest decrease in heart rate compared to that of a saline vehicle control. CCG 203769 (10 mg/kg, IV) has no significant effect upon heart rate when given alone. However, CCG 203769, administered immediately prior to Carbamoylcholine chloride, significantly potentiates the bradycardic effect (p < 0.05). Given the functional role of RGS4 in Parkinson’s disease models, CCG 203769 is tested in a pharmacologic model of D2 antagonist-induced bradykinesia. Raclopride administration in rats causes increased hang time in the bar test, which is rapidly reversed by doses of CCG 203769 ranging from 0.1 to 10 mg/kg. The lowest dose, 0.01 mg/kg has no effect, while 0.1 mg/kg produces a submaximal effect. The higher doses, 1 and 10 mg/kg, produce equivalent effects. Similarly, the raclopride-induced paw drag in mice is reversed by 0.1-10 mg/kg CCG 203769[1].

Name: S-MTC, CAS: 156719-41-4, stock 1.4g, assay 98.3%, MWt: 205.28, Formula: C7H15N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: S-MTC is a selective type I nitric oxide synthase (NOS) inhibitor.
IC50 & Target: NOS[1]
In Vitro: S-MTC (10 or 100 μM) reduces cellular NO release in the absence of Aβ1-42. At 100 μM, S-MTC decreases cell viability. S-MTC (100 μM) significantly lowers nitrite production (11.2±1.1 μM) when compared to control (no NOS inhibitor exposure; 19.6±1.2 μM). Nitrite productions after Aβ1-42 and L-NOARG (100 μM) or Aβ1-42 and S-MTC (100 μM) treatments are significantly lower than Aβ1-42 alone (33.5±2.0 and 34.5±1.6 μM, respectively). S-MTC (100 μM) is able to significantly reduce nitrite production (25.2±1.1 μM) as compared to Aβ1-42 treatment alone (38.3±2.7 μM), when administered after Aβ1-42 at the 1 h time point. S-MTC (100 μM) concentration decreases both MTT (87±1% of control) and NR (80±1% of control, respectively) levels. The co-administration of S-MTC (100 μM) and Aβ1-42 significantly reverses the effects of Aβ1-42 alone (72±2% vs 61±2% of control)[1].
In Vivo: S-MTC (S-methyl-L-thiocitrulline) is a selective neuronal NOS-inhibitor. Following pretreatment with S-MTC (i.c.v.), the HBO2-induced antinociception is significantly antagonized. In Experiment #2, different groups of mice are pretreated with naltrexone hydrochloride (NTX) (3.0 mg/kg, i.p.), L-NAME (1.0 μg/mouse, i.c.v.), S-MTC (1.0 μg/mouse, i.c.v.) or N5-(1-iminoethyl)-L-ornithine (L-NIO) (3.0 mg/kg, s.c.) 15-30 min prior to HBO2 treatment. The antinociceptive effect assessed 90 min after HBO2 treatment is completely abolished by NTX and L-NAME, antagonized by two-thirds by S-MTC and largely unaffected by L-NIO (F=25.57, p<0.0001)[2]. At a dose of 0.3 mg/kg, S-MTC (SMTC) causes a rise in mean blood pressure (BP). At doses of 1.0, 3.0 and 10 mg/kg, S-MTC causes falls in heart rate, rises in BP and vasoconstriction in all three vascular beds[3].

Name: JMV 2959, CAS: 925238-89-7, stock 5.9g, assay 98.6%, MWt: 508.61, Formula: C30H32N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GHSR, Biological_Activity: JMV 2959 is a growth hormone secretagogue receptor type 1a (GHS-R1a) antagonist with an IC50 of 32 nM.
IC50 & Target: IC50: 32 nM (GHS-R1a)
In Vitro: JMV 2959 is a growth hormone secretagogue receptor type 1a (GHS-R1a) antagonist with an IC50 of 32 nM. JMV 2959 does not induce any intracellular calcium mobilization by itself[1].
In Vivo: When administered alone, it does not increase food intake and does not significantly stimulate growth hormone (GH) release[1]. JMV 2959 dose dependently decreases the startle response (F(3.42)=4.4, p<0.01) and increases %prepulse inhibition (PPI) (F(3.42)=3.9, p<0.05) in the prepulse inhibition paradigm. The alteration in the startle response is mainly due to a 27% decrease in the startle seen in the highest dose of JMV 2959 (6 mg/kg) compare to vehicle (p<0.05)[2]. 6 mg/kg JMV 2959 induces a significant suppression of locomotion on days 1 to 7 relative to baseline day 0 (F(7,49)=2.21, p<0.05). Results also reveal a significant interaction between JMV 2959 treatment and day (F(1,14)=4.397, p<0.05)[3].

Name: 3BDO, CAS: 890405-51-3, stock 34.2g, assay 98.9%, MWt: 327.33, Formula: C18H17NO5, Solubility: DMSO : ≥ 150 mg/mL (458.25 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR;Autophagy;Autophagy, Target: Apoptosis;mTOR;Autophagy;Autophagy, Biological_Activity: 3BDO is a new mTOR activator which can also inhibit autophagy.
IC50 & Target: mTOR, autophagy[1]
In Vitro: Phosphorylation of RPS6KB1 and EIF4EBP1 is significantly increased by 3BDO with vector alone but suppressed with FKBP1A overexpression. Rapamycin fails to decrease the phosphorylation of MTOR and RPS6KB1 in the presence of 3BDO. 3BDO suppresses the increase in MAP1LC3B puncta induced with rapamycin. 3BDO also inhibits the effect of rapamycin in HUVECs. The phosphorylation of Ser residues is decreased in HUVECs treated with 10 μM rapamycin, and 60 μM 3BDO reverses the phosphorylation. The results show that 3BDO suppresses the increased MAP1LC3B puncta number, MAP1LC3B-II level and decreased SQSTM1 protein level induced by rapamycin. 3BDO could dose- and time-dependently decrease FLJ11812 level in HUVECs. Overexpression of FLJ11812 reverses the inhibition of autophagy induced by 3BDO[1].
In Vivo: Immunofluorescence assay reveals that 3BDO treatment increases the level of p-p70S6K and decreases the protein level of ATG13 in plaque endothelium of mice. 3BDO does not affect the phosphorylation of mTOR direct downstream targets p70S6K and 4EBP1. As compare with controls, apoE-/- mice show inhibited endothelium autophagy and apoptosis with 3BDO treatment, so 3BDO protects against endothelium injury in atherosclerosis. 3BDO treatment stabilizes established atherosclerotic lesions in apoE-/- mice. In apoE-/-mice, as compare with controls, with 3BDO treatment, the serum level of IL-6 and IL-8 is significantly decreased[2].

Name: Neoseptin 3, CAS: 1622863-21-1, stock 37.8g, assay 98.1%, MWt: 474.59, Formula: C29H34N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: Neoseptin 3 is a Toll-like receptor 4/myeloid differentiation factor 2 (mTLR4/MD-2) agonist with an EC50 of 18.5 μM.
IC50 & Target: EC50: 18.5 μM (mTLR4/MD-2) [1]
In Vitro: Neoseptin 3 is a Toll-like receptor 4/myeloid differentiation factor 2 (mTLR4/MD-2) agonist with an EC50 of 18.5 μM. Neoseptin-3 induces TNFα production by macrophages in a concentration-dependent manner. Neoseptin-3 induces phosphorylation of IκB kinases α (IKKα), IKKβ, p38, c-Jun N-terminal kinase (JNK), and ERK, and degradation of IκBα, consistent with activation of MAPK and canonical NF-κB signaling. TANK-binding kinase 1 (TBK1) and IRF3 phosphorylation also increase in response to Neoseptin-3[1].

Name: Pz-1, CAS: 1800505-64-9, stock 26.7g, assay 98.2%, MWt: 454.52, Formula: C26H26N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;RET, Biological_Activity: Pz-1 is a potent RET and VEGFR2 inhibitor with IC50s of less than 1 nM for both wild type kinases.
IC50 & Target: IC50: < 1 nM (RET and VEGFR2)[1]
In Vitro: Pz-1 is a Type-II tyrosine kinase inhibitor, able to bind the DFG-out conformation of the kinase. In cell-based assays, 1.0 nM of Pz-1 strongly inhibits tyrosine phosphorylation of VEGFR2 and clinically relevant RET mutants, including those refractory to vandetanib and cabozantinib (RETV804M and RETV804L)[1].
In Vivo: Pz-1 is shown active on VEGFR2, which can block blood supply required for RET-stimulated growth. At 1.0 mg/kg/day per os, Pz-1 abrogates formation of tumors induced by RET-mutant fibroblasts and blocks phosphorylation of both RET and VEGFR2 in tumor tissue. Pz-1 features no detectable toxicity up to 100.0 mg/kg, which indicates a large therapeutic window[1].

Name: LP117, CAS: 1056468-55-3, stock 26.1g, assay 98.1%, MWt: 430.95, Formula: C21H23ClN4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Lipoxygenase, Biological_Activity: LP117 is a novel and potent inhibitor of 5-Lipoxygenase (5-LO) product synthesis with an IC50 of 1.1 μM.
IC50 & Target: IC50: 5-LO (1.1 μM)

Name: Protein kinase inhibitors 1, CAS: 1365986-44-2, stock 27g, assay 98.3%, MWt: 383.42, Formula: C18H17N5O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: DYRK, Biological_Activity: Protein kinase inhibitors 1 is a novel inhibitor of HIPK2 with an IC50 of 74 nM and Kd of 9.5 nM.
IC50 & Target: IC50: 74 nM (HIPK2)[1] 
Kd: 9.5 nM (HIPK2)[1]

Name: FHZ, CAS: 1883737-63-0, stock 6.9g, assay 98.9%, MWt: 478.49, Formula: C26H26N2O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FHZ is a fluorescent probe.
In Vitro: After loaded with probe FHZ and treated with HClO and H2O2/EDTA-Fe2+ in order, HeLa cells display the bright fluorescences from both cyan and green channels. FHZ can give out two different fluorescent signals in the presence of both •OH and HClO, suggesting the synchronous discrimination of •OH and HClO by a dual-channel detection model with two exciting wavelengths. Probe FHZ shows very high specificity to the detections of •OH and HClO with the excitations at 410 and 490 nm, respectively. The probe FHZ can efficiently enter the cellular mitochondria and exhibit the differentiable/visual capabilities to the endogenous •OH and HClO by the dual fluorescent responses[1].
In Vivo: Probe FHZ can rapidly be absorbed into the blood circulation system from the zebrafish intestine, and spread out whole zebrafish tissues, and keep its stability in the blood, organs and tissues in the absence of ROS. The probe can keep its stability in biological environments and only selectively react with •OH and HClO species[1].

Name: DPBQ, CAS: 7029-89-2, stock 18.2g, assay 98.5%, MWt: 362.38, Formula: C24H14N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: MDM-2/p53, Biological_Activity: DPBQ is a p53 activator.
IC50 & Target: p53[1]
In Vitro: DPBQ elicits apoptosis and cell death and is selective for effects in 4N cells. DPBQ elicits expression and phosphorylation of p53 and this effect is specific to tetraploid cells. Knockdown of TP53 restores proliferation of tetraploid cells in the presence of DPBQ[1].

Name: CTX1, CAS: 501935-96-2, stock 7g, assay 98.2%, MWt: 234.26, Formula: C14H10N4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Apoptosis, Target: E1/E2/E3 Enzyme;MDM-2/p53, Biological_Activity: CTX1 is a novel small molecule p53 activator.
IC50 & Target: p53[1]
In Vitro: CTX1 induces significant p53-dependent cell death preferentially in HdmX-expressing cells as compare to cells in which p53 is inactivated by Hdm2 overexpression or p53 is knocked down using p53 targeting shRNA. CTX1 can induce p53 protein levels in the p53 mutant cell line, HT29. It is also found that CTX1 exhibits potent activity (LD50 ~1 μM) as a single agent on primary AML patient samples in a similar fashion to AML cell lines. After 16 hr of treatment with CTX1 in HCT116 p53-wild-type cells there is a decrease in S phase from 23% to 3% while HCT116 p53-null cells exhibit a reduction in S phase from 34% to 28%. The combination of low doses of CTX1 and nutlin-3 leads to a significant enhancement of apoptosis in p53-wildtype, but not p53-null cells[1].
In Vivo: CTX1 even as a single agent significantly enhances the survival of mice in this model system. Mice treated with CTX1 alone or in combination with nutlin-3 has a significantly increased survival time (p<0.0001)[1].

Name: SB 258719, CAS: 195199-95-2, stock 21.6g, assay 98.5%, MWt: 338.51, Formula: C18H30N2O2S, 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: SB 258719 is a selective 5-HT7 receptor antagonist with a pKi of 7.5.
IC50 & Target: pKi: 7.5 (5-HT7 receptor)

Name: DDR1-IN-2, CAS: 1429617-90-2, stock 15.3g, assay 98%, MWt: 546.59, Formula: C30H29F3N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Discoidin Domain Receptor, Biological_Activity: DDR1-IN-2 is a potent inhibitor of discoidin domain receptor 1 (DDR1), with an IC50 of 13.1 nM, and also less potently inhibits DDR2, with an IC50 of 203 nM.
IC50 & Target: IC50: 13.1 nM (DDR1), 203 nM (DDR2), 414 nM (Bcr-Abl), 2500 nM (c-Kit)[1]
In Vitro: DDR1-IN-2 (compound 1) is a potent inhibitor of DDR1, with an IC50 of 13.1 nM, and less potently inhibits DDR2, with an IC50 of 203 nM. DDR1-IN-2 also shows inhibitory activities against Bcr-Abl and c-Kit, with IC50s of 414 and 2500 nM, respectively[1].

Name: JPH203 Dihydrochloride, CAS: 1597402-27-1, stock 28g, assay 98.4%, MWt: 545.24, Formula: C23H21Cl4N3O4, Solubility: DMSO : 50 mg/mL (91.70 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: JPH203 Dihydrochloride is a tyrosine analog, acts as a selective inhibitor of L-type amino acid transporter 1 (LAT1), and is used in cancer research.
IC50 & Target: LAT1[1]
In Vitro: JPH203 Dihydrochloride is a selective inhibitor of LAT1. JPH203 (KYT-0353) inhibits 14C-leucine uptake in S2-hLAT1 and HT-29 cells, with IC50s of 0.14 μM and 0.06 μM. JPH203 (3-1000 μM) exhibits concentration-dependent inhibitory effects on S2-hLAT1 cell growth with an IC50 of 16.4 μM. JPH203 also displays inhibitory activities against HT-29 cell growth, with an IC50 value of 4.1 μM[1]. JPH203 (0.001-100 μM) inhibits the 14C-leucine (1.0 μM) uptake in a concentration dependent way by the YD-38 cells with an IC50 value of 0.79 ± 0.06 μM. JPH203 slightly shows such effects in normal human oral keratinocytes (NHOKs). JPH203 (0.01-30 mM, 1-4 d) completely inhibits the proliferation of YD-38 cells in a dose- and time-dependent manner. However, JPH203 slightly inhibits the proliferation of NHOKs. JPH203 (30 mM) induces apoptosis of YD-38 cells. JPH203 (3 mM) also increases the level of cleaved PARP in activation of the caspases cascade[2]. JPH203 (30 mM) induces mitochondria-dependent apoptosis in Saos2 human osteosarcoma cells. JPH203 (0.001-100 µM) inhibits 14C-leucine (1.0 µM) uptake slightly in FOB cells with an IC50 value of 92.12 ± 10.71 µM, but potently exihibts such effects in Saos2 cells with an IC50 value of 1.31 ± 0.27 µM. JPH203 (0.01 to 30 mM, 1-4 d) potently inhibits cell proliferation in Saos2 cells in a dose- and time-dependent manner, with an IC50 of 4.09-0.09 mM, but slightly inhibits that of FOB cells, with an IC50 of 24.1-2.8 mM[3].
In Vivo: JPH203 (6.3, 12.5, and 25.0 mg/kg, i.v. for 14 days) exhibits dose-dependent inhibition on HT-29 tumor growth in nude mice[1].

Name: PBOX 6, CAS: 290814-68-5, stock 38.3g, assay 98.6%, MWt: 396.44, Formula: C25H20N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: PBOX 6 is a pyrrolo-1,5-benzoxazepine (PBOX) compound, acts as a microtubule-depolymerizing agent and an apoptotic agent.
IC50 & Target: Apoptosis[1], Microtubule[3]
In Vitro: PBOX 6 is a potent apoptotic PBOX, but does not elicit a general toxic effect in a rat R2C Leydig cell line. PBOX 6 (0-25 μM, 16 h) results in dose- and time-dependent induction of apoptosis, and also causes DNA fragmentation at 10 μM in HL-60 cells. PBOX 6 (10 μM) induces apoptosis through activation of caspase 3-like proteases in HL-60 cells. PBOX 6 (10 μM) induces apoptosis and exerts an accumulation of cytochromec in the cytosol, but this effect is not triggered by oxidative stress, and is independent of peripheral-type benzodiazepine receptor (PBR) and NF-κB[1]. PBOX 6 (25 μM) induces apoptosis in MCF-7 cells through activation of caspase-7[2]. PBOX 6 (10 μM) induces the redistribution of cypA from the nucleus to the cytosol of the cell in K562 cells. PBOX 6 (10 μM) induces nucleocytoplasmic redistribution of cypA and pin1 through a JNK-dependent manner, also dependent on upstream activation of a trypsin-like serine protease, and this effect correlates with G2/M arrest in K562 cells[3].

Name: PK11000, CAS: 38275-34-2, stock 38.2g, assay 98.7%, MWt: 236.63, Formula: C6H5ClN2O4S, Solubility: DMSO : 100 mg/mL (422.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Apoptosis, Target: DNA Alkylator/Crosslinker;MDM-2/p53, Biological_Activity: PK11000 is an alkylating agent, and stabilizes the DNA-binding domain of both WT and mutant p53 by covalent cysteine modification, without compromising DNA binding[1].
IC50 & Target: p53[1]

Name: ADDA 5 hydrochloride, CAS: 473268-46-1, stock 28.3g, assay 98.9%, MWt: 406.00, Formula: C24H36ClNO2, Solubility: DMSO : 65 mg/mL (160.10 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ADDA 5 hydrochloride is a partial non-competitive inhibitor of cytochrome c oxidase (CcO), with IC50s of 18.93 μM and 31.82 μM for purified CcO from human glioma and bovine heart, respectively.
IC50 & Target: IC50: 18.93 μM (CcO, human glioma), 31.82 μM (CcO, bovine heart)[1]
In Vitro: ADDA 5 hydrochloride is a partial non-competitive inhibitor of CcO, with IC50s of 18.93 μM and 31.82 μM for purified CcO from human glioma and bovine heart, respectively. ADDA 5 inhibits CcO activity in UTMZ and Jx22-derived GSCs, with IC50s of 21.4 ± 3.9 μM and 15.5 ± 2.8 μM. ADDA 5 (25 μM) shows a growth inhibitory effect on UTMZ cells, with an EC50 of 8.17 μM[1].
In Vivo: ADDA 5 (8 mg/kg, i.p.) significantly suppresses the growth of tumor in mice. ADDA 5 does not causes detectable toxicity at up to 80 mg/kg in mice[1].

Name: AGN 193109, CAS: 171746-21-7, stock 23.6g, assay 98.9%, MWt: 392.49, Formula: C28H24O2, Solubility: DMSO : 2 mg/mL (5.10 mM; Need warming), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: RAR/RXR;Autophagy, Biological_Activity: AGN 193109 is a retinoid analog, and acts as a specific and highly effective antagonist of retinoic acid receptors (RARs), with Kds of 2 nM, 2 nM, and 3 nM for RARα, RARβ, and RARγ, respectively.
IC50 & Target: Kd: 2 nM (RARα), 2 nM (RARβ), 3 nM (RARγ)[1]
In Vitro: AGN 193109 is a highly effective antagonist of retinoic acid receptors, with Kds of 2 nM, 2 nM, and 3 nM for RARα, RARβ, and RARγ, respectively. AGN 193109 is completely RAR specific, because it does not bind to or transactivate through any of the RXRs[1]. AGN 193109 (100 nM) inhibits the TTNPB (a retinoic acid receptor agonist)-dependent morphological change in ECE16-1 cells. AGN193109 half-reverses retinoid-dependent growth suppression at 10 nM, and completely shows this effect at 100 nM in ECE16-1 cells. AGN193109 (100 nM) also eliminates TTNPB-induced decrease in levels of K5, K6, K14, K16, and K17 and increase in levels of K7, K8, and K19[2].
In Vivo: AGN 193109 (1.15 μmol/kg) does not causes overt toxicity and has no effect on spleen weight on the mice, but it suppresses TTNPB-induced increase in spleen weight of the mice. AGN 193109 also significantly reduces the cutaneous toxicity induced by ATRA. AGN 193109 (0.30 or 1.20 μmol/kg) by topical treatment significantly reduces both weight loss and cutaneous toxicity caused by oral TTNPB cotreatment[3].

Name: 4-O-Methyl honokiol, CAS: 68592-15-4, stock 19.1g, assay 98.1%, MWt: 280.36, Formula: C19H20O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;NF-κB, Target: PPAR;NF-κB, Biological_Activity: 4-O-Methyl honokiol is a natural neolignan isolated from Magnolia officinalis, acts as a PPARγ agonist, and inhibtis NF-κB activity, used for cancer and inflammation research.
IC50 & Target: PPARγ, NF-κB[1]
In Vitro: 4-O-Methyl honokiol is a natural neolignan isolated from Magnolia officinalis, acts as a PPARγ agonist, and inhibtis NF-κB activity. 4-O-Methyl honokiol (20 μM) increases the expression, transcription and DNA binding activities, and nuclear translocation of PPARγ in both in prostate PC-3 and LNCap cells. 4-O-Methyl honokiol (0-30 μM) inhibits LNCaP and PC-3 cancer cells growth, causes G0/G1 phase arrest and induces apoptotic cell death, and such effects can be reversed by PPARγ antagonist. 4-O-Methyl honokiol inhibits NF-κB activity and cancer cell growth, but such effects as well as its activation of PPARγ can be abolished by knock-down of p21[1]. 4-O-methylhonokiol (0.5, 1 and 2 μM) reduces LPS-induced release of NO, PGE2, ROS, TNF-α and IL-1β in cultured astrocytes, and amyloidogenesis in cultured astrocytes and microglial BV-2 cells[2].
In Vivo: 4-O-Methyl honokiol (40 or 80 mg/kg, i.p. everyday for 4 weeks) inhibits the growth of SW620 and PC3 tumours in SW620 and PC3 xenograft model. 4-O-Methyl honokiol significantly increases the expression of p21 and PPARγ in the tumour tissues[1]. 4-O-Methyl honokiol (0.5 or 1 mg/kg/day daily for 3 weeks) significantly ameliorates LPS-induced memory impairment, and inhibits LPS-induced iNOS and COX-2 expression in mice. 4-O-Methyl honokiol also shows inhibitory activities against the Aβ1-42 accumulation, and activates astrocytes and microglia in LPS-injected mice brain[2].

Name: ATP-Red 1, CAS: 1847485-97-5, stock 28.2g, assay 98.2%, MWt: 561.48, Formula: C34H36BN3O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (89.05 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ATP-Red 1 is a multisite-binding switchable fluorescent probe, and can selectively and rapidly responds to intracellular concentrations of ATP in living cells.
In Vitro: ATP-Red 1 is a multisite-binding switchable fluorescent probe, and can selectively and rapidly responds to intracellular concentrations of ATP in living cells. The maximum absorption and emission wavelength of are 570/566 nm and 590/585 nm. ATP-Red 1 has good membrane permeability, and in the presence of 5 mM ATP, the fluorescence intensity of ATP-Red 1 increases 5.6-fold. ATP-Red 1 (2.5 μM, 20 min) shows much weaker fluorescence after KCN-induced inhibition of OXPHOS, which results in reduced mitochondrial ATP levels in OSCC cells[1].

Name: PL553, CAS: 1456872-74-4, stock 0.7g, assay 98.2%, MWt: 508.49, Formula: C28H23F3N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PL553 is a specific and high-affinity fluorigenic substrate of Leukotriene A4 hydrolase, with a λmax of 210 nm and λem of 410 nm.
In Vitro: PL553 is a specific and high-affinity fluorigenic substrate of Leukotriene A4 hydrolase (LTA4H), with a maximum absorption (λmax) of 210 nm and maximum emission (λem) of 410 nm. PL553 is a better LTA4H substrate than (l)-Ala-β-naphthylamide, and resistant to cleavage by other aminopeptidases, but can be cleaved by FAAH. PL553 (40 μM) is used to evaluate the potencies of known inhibitors toward LTA4H[1].

Name: Soluble epoxide hydrolase inhibitor, CAS: 1241826-88-9, stock 20.9g, assay 99%, MWt: 441.31, Formula: C18H12F5N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Soluble epoxide hydrolase inhibitor is an inhibitor of soluble epoxide hydrolase, and inhibits human soluble epoxide hydrolase (h-sEH) with pIC50 of 8.4, extracted from patent WO 2010096722 A1, example 57.
IC50 & Target: pIC50: 8.4 (h-sEH)[1]
In Vitro: Soluble epoxide hydrolase inhibitor (Example 57) is an inhibitor of soluble epoxide hydrolase, and inhibits human soluble epoxide hydrolase with pIC50 of 8.4[1].

Name: VU591, CAS: 1222810-74-3, stock 11.5g, assay 98%, MWt: 368.30, Formula: C16H12N6O5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (169.70 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: VU591 is a potent, selective renal outer medullary potassium channel (ROMK or Kir1.1) inhibitor, with an IC50 of 0.24 μM[1].
IC50 & Target: IC50: 0.24 μM (ROMK)[1].

Name: Lapatinib GW572016;GW2016, CAS: 231277-92-2, stock 10.4g, assay 98.9%, MWt: 581.06, Formula: C29H26ClFN4O4S, Solubility: DMSO : ≥ 39 mg/mL (67.12 mM), Clinical_Informat: Launched, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Autophagy;Apoptosis, Target: EGFR;EGFR;Autophagy;Ferroptosis, Biological_Activity: Lapatinib (GW572016) is a potent inhibitor of the ErbB-2 and EGFR tyrosine kinase domains with IC50 values against purified EGFR and ErbB-2 of 10.2 and 9.8 nM, respectively[1].
IC50 & Target: IC50: 10.2 nM (EGFR), 9.8 nM (ErbB2)[1]
In Vitro: Lapatinib (GW2016; 0.03-10 µM; 6 hours; BT474 and HN5 cells) treatment inhibits receptor autophosphorylation of EGFR and ErbB-2 in a dose-responsive manner. Phosphorylation of serine 473 of AKT was inhibited by GW2016 in a dose-dependent manner[1]. 
Lapatinib (GW2016; 72 hours; HN5, A-43, BT474, N87, and CaLu-3 cells) treatment has a selective inhibition of the proliferation of human tumor cell lines[1]. 
Lapatinib (GW2016; 1-10 µM; 72 hours; HN5 cells) treatment results in induces G1 arrest[1].
In Vivo: Lapatinib (GW2016; 30-100 mg/kg; oral administration; twice daily; for 21 days; CD-1 nude female mice) treatment inhibits tumor xenograft growth of the HN5 cells in a dose-responsive manner at 30 and 100 mg/kg, with complete inhibition of tumor growth at the higher dose[1].

Name: Pelitinib EKB-569;WAY-EKB 569, CAS: 257933-82-7, stock 30.6g, assay 98.6%, MWt: 467.92, Formula: C24H23ClFN5O2, Solubility: DMSO : 16 mg/mL (34.19 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: Src;EGFR;EGFR, Biological_Activity: Pelitinib (EKB-569;WAY-EKB 569) is an irreversible inhibitor of EGFR with an IC50 of 38.5 nM; also slightly inhibits Src, MEK/ERK and ErbB2 with IC50s of 282, 800, and 1255 nM, respectively.
IC50 & Target: IC50: 38.5 nM (EGFR), 282 nM (Src), 800 nM (MEK/ERK), 1255 nM (ErbB2)[1]
In Vitro: Pelitini has much greater inhibitory activity against the EGFR kinase than against Src, MEK/ERK, Cdk4, c-Met, Raf and ErbB2, for example, the IC50 for EGFR is 32-fold lower than the IC50 for the closely related ErbB2. Pelitinib results in a dramatic reduction in EGFR phosphorylation but no change in the total amount of EGFR protein. It requires at least 10-fold more drug to equivalently inhibit ErbB2 phosphorylation in similar assays, and EKB-569 does not block phosphorylation of another receptor tyrosine kinase (c-Met) assessed in the same manner[1]. EKB-569 is a potent inhibitor of proliferation in NHEK, A431, and MDA-468 cells (IC50=61, 125, and 260 nM, respectively) but not MCF-7 cells (IC50=3600 nM). EKB-569 is also a potent inhibitor of EGF-induced phosphorylated EGF-R (pEGF-R) in A431 and NHEK cells (IC50=20-80 nM)[1].
In Vivo: A single oral dose of 10 mg/kg EKB-569 inhibits EGFR phosphorylation in A431 xenografts within 60 minutes. Twenty-four hours later, EGFR activity is still inhibited by over 50% by this single oral dose. The half-life of EKB-569 in mouse plasma is about 2 hours[1].

Name: Gly-β-MCA, CAS: 66225-78-3, stock 27.9g, assay 98.3%, MWt: 465.62, Formula: C26H43NO6, Solubility: DMSO : 125 mg/mL (268.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: FXR;Autophagy, Biological_Activity: Gly-β-MCA, a bile acid, is a potent, sable, intestine-selective and oral bioactive farnesoid X receptor (FXR) inhibitor that may be a candidate for the treatment of metabolic disorders[1].
IC50 & Target: FXR[1].
In Vitro: Gly-β-MCA, a bile acid, is a potent, sable and intestine-selective and farnesoid X receptor (FXR) inhibitor[1]. 
Gly-β-MCA (Gly-MCA, ) is resistant to hydrolysis by BSH[1].
In Vivo: Gly-β-MCA (Gly-MCA, p.o. 10 and 50 mg/kg) prevents and treats diet-induced and genetic obesity, along with insulin resistance and hepatic steatosis without systemic, hepatic or intestinal toxicities in mice[1]. 
Gly-MCA does not increase faecal LCN-2 levels, indicating that Gly-MCA does not induce intestinal inflammation[1].

Name: CUDC-101, CAS: 1012054-59-9, stock 16.4g, assay 98.5%, MWt: 434.49, Formula: C24H26N4O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (57.54 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Epigenetics;Cell Cycle/DNA Damage, Target: EGFR;EGFR;HDAC;HDAC, Biological_Activity: CUDC-101 is a potent inhibitor of HDAC, EGFR, and HER2 with IC50s of 4.4, 2.4, and 15.7 nM, respectively.
IC50 & Target: IC50: 4.4 nM (HDAC), 2.4 nM (EGFR), and 15.7 nM (HER2)[1]
In Vitro: CUDC-101 inhibits both class I and class II HDACs, but not class III, Sir-type HDACs. CUDC-101 displays broad antiproliferative activity in many human cancer cell types. CUDC-101 is a potent and selective HDAC, EGFR, and HER2 inhibitor with only weak inhibition of the following protein kinases (IC50): KDR (VEGFR2) (849 nM), Src (11000 nM), Lyn (840 nM), Lck (5910 nM), Abl-1 (2890 nM), FGFR-2 (3430 nM), Flt-3 (1500 nM), and Ret (3200 nM)[1]. CUDC-101 (300 nM) inhibits both the full length AR (flAR) and the AR variant AR-V7[2]. CUDC-101 is the most active agent in all three ATC cell lines screened for inhibitors of EGFR and HDACs, with half-maximal inhibitory concentration (IC50) at 0.15 μM for 8505c, and 1.66 μM for both C-643 and SW-1736 cells. CUDC-101 inhibits cancer cell migration and modulates epithelial-mesenchymal transition marker expression in ATC cells. CUDC-101 also inhibits HDAC and MAPK pathway, induces p21, and decreases survivin and XIAP expression in ATC cells[3]. CUDC-101 (1 μM) increases the acetylation of p53 and α-tubulin, nonhistone substrates of HDAC, in treated cancer cells. CUDC-101 modulates RTK activity and expression and exhibits immediate and stable inhibition of RTK and downstream Akt signaling[4].
In Vivo: CUDC-101 (120 mg/kg, iv, daily) induces tumor regression in the Hep-G2 liver cancer model and is more efficacious than erlotinib at its maximum tolerated dose (MTD). In the erlotinib-resistant A549 NSCLC xenograft model, CUDC-101 (120 mg/kg) shows potent inhibition of tumor growth. In the erlotinib-sensitive H358 NSCLC models, CUDC-101 (15, 30, 60 mg/kg, i.v.) inhibits tumor growth in a dose-dependent manner. CUDC-101 (120 mg/kg) causes significant tumor regression in the lapatinib-resistant, HER2-negative, EGFR-overexpressing MDA-MB-468 breast cancer model and the EGFR-overexpressing CAL-27 head and neck squamous cell carcinoma (HNSCC) model. CUDC-101 (120 mg/kg) also inhibits tumor growth in the K-ras mutant HCT116 colorectal and EGFR/HER2 (neu)-expressing HPAC pancreatic cancer models[1]. In an in vivo mouse model of metastatic ATC, CUDC-101 inhibits tumor growth and metastases, and significantly prolongs survival[3]. CUDC-101 (120 mg/kg) is effective against a broad range of tumor types in xenograft models[4].

Name: PF-562271, CAS: 717907-75-0, stock 28.6g, assay 98.1%, MWt: 507.49, Formula: C21H20F3N7O3S, Solubility: DMSO : ≥ 48 mg/mL (94.58 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Pyk2;FAK, Biological_Activity: PF-562271 is a potent ATP-competitive, reversible inhibitor of FAK and Pyk2 kinase, with an IC50 of 1.5 nM and 13 nM, respectively.
IC50 & Target: IC50: 1.5 nM (FAK), 13 nM (Pyk2), 30 nM (CDK2), 47 nM (CDK3), 58 nM (CDK1), 97 nM (CDK7), 97 nM (Flt3)[1]
In Vitro: PF-562271 is shown to be a 30- to 120-nM inhibitor of CDK2/E, CDK5/p35, CDK1/B, and CDK3/E in recombinant enzyme assays, in cell-based assays evaluating the role of CDKs, a 48-hour exposure of 3.3 μM PF-562271 is required to alter cell cycle progression. PF-562271 is potent in an inducible cell-based assay measuring phospho-FAK with a IC50 of 5 nM[1]. PF-562271, a selective inhibitor of both FAK and proline-rich tyrosine kinase 2 (PYK2), a FAK-related family member, on cell growth and colony formation in Ewing sarcoma cell lines. Seven cell lines are treated for 5 days with PF-562271 across a range of concentrations using 2-fold serial dilutions. Treatment with PF-562271 impaires cell viability in all cell lines, with an average IC50 of 2.4 μM after 3 days of treatment. TC32 and A673 are the 2 most sensitive cell lines, with IC50 concentrations of 2.1 and 1.7 μM, respectively[2].
In Vivo: PF-562271 inhibits FAK phosphorylation in vivo in a dose-dependent fashion (calculated EC50 of 93 ng/mL, total) after p.o. administration to tumor-bearing mice[1]. Rats that receive PF-562271 demonstrate a decrease in tumor growth after 2 weeks of treatment with signs of bone healing as evidenced by the deposition of new bone (cortical and cancellous) at sites previously damaged by the tumor[3].

Name: BB-Cl-Amidine, CAS: 1802637-39-3, stock 19.8g, assay 98.7%, MWt: 459.97, Formula: C26H26ClN5O, Solubility: DMSO : 125 mg/mL (271.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Protein Arginine Deiminase, Biological_Activity: BB-Cl-Amidine is a peptidylarginine deminase (PAD) inhibitor.
IC50 & Target: PAD[1].
In Vivo: Treatment with BB-Cl-amidine subtly reduces splenomegaly in MRL/lpr mice, while there is a trend towards increased circulating levels of anti-NET antibodies with PAD inhibitor treatment. However, neither PAD inhibitor affected body weight or total IgG levels. Indeed, treatment with both Cl-amidine and BB-Cl-amidine significantly improves endothelium-dependent vasorelaxation. The BB-Cl-amidine group also shows a strong trend towards downregulation of IRGs. Treatment with either Cl-amidine or BB-Cl-amidine significantly improves muzzle alopecia, in many cases preventing it entirely[1].

Name: Cilofexor GS-9674, CAS: 1418274-28-8, stock 9.6g, assay 98.1%, MWt: 586.85, Formula: C28H22Cl3N3O5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (213.00 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: FXR;Autophagy, Biological_Activity: Cilofexor (GS-9674) is a farnesoid X receptor (FXR) agonist.
IC50 & Target: FXR[1].

Name: Conteltinib CT-707, CAS: 1384860-29-0, stock 1.9g, assay 98.9%, MWt: 635.82, Formula: C32H45N9O3S, Solubility: DMSO : 31.25 mg/mL (49.15 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: FAK, Biological_Activity: Conteltinib (CT-707) is a multi-kinase inhibitor targeting FAK, ALK, and Pyk2. Conteltinib (CT-707) exerts significant inhibitory effect on FAK with an IC50 of 1.6 nM[1].
IC50 & Target: IC50: 1.6 nM (FAK)[1]

Name: Edicotinib JNJ-40346527, CAS: 1142363-52-7, stock 16.4g, assay 98.2%, MWt: 461.60, Formula: C27H35N5O2, Solubility: DMSO : 16.67 mg/mL (36.11 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Fms, Biological_Activity: Edicotinib is a selective and orally available colony-stimulating factor-1 (CSF-1) receptor inhibitor, and has entered phase IIA clinical trial to study rheumatoid arthritis (RA) despite disease.
IC50 & Target: CSF-1 receptor[1]

Name: Baloxavir, CAS: 1985605-59-1, stock 12.5g, assay 98.9%, MWt: 483.49, Formula: C24H19F2N3O4S, Solubility: DMSO : ≥ 50 mg/mL (103.41 mM), Clinical_Informat: Phase 3, Pathway: Anti-infection, Target: Influenza Virus, Biological_Activity: Baloxavir is an anti-influenza agent extracted from patent WO 2017104691 A1.
IC50 & Target: Influenza virus[1]

Name: CT7001 hydrochloride ICEC0942 hydrochloride, CAS: 1805789-54-1, stock 33.8g, assay 98.8%, MWt: 430.97, Formula: C22H31ClN6O, Solubility: DMSO : ≥ 62.5 mg/mL (145.02 mM); H2O : 55 mg/mL (127.62 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CT7001 hydrochloride is a selective CDK7 inhibitor, with IC50s of 41 nM and 578 nM for CDK7/CycH/MAT1 and CDK2/cycE1, respectively.
IC50 & Target: IC50: 41 nM (CDK7/CycH/MAT1), 578 nM (CDK2/cycE1)[1]
In Vitro: CT7001 (ICEC0942) is a selective CDK7 inhibitor, with IC50s of 41 nM and 578 nM for CDK7/CycH/MAT1 and CDK2/cycE1, respectively[1].

Name: Seclidemstat SP-2577, CAS: 1423715-37-0, stock 26.2g, assay 98.4%, MWt: 450.94, Formula: C20H23ClN4O4S, Solubility: DMSO : 100 mg/mL (221.76 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: Seclidemstat (SP-2577) is a potent and orally bioavailable LSD1 inhibitor, with a mean IC50 of 127 nM.
IC50 & Target: IC50: 127 nM (LSD1)[1]
In Vivo: Seclidemstat (Compound 2577) reduces tumor volume at 40, 80 mg/kg by i.p. and also shows such effect at 80 mg/kg via p.o. dosing.

Name: K-80003 TX-803, CAS: 1292821-90-9, stock 23.5g, assay 98.5%, MWt: 336.40, Formula: C22H21FO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: Akt, Biological_Activity: K-80003 is a potent inhibitor of tRXRα-dependent Akt activation and cancer cell growth.
IC50 & Target: Akt[1]
In Vitro: When MCF-7 cells are cotreated with K-80003, TNFα-induced colocalization of tRXRα with p85α in the cytoplasm is inhibited, resulting in tRXRα nuclear localization. Western blotting shows that K-80003-stabilized tetrameric form of tRXRα is found exclusively in the nuclear fraction, while tRXRα monomer is distributed both in the nuclear and cytoplasmic fractions[2].
In Vivo: K-80003 is a potent inhibitor of AKT activation by all-trans-retinoic acid. K-80003 displays enhanced efficacy in inhibiting tRXRα-dependent AKT activation and tRXRα tumor growth in animals. K-80003 has high affinity to RXRα but lacks COX inhibitory activity[1].

Name: GSK2850163, CAS: 2121989-91-9, stock 34.2g, assay 98.8%, MWt: 446.41, Formula: C24H29Cl2N3O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 67.5 mg/mL (151.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: IRE1, Biological_Activity: GSK2850163 is a novel inhibitor of inositol-requiring enzyme-1 alpha (IRE1α) which can inhibit IRE1α kinase activity and RNase activity with IC50s of 20 and 200 nM, respectively.
IC50 & Target: IC50: 20 nM (IRE1α kinase activity), 200 nM (IRE1α RNase activity)[1]
In Vitro: GSK2850163 is a novel inhibitor of inositol-requiring enzyme-1 alpha (IRE1α) which can inhibit IRE1α kinase activity and RNase activity with IC50s of 20 and 200 nM, respectively. The increased autophosphorylation of IRE1α could be reduced in a dose-dependent manner by GSK2850163. Increasing concentrations of GSK2850163 are capable of reducing the increased XBP 1 transcriptional activity. Two additional kinases are weakly inhibited by GSK2850163: Ron (IC50=4.4 μM) and FGFR1 V561M (IC50=17 μM)[1].

Name: Lanraplenib GS-9876, CAS: 1800046-95-0, stock 23.9g, assay 98.4%, MWt: 443.50, Formula: C23H25N9O, Solubility: DMSO : 41.67 mg/mL (93.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Syk, Biological_Activity: Lanraplenib (GS-9876) is a highly selective and orally active SYK inhibitor (IC50=9.5 nM) in development for the treatment of inflammatory diseases. Lanraplenib (GS-9876) inhibits SYK activity in platelets via the glycoprotein VI (GPVI) receptor without prolonging bleeding time (BT) in monkeys or humans[1][2][3].
IC50 & Target: IC50: 9.5 nM (SYK)[1]
In Vitro: Lanraplenib (GS-9876) inhibits anti-IgM stimulated phosphorylation of AKT, BLNK, BTK, ERK, MEK, and PKCδ in human B cells with EC50 values of 24-51 nM. Lanraplenib (GS-9876) inhibits anti-IgM mediated CD69 and CD86 expression on B-cells (EC50=112±10 nM and 164±15 nM, respectively) and anti-IgM /anti-CD40 co-stimulated B cell proliferation (EC50=108±55 nM). In human macrophages, Lanraplenib (GS-9876) inhibits IC-stimulated TNFα and IL-1β release (EC50=121±77 nM and 9±17 nM, respectively)[1]. 
Lanraplenib (GS-9876) inhibits glycoprotein VI (GPVI)-induced phosphorylation of linker for activation of T cells and phospholipase Cγ2, platelet activation and aggregation in human whole blood, and platelet binding to collagen under arterial flow[2].

Name: Licogliflozin LIK066, CAS: 1291094-73-9, stock 32.8g, assay 99%, MWt: 416.46, Formula: C23H28O7, Solubility: H2O : 2 mg/mL (4.80 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel, Target: SGLT, Biological_Activity: Licogliflozin is a sodium glucose cotransporter (SGLT1 and SGLT2) inhibitor.
IC50 & Target: SGLT1, SGLT2[1]
In Vitro: Licogliflozin (LIK066) is a non-anti-fibrotic treatment agent for non-alcoholic steatohepatitis (NASH).

Name: PhiKan 083 hydrochloride, CAS: 1050480-30-2, stock 18g, assay 98.7%, MWt: 274.79, Formula: C16H19ClN2, Solubility: H2O : 2 mg/mL (7.28 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: MDM-2/p53, Biological_Activity: PhiKan 083 hydrochloride is a carbazole derivative, which binds to the surface cavity and stabilizes Y220C (a p53 mutant), with a Kd of 167 μM[1], and a relative binding affinity (Kd) of 150 μM in Ln229 cells[3].
IC50 & Target: Kd: 167 μM (p53-Y220C)[1], 150 μM (p53Y220C, in Ln229 cells)[3]
In Vitro: PhiKan 083 is a carbazole derivative, which binds to the surface cavity and stabilizes Y220C (a p53 mutant), with a Kd of 167 μM[1], shows a relative binding affinity (Kd) of 150 μM for p53Y220C in Ln229 cells[3]. 
PhiKan 083 slows down its thermal denaturation rate[2]. 
PhiKan 083 (125 μM, 48 hours) reduces the cell viability of engineered variants of Ln229 cells[3]. 
PhiKan 083 (100 μM) in conbination with NSC 123127 (1 μM) enhances the pro-apoptotic activity in all variants of Ln229 cells (p53wt, p53Y220C, p53G245S, p53R282W)[3].

Name: Nemorexant ACT-541468, CAS: 1505484-82-1, stock 34g, assay 98.5%, MWt: 450.92, Formula: C23H23ClN6O2, Solubility: DMSO : ≥ 250 mg/mL (554.42 mM), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Orexin Receptor (OX Receptor);Orexin Receptor (OX Receptor), Biological_Activity: Nemorexant (ACT-541468) is a potent orexin receptor antagonist extracted from patent WO2015083094A1, compound example 7, has IC50s of 2 nM and 3 nM for Ox1 receptor and Ox2 receptor, respectively.
IC50 & Target: IC50: 2 nM (Ox1 receptor ), 3 nM (Ox2 receptor)[1]
In Vitro: Nemorexant (Compound example 7) is a orexin receptor antagonist with IC50s of 2 nM and 3 nM for Ox1 receptor and Ox2 receptor, respectively[1].

Name: Nidufexor, CAS: 1773489-72-7, stock 29.6g, assay 98%, MWt: 487.93, Formula: C27H22ClN3O4, Solubility: DMSO : 83.33 mg/mL (170.78 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: FXR;Autophagy, Biological_Activity: Nidufexor is a farnesoid X receptor (FXR) agonist[1].
IC50 & Target: FXR[1]

Name: Parimifasor LYC30937, CAS: 1796641-10-5, stock 33.9g, assay 99%, MWt: 460.21, Formula: C18H11Cl2F4N5O, Solubility: DMSO : ≥ 150 mg/mL (325.94 mM), Clinical_Informat: Phase 1, Pathway: Others, Target: Others, Biological_Activity: Parimifasor (LYC30937) is an immunomodulator, with anti-inflammatory activity.

Name: Ketohexokinase inhibitor 1, CAS: 2102501-84-6, stock 25.7g, assay 98.2%, MWt: 356.34, Formula: C16H19F3N4O2, Solubility: DMS : ≥ 125 mg/mL (350.79 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ketohexokinase inhibitor 1 is an inhibitor of ketohexokinase (KHK), with IC50s of 8.4 nM and 66 nM for KHK-C and KHK-A, respectively, extracted from patent US 20170183328 A1, example 4.
IC50 & Target: IC50: 8.4 nM (KHK-C), 66 nM (KHK-A)[1]
In Vitro: Ketohexokinase inhibitor 1 (Example 4) is an inhibitor of ketohexokinase (KHK), with IC50s of 8.4 nM and 66 nM for KHK-C and KHK-A, sepctively[1].

Name: FT827, CAS: 1959537-86-0, stock 6.7g, assay 98.1%, MWt: 548.61, Formula: C27H28N6O5S, Solubility: DMSO : 125 mg/mL (227.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: FT827 is a selective and covalent ubiquitin-specific protease 7 (USP7) inhibitor (Ki=4.2 µM). FT827 binds to the USP7 catalytic domain (USP7CD; residues 208-560) with an apparent Kd value of 7.8 µM[1].
IC50 & Target: Ki: 4.2 μM (USP7); Kd: 7.8 μM (USP7)[1]
In Vitro: FT827 features a vinylsulfonamide moiety that covalently modifies the catalytic Cys223 of USP7 and inhibits the enzyme with Ki and Kd of 4.2 and 7.8 μM, respectively. FT827 exclusively inhibit USP7 in a panel of 38 deubiquitinases (DUBs) from diverse families. FT827 inhibits USP7 probe reactivity with IC50s of 0.1-2 µM, confirming 10 to 100-fold higher potency as compared to P22077 in crude cell extracts or with intact MCF7 breast cancer cells, followed by incubation with the ubiquitin active site suicide probe haemagglutinin (HA)-tagged ubiquitin bromoethyl (HA-UbC2Br)[1].

Name: GPR120 Agonist 2, CAS: 1234844-11-1, stock 17.2g, assay 98.2%, MWt: 388.88, Formula: C22H25ClO4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 50 mg/mL (128.57 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPR120, Biological_Activity: GPR120 Agonist 2 is a GPR120 agonist extracted from patent US 20110313003 A1, example 209.
IC50 & Target: GPR120[1]
In Vitro: GPR120 Agonist 2 is a GPR120 agonist which is useful for the treatment of metabolic diseases, including Type II diabetes and diseases associated with poor glycemic control[1].

Name: Tinoridine hydrochloride Y-3642 hydrochloride, CAS: 25913-34-2, stock 4.4g, assay 98.1%, MWt: 352.88, Formula: C17H21ClN2O2S, Solubility: DMSO : 16.67 mg/mL (47.24 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Glutathione Peroxidase, Biological_Activity: Tinoridine hydrochloride is a nonsteroidal anti-inflammatory drug and also has potent radical scavenger and antiperoxidative activity.
In Vitro: Tinoridine reduces a stable free radical, diphenyl-p-picrylhydrazyl, in the molar ratio of about 1:2, indicating its free radical scavenging ability. Tinoridine inhibits the lipid peroxidation in rat liver microsomes induced by xanthine-xanthine oxidase system in the presence of ADP and Fe2+, in which hydroxyl radical is formed. Tinoridine is demonstrated to be oxidized in the course of the lipid peroxidation by following the fluorescence derived from the oxidation product of tinoridine. It is also oxidized by the xanthine-xanthine oxidase system in the presence of Fe2+, but its oxidation is slow in the absence of Fe2+ and almost completely inhibited by catalase. Tinoridine is also oxidized by H2O2-Fe2+ system producing OH (Fenton reaction), but it does not affect the reduction of cytochrome c caused by superoxide radical[1].
In Vivo: CCl4 aministration produces a marked decrease in the concentrations of liver microsomal cytochrome P-450 and G6Pase, indicating that hepatic endoplasmic reticulum function is disrupted. Prior treatment of the animals with tinoridine (100 mg/kg) significantly reduces the CCl4-induced alterations in the enzyme activities, and a rapid recovery toward the normal values is observed[2].

Name: Pemigatinib, CAS: 1513857-77-6, stock 15.7g, assay 98.9%, MWt: 487.50, Formula: C24H27F2N5O4, Solubility: DMSO : 41.67 mg/mL (85.48 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK, Target: FGFR, Biological_Activity: Pemigatinib is a selective FGFR inhibitor in development for the treatment of patients with cholangiocarcinoma.
IC50 & Target: Target: FGFR[1]

Name: Risdiplam RG7916;RO7034067, CAS: 1825352-65-5, stock 13.4g, assay 98.9%, MWt: 401.46, Formula: C22H23N7O, Solubility: Ethanol : < 1 mg/mL (insoluble); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Phase 3, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: Risdiplam (RG7916; RO7034067) is an orally administered, centrally and peripherally distributed SMN2 pre-mRNA splicing modifier that increases survival motor neuron (SMN) protein levels.
IC50 & Target: SMN2
In Vitro: Risdiplam modulates SMN2 pre-mRNA splicing towards the production of full-length SMN2 mRNA and increases SMN protein levels. Risdiplam is a modifier of SMN2 splicing, leading to an increase in SMN2 full length transcript and thus functional SMN protein. Spinal muscular atrophy (SMA) type I remains the most common genetic disease resulting in death in infancy. Characterized by progressive motor and respiratory muscle weakness, this autosomal recessive neuromuscular disorder is caused by low levels of the survival motor neuron protein (SMN) due to inactivating bi-allelic deletions and other disabling mutations in the survival motor neuron 1 (SMN1) gene[1].

Name: Telratolimod MEDI 9197;3M 052, CAS: 1359993-59-1, stock 21g, assay 98.6%, MWt: 593.89, Formula: C36H59N5O2, Solubility: DMSO : 5 mg/mL (8.42 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: Telratolimod is a toll like receptors 7/8 (TLR7/8) agonist, with antitumor activity.
IC50 & Target: TLR7/8[1]
In Vitro: Telratolimod (3M-052) is a toll like receptors 7/8 (TLR7/8) agonist, with antitumor activity[1].
In Vivo: Telratolimod (50 μg) inhibits the tumor volume, and more potently blocks tumor gowth in combination with CpG ODN in BALB/c mice bearing CT26 colon carcinoma cells. Telratolimod (100 μg) plus 200 μg of CpG ODN slows tumor growth and prolongs survival of mice bearing large tumors[1].

Name: Tepilamide fumarate XP-23829, CAS: 1208229-58-6, stock 37.4g, assay 98.8%, MWt: 243.26, Formula: C11H17NO5, Solubility: DMSO : ≥ 125 mg/mL (513.85 mM), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Tepilamide fumarate (XP-23829) is an oral fumaric acid ester, acts as a prodrug of monomethyl fumarate, and is used in the research of moderate to severe chronic plaque psoriasis[1].

Name: FN-1501, CAS: 1429515-59-2, stock 19.3g, assay 98.4%, MWt: 431.49, Formula: C22H25N9O, Solubility: DMSO : ≥ 50 mg/mL (115.88 mM), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;Protein Tyrosine Kinase/RTK, Target: CDK;FLT3, Biological_Activity: FN-1501 is a potent inhibitor of FLT3 and CDK, with IC50s of 2.47, 0.85, 1.96, and 0.28 nM for CDK2/cyclin A, CDK4/cyclin D1, CDK6/cyclin D1 and FLT3, respectively. FN-1501 has anticancer activity.
IC50 & Target: IC50: 2.47 nM (CDK2/cyclin A), 0.85 nM (CDK4/cyclin D1), 1.96 nM (CDK6/cyclin D1), 0.28 nM (FLT3)[1]
In Vitro: FN-1501 is a potent inhibitor of FLT3 and CDK, with IC50s of 2.47 ± 0.21, 0.85 ± 0.28, 1.96 ± 0.08 and 0.28 ± 0.01 nM for CDK2/cyclin A, CDK4/cyclin D1, CDK6/cyclin D1 and FLT3, respectively. FN-1501 shows potent inhibitory activity against several tumor cells, such as MGC803, RS4;11, MCF-7, HCT-116, and NCI-H82, with GI50s of 0.37 ± 0.04, 0.05 ± 0.01, 2.84 ± 0.25, 0.09 ± 0.04, 0.11 ± 0.02 nM, respectively[1].
In Vivo: FN-1501 exhibits potent antitumor activity, and shows little cytotoxicity on normal lymphocyte cells, with LD50 of 185.67 mg/kg in ICR mice. FN-1501 (15. 30, or 40 mg/kg/d, i.v.) dose-dependently and significantly suppresses the growth of tumor in MV4-11-cell-inoculated-xenograft mice[1].

Name: MK8722, CAS: 1394371-71-1, stock 7.1g, assay 98.7%, MWt: 449.89, Formula: C24H20ClN3O4, Solubility: DMSO : ≥ 62.5 mg/mL (138.92 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: MK8722 is a potent and systemic pan-AMPK activator.
IC50 & Target: AMPK[1]
In Vitro: MK8722 (MK-8722) is a potent, direct, allosteric activator of all 12 mammalian AMPK complexes. MK8722 activates pAMPK complexes with increased potency and magnitude versus AMP, with EC50 values of ~1 to 60 nM and increased activation by factors of ~4 to 24. Although MK8722 exhibits higher affinity for β1-containing (~1 to 6 nM) versus β2-containing (~15 to 63 nM) pAMPK complexes, it is the most potent activator of β2 complexes reported to date. pAMPK activation by maximal AMP plus MK8722 is synergistic, demonstrating that the agents act at distinct sites[1].
In Vivo: Chronic antihyperglycemic efficacy of MK8722 (MK-8722) is evaluated in db/db mice, a leptin receptor-deficient T2DM model. Once-daily administration of MK8722 results in dose-dependent lowering of ambient blood glucose. On treatment day 12, glucose reductions after MK8722 treatment (30 mpk/day) are comparable to those observed with the PPARγ agonist BRL49653 (3 mpk/day). Unlike BRL49653, the glucose-lowering action of MK8722 manifests without significant effects on body weight, which is a consistent finding. Dose-dependent increases in tissue pACC are maintained throughout the dosing period. Chronic efficacy, without tachyphylaxis, is also observed in additional dysmetabolic and diabetic rodent models. In all cases, efficacy is associated with trough MK8722 plasma levels comparable to the concentrations required to acutely stimulate skeletal muscle glucose uptake. Chronic MK8722 dosing in mice also increases muscle Glut4 protein levels, possibly contributing to efficacy[1].

Name: TES-1025, CAS: 1883602-21-8, stock 30.1g, assay 98%, MWt: 383.44, Formula: C18H13N3O3S2, Solubility: DMSO : 100 mg/mL (260.80 mM; Need warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TES-1025 is a potent and selective human α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) inhibitor with an IC50 of 13±3 nM.
IC50 & Target: IC50: 13±3 nM (human ACMSD)[1]
In Vitro: TES-1025 is a low nanomolar human ACMSD inhibitor, which increases NAD+ levels in cellular systems[1].
In Vivo: TES-1025 is subjected to in vivo pharmacokinetic studies, following intravenous (IV) and oral (PO) dosings of male CD-1 mice. After the intravenous administration of 0.5 mg/kg, TES-1025 shows low blood clearance, with low volumes of distribution and half-lives (t1/2) of about 5.33 h, although after oral administration at 5 mg/kg, the blood concentration of TES-1025 is quantifiable for up to 8 h. A good systemic exposure is recorded for TES-1025, with a Cmax of 2570 ng/mL reaches at 2 h after dosing. The greater oral exposure of TES-1025 is further confirmed in the liver and kidneys with AUC0-8h of 19 200 h•ng/mL and 36 600 h•ng/mL, respectively[1].

Name: PF-05180999, CAS: 1394033-54-5, stock 22g, assay 98.6%, MWt: 414.39, Formula: C19H17F3N8, Solubility: DMSO : 50 mg/mL (120.66 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: PF-05180999 is a phosphodiesterase 2A (PDE2A) inhibitor, with an IC50 of 1.6 nM.
IC50 & Target: IC50: 1.6 nM (PDE2A)[1]
In Vitro: PF-05180999 is a phosphodiesterase 2A (PDE2A) inhibitor, with an IC50 of 1.6 nM. PF-05180999 binds to the rat, dog and monkey PDE2A, with Kis of 4.2, 8.4, and 5.5 nM and IC50s of 2.6, 5.2, and 3.4 nM, respectively. PF-05180999 shows weak activity against PDE, with IC50s of 2.03 μM (PDE10A1), 26.969 μM (PDE7B), 50.09 μM (PDE11A4), and >56.25 μM (PDE1B1, PDE3A1, PDE4D3, PDE5A1, PDE6 (bovine), PDE8B, PDE9A1), respectively. PF-05180999 is also a weak inducer of CYP3A4, and with no direct inhibition of human recombinant cytochrome P450 (CYP) enzymes (1A2, 2B6, 2C8, 2C9, 2C19, 2D6, and 3A) and no induction of CYP1A2[1].
In Vivo: PF-05180999 (Compound 30; 0.032-0.32 mg/kg mg/kg, s.c.) dramatically reduces the working memory errors produced by ketamine in a working memory radial arm maze (RAM) model in rats. PF-05180999 causes acute and exposure-dependent elevation in the accumulation of cGMP bulk levels in the cortex, striatum, and hippocampus, but with no changes in cAMP and the associated downstream phospho-cAMP response element-binding protein (p-CREB) in mice[1].

Name: CCG-63802, CAS: 620112-78-9, stock 11.9g, assay 98.9%, MWt: 450.51, Formula: C26H18N4O2S, Solubility: DMSO : 1.67 mg/mL (3.71 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: RGS Protein, Biological_Activity: CCG-63802 is a reversible inhibitor of regulator of G-protein signaling (RGS) protein; with greatest potency at RGS4.
IC50 value:
Target: RGS
CCG-63802 is selective amongst RGS proteins, with greatest potency at RGS4. CCG-63802 inhibits GTPase accelerating protein activity of RGS4 and blocks its interaction with Gαo. Retains activity under reducing conditions.

Name: NMDI14, CAS: 307519-88-6, stock 35.6g, assay 98.4%, MWt: 415.51, Formula: C21H25N3O4S, Solubility: DMSO : ≥ 25 mg/mL (60.17 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NMDI14 is a nonsense mediated RNA decay (NMD) inhibitor.
IC50 & Target: NMD[1]
In Vitro: NMDI14 is a nonsense mediated RNA decay (NMD) inhibitor. Treating cells with NMDI14 for 6 hours leads to an increase of PTC 39 β globin to 12%, a relative four-fold increase that, if resulting in biologically active hemoglobin, would be sufficient to ameliorate the clinical symptoms of thalassemia. Three days of treatment with NMDI14 results in no decrease in cell counts, demonstrating that the pharmacological inhibition of NMD can be achieved without subtle changes in proliferation. 941 genes are increased >1.5 fold with NMDI14. The treatment of N417 cells with NMDI14 for 6 hours leads to a steady state expression of p53 similar to that seen in U2OS cells. NMDI14 significantly increases the stability of PTC mutated p53 mRNA in N417 cells, without altering the stability of wild-type p53 in NMDI treated U2OS cells[1].

Name: 6,2'-Dihydroxyflavone, CAS: 92439-20-8, stock 32g, assay 98%, MWt: 254.24, Formula: C15H10O4, Solubility: DMSO : 155 mg/mL (609.66 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: 6,2'-Dihydroxyflavone is a novel antagonist of GABAA receptor.
IC50 & Target: GABAA receptor[1]
In Vitro: 6,2'-Dihydroxyflavone is a novel antagonist of GABAA receptor. 6,2'-Dihydroxyflavone inhibits [3H]-flunitrazepam binding to the rat cerebral cortex membranes with a Ki of 37.2±4.5 nM. The current elicited with the EC50 concentration of GABA is decreased to 73.6±1.9% of control by co-application of 5 μM 6,2'-Dihydroxyflavone (n=5), compare to a decrease to 65.9±3.0% by 1 μM FG-7142 (n=5). The EC50 for GABA dose response increases from 47.6 to 59.7 μM upon co-application of 5 μM 6,2'-Dihydroxyflavone, and the maximal GABA-current is decreased[1].
In Vivo: 6,2'-Dihydroxyflavone-treated mice exhibit significant differences from control mice with respect to the percentage of open arms entries [F(4,73)=8.01, P<0.0001] and the percentage of time spent in open arms [F (4,73)=5.19, P<0.002], but not the number of entries to closed arms [F(4,73)= 0.79,P=0.54]. The post-hoc NewmaneKeuls’ tests confirm that 6,2'-Dihydroxyflavone significantly decreases the percentage of open arm entries and time spent in open arms at the doses of 8 and 16 mg/kg. 6,2'-Dihydroxyflavone treatment similarly increases step-through latency [F(4,75)=4.71, P<0.002], suggesting enhanced cognitive performance[1].

Name: 3'-Methoxyflavonol, CAS: 76666-32-5, stock 25.3g, assay 98.7%, MWt: 268.26, Formula: C16H12O4, Solubility: DMSO : 155 mg/mL (577.80 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3'-Methoxyflavonol is a selective agonist of neuromedin U 2 receptor (NMU2R).
IC50 & Target: NMU2R[1]
In Vitro: 3'-Methoxyflavonol (NRA 10) is a selective agonist of neuromedin U 2 receptor (NMU2R)[1].

Name: 6-Methylflavone, CAS: 29976-75-8, stock 22.8g, assay 98.7%, MWt: 236.27, Formula: C16H12O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (211.62 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: 6-Methylflavone is an activator of α1β2γ2L and α1β2 GABAA receptors.
IC50 & Target: α1β2γ2L GABAA receptor, α1β2 GABAA receptor[1]
In Vitro: 6-Methylflavone is an activator of α1β2γ2L and α1β2 GABAA receptors. 6-Methylflavone enhances the normal response to GABA at recombinant α1β2γ2L and α1β2 GABAA receptors (P<0.0001) at concentrations from 1 to 100 μM. 6-Methylflavone (60 μM) shifts the GABA dose-response curve to the left (n=4, F=16.38, P=0.0004), decreasing the mean EC50 at α1β2γ2L GABAA receptors by 33±5.4%[1].

Name: 7-Methoxyisoflavone, CAS: 1621-56-3, stock 11.7g, assay 98.6%, MWt: 252.26, Formula: C16H12O3, Solubility: DMSO : 62 mg/mL (245.78 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: 7-Methoxyisoflavone is an isoflavone derivative and also an activator of adenosine monophosphate-activated protein kinase (AMPK).
IC50 & Target: AMPK[1]
In Vitro: 7-Methoxyisoflavone is an isoflavone derivative and also an activator of adenosine monophosphate-activated protein kinase (AMPK). When serum-starved cells are treated with 10 % FBS in the presence of 7-methoxyisoflavone, the serum-induced decrease in AMPK phosphorylation is prevented[1].

Name: Amine-PEG3-Biotin, CAS: 359860-27-8, stock 15.1g, assay 98.5%, MWt: 418.55, Formula: C18H34N4O5S, Solubility: H2O : ≥ 50 mg/mL (119.46 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Amine-PEG3-Biotin is used as a signal amplification label.

Name: Casein Kinase II Inhibitor IV, CAS: 863598-09-8, stock 24.7g, assay 98.8%, MWt: 429.47, Formula: C24H23N5O3, Solubility: DMSO : ≥ 250 mg/mL (582.11 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: Casein Kinase;Casein Kinase, Biological_Activity: Casein Kinase II Inhibitor IV is a small-molecule inducer of epidermal keratinocyte differentiation.
IC50 & Target: Target: Casein Kinase[1]
In Vitro: Treatment of human epidermal keratinocytes (NHEKs) with Casein Kinase II Inhibitor IV leads to an increase in the early differentiation markers keratins 1 and 10 at 48 h. Increased levels of IVL and TGM are observed in cells treated with Casein Kinase II Inhibitor IV at 72 h and persisted at 96 h. In addition, treated with Casein Kinase II Inhibitor IV expressesloricrin, a terminal differentiation marker, at later time points. Similar results are observed by messenger RNA (mRNA) expression analysis of NHEKs treated with Casein Kinase II Inhibitor IV. At early time points (12 and 24 h), treatment with Casein Kinase II Inhibitor IV leads to the upregulation of keratinocyte early differentiation marker genes, including keratin 1 (5.4-fold) and keratin 10 (5.4-fold). Terminal differentiation marker genes, including IVL (1.8-fold), TGM 1 (4.8-fold), loricrin (3.3-fold), and filaggrin (5.6-fold), are upregulated at late time points (36 and 48 h). These results are again consistent with the ability of Casein Kinase II Inhibitor IV to induce differentiation of epidermal progenitor cells into terminally differentiated keratinocytes[1].

Name: EHT 5372, CAS: 1425945-60-3, stock 25.7g, assay 99%, MWt: 383.40, Formula: C18H14FN5O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (65.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Stem Cell/Wnt;PI3K/Akt/mTOR;Cell Cycle/DNA Damage, Target: DYRK;GSK-3;GSK-3;CDK, Biological_Activity: EHT 5372 is a strong inhibitor of DYRK’s family kinases, with IC50s of 0.22, 0.28 nM for DYRK1A and DYRK1B, respectively.
IC50 & Target: IC50: 0.22/0.28 nM (DYRK1A/1B)[1].
In Vitro: EHT 5372 is a strong inhibitor of DYRK’s family kinases, with IC50s of 0.22, 0.28 nM for DYRK1A and DYRK1B, respectively[1][2]. IC50 for DYRK2 and DYRK3 were higher (10.8 and 93.2 nM, respectively) and there was no inhibition on DYRK4. EHT 5372 displayed minimal impact on the CDC2-like kinase (CLK) family, with more than 100x selectivity over CLK1 (CLK1: IC50=22.8 nM; CLK2: IC50=88.8 nM; CLK3: IC50>10 lM; CLK4: no inhibition) and on the glycogen synthase kinase 3 (GSK3) family (GSK3α: IC50=7.44 nM; GSK3β: IC50=221 nM). EHT 5372 inhibits the direct phosphorylation of Tau by DYRK1A. EHT 5372 also normalizes both Aβ-induced Tau phosphorylation and DYRK1A-stimulated Aβ production[2].

Name: BI-3812, CAS: 2166387-64-8, stock 15.8g, assay 98.1%, MWt: 558.03, Formula: C26H32ClN7O5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 20.83 mg/mL (37.33 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BI-3812 is potent and efficacious BCL6 inhibitor, inhibiting the BTB domain of BCL6, with an IC50 of ≤3 nM; BI-3812 has antitumor activity.
IC50 & Target: IC50: ≤3 nM (BCL6 BTB)[1]
In Vivo: BI-3812 is a BCL6 inhibitor, with an IC50 of ≤3 nM. BI-3812 shows an IC50 of 40 nM for the cellular BCL6[1].

Name: Diphenylterazine DTZ, CAS: 344940-63-2, stock 23.7g, assay 98.5%, MWt: 377.44, Formula: C25H19N3O, Solubility: DMSO : ≥ 19 mg/mL (50.34 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diphenylterazine is a bioluminescence agent.
In Vitro: Diphenylterazine is a bioluminescence agent. Diphenylterazine alone yields very little background, leading to excellent signal-to-background ratios. Furthermore, Diphenylterazine elicits minimal cell toxicity at millimolar concentrations. Diphenylterazine injections into untransfected BALB/c mice do not yield any background emission. The bioluminescence resulting from intraperitoneally injected Diphenylterazine displays extended kinetics[1].

Name: LX2343, CAS: 333745-53-2, stock 39.1g, assay 99%, MWt: 474.91, Formula: C22H19ClN2O6S, Solubility: DMSO : ≥ 155 mg/mL (326.38 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;PI3K/Akt/mTOR;Neuronal Signaling;Autophagy, Target: Amyloid-β;PI3K;Beta-secretase;Autophagy, Biological_Activity: LX2343 is a BACE1 enzyme inhibitor with an IC50 value of 11.43±0.36 μM. LX2343 acts as a non-ATP competitive PI3K inhibitor with an IC50 of 15.99±3.23 μM. LX2343 stimulates autophagy in its promotion of Aβ clearance.
IC50 & Target: IC50: 11.43±0.36 μM (BACE1), 15.99±3.23 μM (PI3K)[1] 
Amyloid-β, Autophagy[1]
In Vitro: LX2343 (5-20 μM) dose-dependently decreased Aβ accumulation in HEK293-APPsw and CHO-APP cells, and promotes Aβ clearance in SH-SY5Y cells and primary astrocytes. LX2343 ameliorates cognitive dysfunction in APP/PS1 transgenic mice via both Aβ production inhibition and clearance promotion, which highlights the potential of LX2343 in the treatment of AD. Western blot results in both HEK293-APPsw cells and CHO-APP cells demonstrate that LX2343 fails to regulate BACE1 protein levels, while in vitro BACE1 enzymatic activity assays indicated that LX2343 dose-dependently decreases BACE1 activity (TDC as a positive control) with an IC50 of 11.43±0.36 μM. To test whether competition exists between LX2343 and ATP, we investigated the effects of ATP at different concentrations on the inhibitory activity of LX2343. The result demonstrated that the inhibition of LX2343 against PI3K is virtually unaffected by ATP. Thus, this result suggested that LX2343 is a non-ATP competitive inhibitor of PI3K. In the presence of 10 μM of ATP, the IC50 of LX2343 is 13.11±1.47 μM, in the presence of 50 μM ATP, the IC50 of LX2343 is 13.86±1.12 μM, in the presence of 100 μM ATP, the IC50 of LX2343 is 15.99±3.23 μM [1].
In Vivo: APP/PS1 mice express chimeric human Swedish mutant APP and a mutant human presenilin 1 protein and are widely used as an effective animal model for AD dementia. The amelioration of memory impairment by LX2343 is evaluated t in this model using the MWM test. In 8-d training trials, the path lengths and escape latencies used to find the platform for APP/PS1 transgenic mice are remarkably longer than those for non-transgenic mice, while 10 mg/kg LX2343 administration obviously antagonizes the prolonged path lengths and escape latencies at d 7 and 8. In the probe trial assay, the LX2343-administered transgenic mice cross over the hidden location of the platform more frequently compared with the vehicle-administered transgenic mice[1].

Name: E-7386, CAS: 1799824-08-0, stock 37g, assay 98.3%, MWt: 725.85, Formula: C39H48FN9O4, Solubility: DMSO : 125 mg/mL (172.21 mM; Need ultrasonic); Methanol : 250 mg/mL (344.42 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: E-7386 is an orally active CBP/beta-catenin modulator.
IC50 & Target: CBP/beta-catenin[1]
In Vivo: E-7386 is an orally active CBP/beta-catenin modulator which can induce T cells infiltration into tumor and enhance antitumor activity of anti-PD-1 mAb in Wnt1 tumor syngeneic mice model. E-7386 shows significant antitumor activity in Wnt1 model. Infiltration of T cells is limited in vehicle control group, but T cell infiltration into tumors is clearly observed in E-7386 treatment group[1].

Name: IDF-11774, CAS: 1429054-28-3, stock 22.9g, assay 98.3%, MWt: 368.51, Formula: C23H32N2O2, Solubility: DMSO : 60 mg/mL (162.82 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIF/HIF Prolyl-Hydroxylase, Biological_Activity: IDF-11774 is a novel hypoxia-inducible factor α (HIFα)-1 inhibitor with an IC50 of 3.65 μM.
IC50 & Target: IC50: 3.65 μM (HIF-1α)[1]
In Vitro: IDF-11774 is a novel hypoxia-inducible factor (HIF)-1 inhibitor with an IC50 of 3.65 μM in cancer cell line. IDF-11774 has been approved as a clinical candidate for a phase I study. Human umbilical vascular endothelial cells (HUVECs) treated with IDF-11774 show reduced capillary network formation on Matrigel. IDF-11774 treatment leads to reduced mRNA expression of GLUT1 and pyruvate dehydrogenase kinase 1 (PDK1). In addition, intracellular ATP levels are significantly reduced in the presence of IDF-11774 and are affected to a greater degree under low glucose conditions (5.5 mM)[1].
In Vivo: Luciferase activity and HIF-1α accumulation are strongly suppressed in the tumors of mice treated by oral administration of IDF-11774, compare with the control. When IDF-11774 is orally administered daily for two weeks, significant dose-dependent tumor regression is observed in the mouse model[1].

Name: SEL120-34A, CAS: 1609522-33-9, stock 19.6g, assay 98%, MWt: 414.14, Formula: C15H18Br2N4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: SEL120-34A is a potent, selective, orally available, ATP-competitive CDK8 inhibitor, with IC50s of 4.4 nM and 10.4 nM for CDK8/CycC and CDK19/CycC, respectively, with antitumor activity.
IC50 & Target: IC50: 4.4 nM (CDK8/CycC), 10.4 nM (CDK19/CycC)[1]
In Vitro: SEL120-34A is a selective, ATP-competitive CDK8 inhibitor, with IC50 of 4.4 nM and 10.4 nM for CDK8/CycC and CDK19/CycC, respectively. SEL120-34A shows no obvious inhibition on CDK1, 2, 4, 6, 5, 7, and only weakly suppresses CDK9 (IC50, 1070 nM). SEL120-34A is active against a panel of AML cell lines (GI50<1 μM), such as SKNO-1, KG-1, HEL-60, MOLM-16, MV-4-11, OciAML-2, MOLM-6 and OciAML-3 cells, consistent with the effective inhibition range of STAT1 S727 and STAT5 S726[1].
In Vivo: SEL120-34A (30, 60 mg/kg, p.o.) inhibits the growth of tumor in mice bearing MV4-11 cancer cells, and also arrests the growth of KG-1-derived tumors at 30 mg/kg via oral administration[1].

Name: Siremadlin R Enantiomer NVP-HDM201 R Enantiomer;HDM201 R Enantiomer, CAS: 1448867-42-2, stock 1.9g, assay 98.3%, MWt: 555.41, Formula: C26H24Cl2N6O4, Solubility: DMSO : ≥ 56.75 mg/mL (102.18 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Siremadlin R Enantiomer (NVP-HDM201 R Enantiomer) is the R enantiomer of Siremadlin. Siremadlin is a potent and highly specific MDM-2/p53 inhibitor.

Name: Resazurin (sodium) Diazoresorcinol (sodium), CAS: 62758-13-8, stock 20.2g, assay 98.1%, MWt: 251.17, Formula: C12H6NNaO4, Solubility: DMSO : 150 mg/mL (597.21 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Resazurin sodium (Diazoresorcinol sodium) is commonly used to measure bacterial and eukaryotic cell viability through its reduction to the fluorescent product resorufin.
In Vitro: Resazurin sodium (Diazoresorcinol sodium) is commonly used to measure bacterial and eukaryotic cell viability through its reduction to the fluorescent product resorufin. No viable bacteria are detected 24 h post-inoculation following inclusion of Resazurin sodium in TSBc cultures of F. tularensis LVS at the concentration of 44 μM. Lowering the Resazurin sodium concentration to as little as 4.4 μM still results in a 10-fold reduction in viable F. tularensis LVS compare to growth medium alone. Both Resazurin sodium treatments result in a significant decrease in viable F. tularensis LVS bacteria over 22 h. Treatment with Resazurin sodium significantly reduces the number of viable F. tularensis LVS bacteria in HEK293 cells 22 h post-infection[1].

Name: ALB-127158(a), CAS: 1173154-32-9, stock 10.4g, assay 98.4%, MWt: 404.44, Formula: C23H21FN4O2, Solubility: Ethanol : 2 mg/mL (4.95 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: ALB-127158(a) is a potent and selective melanin concentrating hormone 1 (MCH1) receptor antagonist.
IC50 & Target: MCH1 receptor[1]
In Vitro: ALB-127158(a) has high affinity for the MCH1 receptor (7 nM) with good selectivity over a range of other G-protein coupled receptors (GPCRs), ion channels and transporters, including the MCH2 receptor. In vitro functional assays confirmed that ALB-127158(a) is a potent and selective MCH1 receptor antagonist[1].
In Vivo: In a mouse diet induced obesity (DIO) model, ALB-127158(a) produces a significant sustained decrease in body weight and food intake in the range of 5-15 mg/kg bid. The weight reduction is predominantly due to a decrease in fat content. In high fat diet (HFD) rats, ALB-127158(a) produces significant weight loss and food reduction at doses as low as 1.25 mg/kg po. Doses > 1.25 mg/kg po produces weight loss > 6%, maximal weight loss of about 10% in rats is observed at 10 mg/kg. Following single and multiple oral administration of ALB-127158(a), ALB-127158(a) is rapidly absorbed (median tmax attains between 1 and 3 h post dose in lean and overweight/obese subjects) with a trend to decrease over dose suggesting a slower absorption rate of ALB-127158(a) at lower doses. After single doses, ALB-127158(a) has a mean half-life (t1/2) of 18 to 21 h. Slightly longer mean t1/2 estimates of approximately 26 h are obtained following multiple dosing in overweight/obese subjects; steady-state plasma ALB-127158(a) is attained within 6 to 8 days of dosing[1].

Name: Corn oil, CAS: 8001-30-7, stock 7.9g, assay 98.1%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Corn oil, extracted from the germ of corn, can be used as a carrier for drug molecules.
In Vivo: Corn oil-gavaged rats have ~25% lower MNCL incidence as well as longer MNCL latency and increase survival. Corn oil-gavaged rats have 54% lower serum growth hormone (GH) levels, and replacement of GH into corn oil-gavaged rats by osmotic minipump infusion increase in situ MNCL cell proliferation to rates observed in water-gavaged animals. Corn oil-gavaged rats, which receive 5 mL corn oil /kg body wt/day for 5 days/week, have a 3-fold increase in fat intake compared to nongavaged or water-gavaged control rats[1]. Intraperitoneal injection of trace amounts of corn oil prior to and following the injection of 40u201350 mg of tissue from hepatoma 7777 or 7800 into the thigh of adult male Buffalo rats result in a marked decrease in the growth rate of both tumors[2].

Name: Cremophor EL, CAS: 61791-12-6, stock 13.4g, assay 98.5%, MWt: 1000, Formula: N/A, Solubility: H2O : 25 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cremophor EL is a polyethoxylated surfactant.
In Vitro: Cremophor EL is a widely used excipient. In the first 10 h, Cremophor EL at 5 mg/mL increases the impedance, then decreases it, and after 20 h of treatment, epithelial cell death is detected. Cremophor EL decreases cell viability and increases cell toxicity more than RH40. Both epithelial viability and monolayer integrity are seriously impaired at 10 to 50 mg/mL concentrations of Cremophor EL at 24-h treatment. Cremophor EL also enhances cell detachment[1].

Name: Tween 80, CAS: 9005-65-6, stock 37.2g, assay 98.4%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tween 80 is a surfactant which can also reduce bacterial attachment and inhibit biofilm formation.
In Vitro: Tween 80 is a surfactant which can also reduce bacterial attachment and inhibit biofilm formation[1]. Solubility enhancement as high as 100-fold is achieved using 1% Tween 80 in vitro[2].

Name: Gelucire 14/44, CAS: 121548-04-7, stock 1.4g, assay 98.8%, MWt: 1000, Formula: N/A, Solubility: Ethanol : 50 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gelucire 44/14 is a potential and safe absorption enhancer for improving the absorption of poorly absorbable drugs including insulin and calcitonin by pulmonary delivery.
In Vivo: Gelucire 44/14 is a potential and safe absorption enhancer for improving the absorption of poorly absorbable drugs including insulin and calcitonin by pulmonary delivery. It is found that pulmonary absorptions of FD4, FD10 and FD70 are enhanced in different degree by Gelucire 44/14 in a concentration-dependent manner, and the maximal absorption-enhancing effect is obtained when the concentration of Gelucire 44/14 reaches to 2.0% (w/v). It is also found that the absorption enhancing ability of Gelucire 44/14 is correlated with the molecular weight of model drugs, and the highest absorption enhancement ratio of Gelucire 44/14 is observed when the molecular weight of model drugs reaches to nearly 10000 Da[1].

Name: Solutol HS-15, CAS: 61909-81-7, stock 17g, assay 98.4%, MWt: 1000, Formula: (C2H4O)nC18H36O3, Solubility: H2O : 25 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Solutol HS-15 is a permeability enhancer.
In Vitro: Solutol HS-15 is a permeability enhancer. A general decline in cell metabolic activity is seen for all three tested cell lines as the concentration of Solutol HS-15 solution is increased. Results demonstrate that Solutol HS-15 promotes the apical-to-basolateral translocation of a model protein (insulin) across Calu-3 monolayers when applied at 37°C. Furthermore there is no statistically significant increase in insulin permeability in the presence of Solutol HS-15, relative to the respective control, at 4°C. Solutol HS-15 treated cells show a statistically significant increase in permeability towards lower molecular weight permeants (5 to 22 kDa) and an absence of a statistically significant increase in permeability of proteins with larger molecular weight, namely albumin and IgG (P>0.05 relative to control)[1].

Name: SR-4370, CAS: 1816294-67-3, stock 22.5g, assay 98.4%, MWt: 304.33, Formula: C17H18F2N2O, Solubility: DMSO : ≥ 150 mg/mL (492.89 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: SR-4370 is an inhibitor of HDAC, with IC50s of 0.13 μM, 0.58 μM, 0.006 μM, 2.3 μM, and 3.4 μM for HDAC1, HDAC2, HDAC3, HDAC8, and HDAC6, respectively.
IC50 & Target: IC50: 0.13 μM (HDAC1), 0.58 μM (HDAC2), 0.006 μM (HDAC3), 2.3 μM (HDAC8), 3.4 μM (HDAC6)[1]
In Vitro: SR-4370 is an inhibitor of HDAC, with IC50s of 0.13 μM, 0.58 μM, 0.006 μM, 2.3 μM, and 3.4 μM for HDAC1, HDAC2, HDAC3, HDAC8, and HDAC6, respectively. SR-4370 is cytotoxic to the breast cancer cells (MDA-MB-231), with an IC50 of 12.6 μM[1].

Name: (2S,3R,4S,5R)-2-Amino-3,4,5,6-tetrahydroxyhexanal hydrochloride, CAS: 5505-63-5, stock 34.2g, assay 98.2%, MWt: 215.63, Formula: C6H14ClNO5, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: MK-8353 SCH900353, CAS: 1184173-73-6, stock 23.8g, assay 98.4%, MWt: 691.84, Formula: C37H41N9O3S, Solubility: DMSO : 125 mg/mL (180.68 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway, Target: ERK;ERK, Biological_Activity: MK-8353 (SCH900353) is a potent, selective and orally available ERK1/2 inhibitor, with IC50s of 23.0 nM and 8.8 nM, respectively; MK-8353 has antitumor activity.
IC50 & Target: IC50: 23.0 nM (ERK1), 8.8 nM (ERK2)[1]
In Vitro: MK-8353 is a potent, selective and orally available ERK1/2 inhibitor, with IC50s of 23.0 nM and 8.8 nM, respectively; MK-8353 has antitumor activity. MK-8353 only at 1 μM shows >50% inhibition on 3 kinases (CLK2, FLT4, and Aurora B), and no other kinases tested are inhibited by >35% at 0.1 μM. MK-8353 also shows potent antitumor activity against various cancer cell lines, such Malme-3M cells (Melanoma), Colo-205 cells (Colon), NCI-H292 cells (Lung), A-549 cells (NSCLC), 8505C cells (Thyroid), SW-626 cells (Ovarian), with EC50s of 21 nM, 19 nM, 130 nM, 230 nM, 210 nM, 108 nM[1].
In Vivo: MK-8353 (60 mg/kg, p.o., bid (twice daily)) causes at least 50% tumor growth inhibition or regression in 83% of the animal models bearing different tumor cells, including LOX, Colo-205, MIA PaCa-2, and Calu-6 cells[1].

Name: EOAI3402143, CAS: 1699750-95-2, stock 15.1g, assay 98.6%, MWt: 503.42, Formula: C25H28Cl2N4O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (99.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: EOAI3402143 is a deubiquitinase (DUB) inhibitor, which inhibits dose-dependently inhibits Usp9x/Usp24 and Usp5.
IC50 & Target: Usp5[1] 
Usp9x[1][2][3] 
Usp24[2] 
In Vitro: EOAI3402143 retains potent Usp9x and Usp5 inhibitory activity[1]. EOAI3402143 dose-dependently inhibits Usp9x and Usp24 activity, increases tumor cell apoptosis[2]. Treatment of UM-2, UM-6, UM-16, and UM-76 with Usp9x inhibitor EOAI3402143 (G9) dose-dependently suppresses cell survival, while 600 nM of EOAI3402143 completely suppresses UM-2 3D colony growth when compared to untreated vehicle controls[3].
In Vivo: To examine this potential, the effect of EOAI3402143 (G9) treatment is investigated on human MIAPACA2 tumor xenografts. Human MIAPACA2 cells are injected subcutaneously into NSG mice. Primary tumor development is monitored by caliper measurements, and once measurable, mice are separated into two groups and are treated with either vehicle control (PEG300/DMSO) or G9 at 15 mg/kg. Tumor growth, animal weight, behavior, and mobility are monitored during treatment. In parallel, murine 8041 tumors are also established and subjected to similar G9 treatment and tumor monitoring regimen as the human MIAPACA2 xenografts. Consistent with the in vitro findings, Usp9x inhibition results in the suppression of tumor growth in human tumor xenografts, but any significant effect on the growth of 8041 tumors xenografts is not observed, although the Usp9x activity is inhibited effectively by EOAI3402143 treatment in both human MIAPACA2 and mouse 8041 xenograft tumors[3].

Name: DAAO inhibitor-1, CAS: 2065250-25-9, stock 33.8g, assay 98%, MWt: 152.13, Formula: C7H5FN2O, Solubility: DMSO : 125 mg/mL (821.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DAAO inhibitor-1 is a potent D-amino acid oxidase (DAAO) inhibitor with an IC50 of 0.12 μM.
IC50 & Target: IC50: 0.12 μM (DAAO)[1]

Name: c(phg-isoDGR-(NMe)k), CAS: 1844830-65-4, stock 25g, assay 98.8%, MWt: 603.67, Formula: C27H41N9O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: c(phg-isoDGR-(NMe)k) is a selective and potent α5β1-integrin ligand with an IC50 of 2.9 nM[1].
IC50 & Target: IC50: 2.9 nM (α5β1)[1]
In Vivo: c(phg-isoDGR-(NMe)k) is trimerized with the chelator TRAP and used as a positron-emission tomography tracer for monitoring α5β1 integrin expression in a M21 mouse xenograft[1].

Name: EBI-2511, CAS: 2098546-05-3, stock 5g, assay 98.5%, MWt: 576.77, Formula: C34H48N4O4, Solubility: DMSO : 5 mg/mL (8.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: EBI-2511 is a highly potent and orally active EZH2 inhibitor, with an IC50 of 6 nM in Pfeffiera cell lines, respectively.
IC50 & Target: IC50: 6 nM (EZH2)[1].
In Vitro: EBI-2511 (Compound 34) significantly reduces cellular H3K27me3 levels in a dose-dependent manner with an approximate IC50 of 8 nM, which is 3-fold more potent than EPZ-6438. In addition to Pfeffier cell line, EBI-2511 was shown active with IC50 value of 55 nM against WSU-DLCL2[1].
In Vivo: EBI-2511 displays a dose-dependent inhibition on the tumor growth, resulting in 28% (10mg/kg), 83% (30mg/kg), and 97% (100mg/kg) reduction in tumor size. At the same dosage level, EBI-2511 shows a superior anti-tumor efficacy to EPZ-6438 (P<0.01). It is noteworthy that no significant changes in body weights of all treatment groups are observed[1].

Name: PLX51107, CAS: 1627929-55-8, stock 17.5g, assay 98.4%, MWt: 438.48, Formula: C26H22N4O3, Solubility: DMSO : 75 mg/mL (171.05 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: PLX51107 is a potent and selective BET inhibitor, with Kds of 1.6, 2.1, 1.7, and 5 nM for BD1 and 5.9, 6.2, 6.1, and 120 nM for BD2 of BRD2, BRD3, BRD4, and BRDT, respectively; PLX51107 also interacts with the bromodomains of CBP and EP300 (Kd, in the 100 nM range).
IC50 & Target: Kd: 1.6 nM (BRD2-BD1), 2.1 nM (BRD3-BD1), 1.7 nM (BRD4-BD1), 5 nM (BRDT-BD1), 5.9 nM (BRD2-BD2), 6.2 nM (BRD3-BD2), 6.1 nM (BRD4-BD2), 120 nM (BRDT-BD2), ∼100 nM (CBP), ∼100 nM (EP300)[1]
In Vitro: PLX51107 is a potent and selective BET inhibitor, with Kds of 1.6, 2.1, 1.7, and 5 nM for BD1 and 5.9, 6.2, 6.1, and 120 nM for BD2 of BRD2, BRD3, BRD4, and BRDT, respectively. PLX51107 also interacts with the bromodomains of CBP and EP300 (Kd, in the 100 nM range). PLX51107 (0.156-10 μM) suppresses the CpG-induced proliferation of primary chronic lymphocytic leukemia (CLL) cells. PLX51107 also causes accumulation of p21 and IκBα, reduces c-MYC level, and modulates proapoptotic and antiapoptotic proteins. PLX51107 selectively modulates CLL driver genes[1].
In Vivo: PLX51107 (2 mg/kg, p.o.) inhibits splenomegaly by 75% in the Ba/F3 (murine IL3-dependent pro-B-cell line) splenomegaly mouse model, with the similar effect of 25 mg/kg OTX015. PLX51107 (20 mg/kg, qd, p.o.) exhibits potent antileukemic effects in disease models of aggressive chronic lymphocytic leukemia (CLL) and Richter transformation (RT) via oral administration once daily[1].

Name: SSE15206, CAS: 1370046-40-4, stock 38.9g, assay 98.5%, MWt: 371.45, Formula: C19H21N3O3S, Solubility: DMSO : 150 mg/mL (403.82 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: SSE15206 is a microtubule polymerization inhibitor (GI50 = 197 nM in HCT116 cells) that overcomes multidrug resistance. Causes aberrant mitosis resulting in G2/M arrest due to incomplete spindle formation in cancer cells[1].
IC50 & Target: GI50: 197 nM (microtubule)[1].
In Vitro: SSE15206 induces apoptosis in cells irrespective of MDR-1 overexpression cell lines (KB-V1, A2780-Pac-Res), highly resistant to paclitaxel cells (HCT116-Pac-Res) and parental cells at the concentration of 5 × and 10 × GI50 values. To conclude, SSE15206 is able to overcome resistance to chemotherapeutic drugs such as paclitaxel in different cancer cell lines[1].

Name: Glycocyamine Guanidinoacetic acid, CAS: 352-97-6, stock 2.7g, assay 98%, MWt: 117.11, Formula: C3H7N3O2, Solubility: H2O : < 0.1 mg/mL (insoluble); 1M HCl : 50 mg/mL (426.95 mM; ultrasonic and adjust pH to 1 with HCl), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Glycocyamine (Guanidinoacetic acid), a precursor of creatine, is a replacement of dietary arginine and could support overall energy homeostasis of the bird.

Name: SEL120-34A HCl, CAS: 1609452-30-3, stock 36.6g, assay 98.4%, MWt: 1000, Formula: C15H18Br2N4.xHCl, Solubility: DMSO : 62.5 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: SEL120-34A HCl is a potent, selective, orally available, ATP-competitive CDK8 inhibitor, with IC50s of 4.4 nM and 10.4 nM for CDK8/CycC and CDK19/CycC, respectively, with antitumor activity.
IC50 & Target: IC50: 4.4 nM (CDK8/CycC), 10.4 nM (CDK19/CycC)[1]
In Vitro: SEL120-34A HCl is a selective, ATP-competitive CDK8 inhibitor, with IC50 of 4.4 nM and 10.4 nM for CDK8/CycC and CDK19/CycC, respectively. SEL120-34A HCl shows no obvious inhibition on CDK1, 2, 4, 6, 5, 7, and only weakly suppresses CDK9 (IC50, 1070 nM). SEL120-34A HCl is active against a panel of AML cell lines (GI50<1 μM), such as SKNO-1, KG-1, HEL-60, MOLM-16, MV-4-11, OciAML-2, MOLM-6 and OciAML-3 cells, consistent with the effective inhibition range of STAT1 S727 and STAT5 S726[1].
In Vivo: SEL120-34A (30, 60 mg/kg, p.o.) inhibits the growth of tumor in mice bearing MV4-11 cancer cells, and also arrests the growth of KG-1-derived tumors at 30 mg/kg via oral administration[1].

Name: Sultopride LIN-1418, CAS: 53583-79-2, stock 22.4g, assay 98.8%, MWt: 354.46, Formula: C17H26N2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Sultopride (LIN-1418) is a selective antagonist of dopamine D2 receptor.
IC50 & Target: Dopamine D2 receptor[1]
In Vivo: Sultopride (LIN-1418) is a selective antagonist of dopamine D2 receptor. DOPAC and HVA levels in the striatum, the nucleus accumbens and the medial prefrontal cortex are higher in the rats treated with Sultopride and sulpiride than those of the controls. In the striatum, DOPAC and HVA levels are higher in the Sultopride-treated rats than the sulpiride-treated rats (p<0.05). In the nucleus accumbens, DOPAC levels are higher in the Sultopride-treated rats than sulpiride treated rats (p<0.05). In the Sultopride-treated rats, DOPAC and HVA levels are higher in the striatum or in the nucleus accumbens than in the medial prefrontal cortex (p<0.05)[1].

Name: Sultopride hydrochloride LIN-1418 hydrochloride, CAS: 23694-17-9, stock 28.5g, assay 98.1%, MWt: 390.93, Formula: C17H27ClN2O4S, Solubility: DMSO : 50 mg/mL (127.90 mM; Need ultrasonic); H2O : 50 mg/mL (127.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Sultopride hydrochloride (LIN-1418 hydrochloride) is a selective antagonist of dopamine D2 receptor.
IC50 & Target: Dopamine D2 receptor[1]
In Vivo: Sultopride hydrochloride (LIN-1418 hydrochloride) is a selective antagonist of dopamine D2 receptor. DOPAC and HVA levels in the striatum, the nucleus accumbens and the medial prefrontal cortex are higher in the rats treated with Sultopride hydrochloride and sulpiride than those of the controls. In the striatum, DOPAC and HVA levels are higher in the Sultopride hydrochloride-treated rats than the sulpiride-treated rats (p<0.05). In the nucleus accumbens, DOPAC levels are higher in the Sultopride hydrochloride-treated rats than sulpiride treated rats (p<0.05). In the Sultopride hydrochloride-treated rats, DOPAC and HVA levels are higher in the striatum or in the nucleus accumbens than in the medial prefrontal cortex (p<0.05)[1].

Name: YAP/TAZ inhibitor-1, CAS: 2093565-23-0, stock 30.6g, assay 98.1%, MWt: 621.81, Formula: C33H39N3O5S2, Solubility: DMSO : 62.5 mg/mL (100.51 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: YAP, Biological_Activity: YAP/TAZ inhibitor-1 is a YAP/TAZ inhibitor extracted from patent WO2017058716A1, Compound 1, has an IC50 of <0.100 μΜ in firefly luciferase assay[1].
IC50 & Target: YAP/TAZ
In Vitro: YAP and TAZ are transcriptional co-activators of the Hippo pathway network and regulate cell proliferation, migration, and apoptosis. YAP/TAZ inhibitor-1 is an inhibitor of transcriptional coactivator with PDZ binding motif/Yes- associated protein transcriptional coactivator (TAZ/YAP).

Name: 1-Ethynylnaphthalene, CAS: 15727-65-8, stock 19.8g, assay 99%, MWt: 152.19, Formula: C12H8, Solubility: DMSO : ≥ 125 mg/mL (821.34 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: 1-Ethynylnaphthalene is a selective inhibitor of cytochrome P450 1B1.
IC50 & Target: P450 1B1[1]
In Vitro: 1-Ethynylnaphthalene, selective inhibitor of cytochrome P450 IB1, does not affect 2-hydroxylation but inhibits 4-hydroxylation by 38%. At higher concentrations, 1-Ethynylnaphthalene inhibits 2-hydroxylation of 2-Hydroxylation of estradiol (E2) by ~30% and 4-hydroxylation of E2 by up to 80%[1].

Name: Vactosertib (Hydrochloride) EW-7197 (Hydrochloride);TEW-7197 (Hydrochloride), CAS: 1352610-25-3, stock 31.8g, assay 98.3%, MWt: 435.88, Formula: C22H19ClFN7, Solubility: H2O : 50 mg/mL (114.71 mM; Need ultrasonic); DMSO : 50 mg/mL (114.71 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: Vactosertib Hydrochloride (EW-7197 Hydrochloride) is a potent, orally active and ATP-competitive activin receptor-like kinase 5 (ALK5) inhibitor with an IC50 of 12.9 nM. Vactosertib Hydrochloride also inhibits ALK2 and ALK4 (IC50 of 17.3 nM) at nanomolar concentrations. Vactosertib Hydrochloride has potently antimetastatic activity and anticancer effect[1][2].
IC50 & Target: IC50: 12.9 nM (ALK5)[1]
In Vitro: Vactosertib (10-1000 nM; 30 minutes; 4T1 cells) treatment blocks the TGFβ-induced phosphorylation of Smad2 or Smad3 in a dose-dependent manner in 4T1 cells[1]. 
Vactosertib suppresses the TGFβ-induced nuclear translocation of Smad2/3 in 4T1 cells and MCF10A cells. The IC50 value of Vactosertib on pSmad3 in 4T1 cells is 10-30 nM[1]. 
Vactosertib abrogates TGFb1-induced tumor cell migration and invasion[1]. 
TGFβ1 downregulated the mRNA level of CDH1 and upregulated the mRNA levels of FN1, HMGA2 (high-mobility group AT-hook 2), SNAI1, and SNAI2 (Snail family zinc finger 1 and 2, respectively). Moreover, Vactosertib abolishes the TGFβ1-induced effects on genes related to epithelial-to-mesenchymal transition (EMT)[1].
In Vivo: Vactosertib (40 mg/kg; intraperitoneal injection; every other day; for 10 weeks; MMTV/c-Neu female mice) treatment inhibits Smad/TGFβ signaling, cell migration, invasion, and lung metastasis in MMTV/c-Neu mice[1]. 
Vactosertib also inhibits the epithelial-to-mesenchymal transition (EMT) in both TGFβ-treated breast cancer cells and 4T1 orthotopic-grafted mice. Furthermore, Vactosertib enhances cytotoxic T lymphocyte activity in 4T1 orthotopic-grafted mice and increased the survival time of 4T1-Luc and 4T1 breast tumor-bearing mice[1].

Name: p-Methylphenyl potassium sulfate, CAS: 91978-69-7, stock 6g, assay 98.1%, MWt: 226.29, Formula: C7H7KO4S, Solubility: DMSO : ≥ 300 mg/mL (1325.73 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: p-Methylphenyl potassium sulfate is a prototype protein-bound uremic toxin.

Name: BRD4 degrader AT1, CAS: 2098836-45-2, stock 0.2g, assay 98.5%, MWt: 972.68, Formula: C48H58ClN9O5S3, Solubility: DMSO : 100 mg/mL (102.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: BRD4 degrader AT1 is a highly selective Brd4 degrader based on PROTAC technology, with a Kd of 44 nM for Brd4BD2 in cells.
IC50 & Target: Kd: 44 nM (Brd4BD2, cell assay), 38.8 nM (Brd4BD2 QVK, cell assay), 111 nM (Brd2BD1, cell assay), 94 nM (Brd2BD2, cell assay), 35 nM (Brd3BD1, cell assay), 39 nM (Brd3BD2, cell assay), 75 nM (Brd4BD1, cell assay), 35 nM (Brd2BD1 KEA, cell assay)[1]
In Vitro: BRD4 degrader AT1 is a highly selective Brd4 degrader, with a Kd of 44 nM, for Brd4BD2 in cells. BRD4 degrader AT1 also shows Kds of 38.8 nM for a mutant Brd4BD2 (QVK), 111 ± 14 nM for Brd2BD1, 94 ± 9 nM for Brd2BD2, 35 ± 3 nM for Brd3BD1, 39 ± 8 nM for Brd3BD2, 75 ± 23 nM for Brd4BD1 and 35 ± 4 nM for a Brd2BD1 mutant (KEA). BRD4 degrader AT1 (1-3 μM) causes remarkable Brd4-selective depletion and has no or little activity against Brd2 and Brd3[1].

Name: Itacitinib adipate, CAS: 1334302-63-4, stock 22.6g, assay 98.2%, MWt: 699.66, Formula: C32H33F4N9O5, Solubility: DMSO : ≥ 137.5 mg/mL (196.52 mM), Clinical_Informat: Phase 3, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: Itacitinib adipate is an orally bioavailable and selective JAK1 inhibitor which has been tested for efficacy and safety in a phase II trial in myelofibrosis.
IC50 & Target: JAK1[1]

Name: NT 13 TPPT, CAS: 117928-93-5, stock 14.2g, assay 98.3%, MWt: 414.45, Formula: C18H30N4O7, Solubility: DMSO : ≥ 122.5 mg/mL (295.57 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: NT 13 (TPPT) is a tetrapeptide having the amino acid sequence L-threonyl-L-prolyl-L-prolyl-L-threonine amide. NT 13 is a partial N-methyl-D-aspartate receptor (NMDAR) agonist used in the study of depression, anxiety, and other related diseases.
IC50 & Target: Target: NMDAR[1]
In Vitro: NT 13 derivatives are used in the study of depression, anxiety, and other related diseases. Some NT 13 derivatives are NMDAR partial agonist[1].

Name: Rapastinel (Trifluoroacetate) GLYX-13 (Trifluoroacetate), CAS: 1435786-04-1, stock 18.3g, assay 98.6%, MWt: 527.49, Formula: C20H32F3N5O8, Solubility: DMSO : 125 mg/mL (236.97 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Rapastinel Trifluoroacetate (GLYX-13 Trifluoroacetate) is an NMDA receptor modulator with glycine-site partial agonist properties and currently in a phase II clinical development program as an adjunctive therapy for major depressive disorder.
IC50 & Target: NMDA receptor[1]
In Vivo: Rapastinel Trifluoroacetate is an NMDA receptor modulator with glycine-site partial agonist properties and currently in a phase II clinical development program as an adjunctive therapy for major depressive disorder. Mice given Rapastinel Trifluoroacetate (1.0 mg/kg) prior to acute ketamine (30 mg/kg) show clear preference for novel compare to familiar objects (P<0.01)[1]. Rapastinel Trifluoroacetate produces an antidepressant like effect in the USVs test, as indexed by an increase in hedonic 50-kHz USVs [F(1,20)=12.4, P<0.05] and a decrease in aversive 20-kHz USVs [F(1,20)=6.8, P<0.05]. Rapastinel Trifluoroacetate also produces an anxiolytic effect in the open field, as indexed by increased center time [F(1,20)=19.2, P<0.05] without altering locomotor activity as measured by line crosses [F(1,20)=0.0, P>0.05][2].

Name: 1,4-Chrysenequinone Chrysene-1,4-dione, CAS: 100900-16-1, stock 20.8g, assay 98.3%, MWt: 258.27, Formula: C18H10O2, Solubility: DMSO : 3.33 mg/mL (12.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Aryl Hydrocarbon Receptor, Biological_Activity: 1,4-Chrysenequinone, a polycyclic aromatic quinone, acts as an activator of aryl hydrocarbon receptor (AhR).
IC50 & Target: AhR[1]
In Vitro: 1,4-Chrysenequinone shows significant AhR ligand activity, with ECTCDD25s (concentration equivalent with 25% of TCDD max) of 9.7 nM and 1.9 μM in yeast and mouse hepatoma cell systems, respectively[1].

Name: TR antagonist 1, CAS: 500794-88-7, stock 6.5g, assay 98.8%, MWt: 561.26, Formula: C25H23Br2NO4, Solubility: DMSO : ≥ 83.3 mg/mL (148.42 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Thyroid Hormone Receptor, Biological_Activity: TR antagonist 1 is a high-affinity thyroid hormone receptor (TR) antagonist with IC50s of 36 and 22 nM for TRα and TRβ, respectively.
IC50 & Target: IC50: 36 nM (Thyroid hormone α), 22 nM (Thyroid hormone α)[1]
In Vitro: TR antagonist 1 displays high affinity for both thyroid hormone TRα and TRβ (IC50=36 and 22 nM, respectively). TR antagonist 1 acts as a full antagonist in the TRAFR cell assay and the IC50 32 nM for both TRAFα1 and TRAFβ1[1].
In Vivo: TR antagonist 1 treatment lowers heart rate and shows a possible trend toward an increase of low-density lipoprotein cholesterol (LDL-C) in the cholesterol fed rat model[1].

Name: Auxinole, CAS: 86445-22-9, stock 4.7g, assay 98.3%, MWt: 321.37, Formula: C20H19NO3, Solubility: DMSO : ≥ 125 mg/mL (388.96 mM); Ethanol : 12.5 mg/mL (38.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Auxinole is a potent auxin antagonist of TIR1/AFB receptors, binding TIR1 to block the formation of the TIR1-IAA-Aux/IAA complex and so inhibits auxin-responsive gene expression.
IC50 & Target: TIR1/AFB receptor[1]
In Vitro: Auxinole is a potent auxin antagonist of TIR1/AFB receptors, and binds TIR1 to block the formation of the TIR1-IAA-Aux/IAA complex and then inhibits auxin-responsive gene expression. In addition, Auxinole competitively inhibits various auxin responses in planta[1]. Auxinole causes reduction in IAA-triggered depolarization in root hair cells. Auxinole (20 µM) also represses the transient increase in [Ca2+]cyt completely, and blocks Ca2+ response[2].

Name: CeMMEC1, CAS: 440662-09-9, stock 10.1g, assay 98.5%, MWt: 336.34, Formula: C19H16N2O4, Solubility: DMSO : 100 mg/mL (297.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Epigenetic Reader Domain;DNA/RNA Synthesis, Biological_Activity: CeMMEC1 is an inhibitor of BRD4, and also has high affinity for TAF1, with an IC50 of 0.9 μM for TAF1, and a Kd of 1.8 μM for TAF1 (2).
IC50 & Target: Kd: 1.8 μM (TAF1 (2))[1] 
IC50: 0.9 μM (TAF1)[1]
In Vitro: CeMMEC1 is an inhibitor of BRD4, and also has high affinity for TAF1, with an IC50 of 0.9 μM for TAF1, and a Kd of 1.8 μM for TAF1 (2) and slso shows high affinity for the bromodomains of CREBBP, EP300, BRD9. CeMMEC1 (1, 10, 20 μM) decreases the number of THP1 cells in S phase in a dose manner. CeMMEC1 also induces apoptosis. CeMMEC1 in combination with (S)-JQ1 displays potently impaired cell viability than treatment alone[1].

Name: AHR antagonist 1, CAS: 2162982-11-6, stock 5.5g, assay 98.7%, MWt: 401.82, Formula: C20H17ClFN3O3, Solubility: DMSO : ≥ 250 mg/mL (622.17 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Aryl Hydrocarbon Receptor, Biological_Activity: AHR antagonist 1 is an aryl hydrocarbon receptor (AHR) antagonist extracted from patent WO2017202816A1, example 23, has an IC50 of 39.9 nM in human cell line[1].
IC50 & Target: IC50: 39.9 nM (AHR in human cell line)[1]

Name: AZD7594 AZ13189620, CAS: 1196509-60-0, stock 40g, assay 98.5%, MWt: 606.62, Formula: C32H32F2N4O6, Solubility: DMSO : ≥ 83.3 mg/mL (137.32 mM), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: AZD7594 is a potent selective nonsteroidal glucocorticoid receptor modulator, with an IC50 of 0.9 nM.
IC50 & Target: IC50: 0.9 nM (Glucocorticoid receptor)[1]
In Vitro: AZD7594 is a potent selective nonsteroidal glucocorticoid receptor modulator, with an IC50 of 0.9 nM. AZD7594 shows no effect on progesterone receptor, mineralocorticoid receptor, Androgen receptor, ERα or ERβ (IC50, > 10 μM).
In Vivo: AZD7594 has anti-inflammatory activity, and efficiently inhibits rat lung edema[1].

Name: SR17018, CAS: 2134602-45-0, stock 13.5g, assay 98.6%, MWt: 410.72, Formula: C19H18Cl3N3O, Solubility: DMSO : 6.4 mg/mL (15.58 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: SR17018 is an mu-opioid-receptor (MOR) agonist, binding with GTPγS, with an EC50 of 97 nM.
IC50 & Target: EC50: 97 nM (MOR)[1]
In Vitro: SR17018 is an mu-opioid-receptor (MOR) agonist, binding with GTPγS, with an EC50 of 97 nM. SR17018 shows no obvious effect on inducing βarrestin2 recruitment to the MOR at below 10 μM. SR17018 promotes signaling through G proteins or βarrestin2[1].

Name: l-Atabrine dihydrochloride, CAS: 56100-42-6, stock 35.5g, assay 98.4%, MWt: 472.88, Formula: C23H32Cl3N3O, Solubility: DMSO : 20 mg/mL (42.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: l-Atabrine dihydrochloride is a less active enantiomer of quinacrine which displays antiprion activity.

Name: d-Atabrine dihydrochloride, CAS: 56100-41-5, stock 19.3g, assay 98.9%, MWt: 472.88, Formula: C23H32Cl3N3O, Solubility: DMSO : 16.67 mg/mL (35.25 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: d-Atabrine dihydrochloride is an active enantiomer of quinacrine which displays antiprion activity.

Name: LP-211, CAS: 1052147-86-0, stock 14.1g, assay 98.4%, MWt: 466.62, Formula: C30H34N4O, Solubility: DMSO : ≥ 106.6 mg/mL (228.45 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: LP-211 is a selective and blood−brain barrier penetrant 5-HT7 receptor agonist, with a Ki of 0.58 nM, with high selectivity over 5-HT1A receptor (Ki, 188 nM) and D2 receptor (Ki, 142 nM).
IC50 & Target: Ki: 0.58 nM (5-HT7 receptor), 188 nM (5-HT1A receptor), 142 nM (D2 receptor)[1]
In Vitro: LP-211 is a selective 5-HT7 receptor agonist, with a Ki of 0.58 nM, 324- and 245-fold selectivity over 5-HT1A receptor (Ki, 188 nM) and D2 receptor (Ki, 142 nM). LP-211 shows agonist properties with an EC50 of 0.6 μM[1].
In Vivo: LP-211 (10 mg/kg, i.p.) rapidly reaches the systemic circulation in the mouse, with mean Cmax of 0.76 ± 0.32 μg/mL at 30 min[1]. LP-211 (0.003-0.3 mg/kg, i.p.) significantly increases the micturition volume in a dose-dependent manner, and causes significant increases in voiding efficiency in spinal cord-injured (SCI) rats, and such effects can be completely reversed by SB-269970[2]. LP-211 (0.25 and 0.50 mg/kg i.p.) improves consolidation of chamber-shape memory in rats, resulting in significant novelty-induced hyperactivity and recognition[3].

Name: CCG-63808, CAS: 620113-73-7, stock 6.1g, assay 98.4%, MWt: 454.48, Formula: C25H15FN4O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 1 mg/mL (2.20 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: RGS Protein, Biological_Activity: CCG-63808 is a reversible inhibitor of regulator of G-protein signaling (RGS) proteins.

Name: BAY-677, CAS: 2117404-84-7, stock 0.8g, assay 98.9%, MWt: 400.35, Formula: C20H15F3N4O2, Solubility: DMSO : ≥ 50 mg/mL (124.89 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BAY-677 is an inactive control for BAY-678. BAY-678 is an orally bioavailable, highly potent, selective and cell-permeable inhibitor of human neutrophil elastase (HNE), with an IC50 of 20 nM[1]. BAY-678 is also nominated as a chemical probe to the public via the Structural Genomics Consortium (SGC)[2].

Name: BAY-678, CAS: 675103-36-3, stock 14.5g, assay 98.6%, MWt: 400.35, Formula: C20H15F3N4O2, Solubility: DMSO : ≥ 100 mg/mL (249.78 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Elastase, Biological_Activity: BAY-678 is an orally bioavailable, highly potent, selective and cell-permeable inhibitor of human neutrophil elastase (HNE), with an IC50 of 20 nM. BAY-678 is also nominated as a chemical probe to the public via the Structural Genomics Consortium (SGC).
IC50 & Target: IC50: 20 nM (HNE)[1].
In Vitro: BAY-678 is an orally bioavailable, highly potent, selective and cell-permeable inhibitor of human neutrophil elastase (HNE), with an IC50 of 20 nM. The Ki value of BAY-678 for MNE is 700 nM. BAY-678 is the 4th generation inhibitor of HNE[1]. BAY-678 is also nominated as a chemical probe to the public via the Structural Genomics Consortium (SGC)[2]. BAY-678 has more than 2,000-fold selectivity in a panel of 21 serine proteases[3].
In Vivo: BAY-678 (17) reveals significant efficacy in preclinical models of ALI and lung emphysema, demonstrating their anti-inflammatory and anti-remodeling mode of action. Additionally, BAY-678 (17) has shown significant beneficial pulmonary hemodynamic and vascular effects in models of PAH in rats and mice[2].

Name: Porcn-IN-1, CAS: 2036044-77-4, stock 19.5g, assay 98.6%, MWt: 410.44, Formula: C25H19FN4O, Solubility: DMSO : ≥ 100 mg/mL (243.64 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: Porcupine, Biological_Activity: Porcn-IN-1 is potent porcupine inhibitor with an IC50 of 0.5±0.2 nM.
IC50 & Target: IC50: 0.5±0.2 nM (Porcupine inhibitor)[1]
In Vitro: Porcupine is an enzyme that catalyses the addition of palmitoleate to a serine residue in Wnt proteins, a process which is required for the secretion of Wnt proteins. Porcupine-IN-1 is as potent as the clinical compound LGK974 in a cell based STF reporter gene assay. Porcn-IN-1 potently inhibits the secretion of Wnt3A, therefore is confirmed to be a porcupine inhibitor[1].
In Vivo: Porcn-IN-1 demonstrates moderate clearance under the treatment of human liver microsomes (57 mL/min/kg) and rat liver microsomes (24 mL/min/kg). It exhibits high clearance when treated with mouse microsomes (109 mL/min/kg)[1].

Name: 3-(3,4,5-Trimethoxyphenyl)propanoic acid, CAS: 25173-72-2, stock 18.2g, assay 98.1%, MWt: 240.25, Formula: C12H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-(3,4,5-Trimethoxyphenyl)propanoic acid is found in herbs and spices. 3-(3,4,5-Trimethoxyphenyl)propanoic acid is a constituent of Piper longum (long pepper) and Piper retrofractum (Javanese long pepper).

Name: SM 16, CAS: 614749-78-9, stock 9.1g, assay 99%, MWt: 430.50, Formula: C25H26N4O3, Solubility: DMSO : 65 mg/mL (150.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: SM 16 is a ALK5/ALK4 kinase inhibitor with Kis of 10 and 1.5 nM, respectively.
IC50 & Target: Ki: ALK5 (10 nM), ALK4 (1.5 nM)[1]
In Vitro: SM 16 inhibits TGFβ-induced plasminogen activator inhibitor-luciferase activity (IC50=64 nM) and TGFβ- or activin-induced Smad2 phosphorylation at concentrations between 100 and 620 nM. SM 16 is tested against >60 related and unrelated kinases and shows moderate off-target activity only against Raf (IC50=1 μM) and p38/SAPKa (IC50=0.8 μM). SM 16 exhibits no inhibitory activity against ALK family members ALK1 and ALK6[1].
In Vivo: SM 16 penetrates tumor cells in vivo, suppressing tumor phosphorylated Smad2/3 levels for at least 3 h following treatment of tumor-bearing mice with a single i.p. bolus of 20 mg/kg SM 16. The growth of established AB12 tumors is significantly inhibited by 5 mg/kg/d SM 16 (P<0.001) delivered via s.c. miniosmotic pumps over 28 days[1].

Name: AZD-0364, CAS: 2097416-76-5, stock 15.7g, assay 98.9%, MWt: 494.50, Formula: C24H24F2N8O2, Solubility: DMSO : ≥ 100 mg/mL (202.22 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway, Target: ERK;ERK, Biological_Activity: AZD-0364 is a potent and selective ERK2 inhibitor extracted from patent WO2017080979A1, compound example 18, has an IC50 of 0.6 nM.
IC50 & Target: IC50: 0.6 nM (ERK2)[1]
In Vitro: AZD-0364 is measured in the ERK2 mass spectrometry and A375 phospho-p90RSK assays with IC50s of 0.6 nM and 5.7 nM, respectively. AZD-0364 can inhibit the growth of a panel of cancer cell lines (A549, H2122, H2009, and Calu6 cell lines) with KRAS mutations as a monotherapy and this effect is synergistically enhanced by treatment with Selumetinib[1].
In Vivo: Tumor growth inhibition by AZD-0364 ethanesulfonic acid (Example 18a) in combination with MEK inhibitor Selumetinib is measured. Studies are performed in the A549 xenograft model. Selumetinib is dosed twice daily (BiD) 8 hours apart and AZD-0364 ethanesulfonic acid is dosed once daily (QD) 4 hours after the first Selumetinib dose. Both compounds are dosed continuously for 3 weeks. Both vehicles are dosed in the vehicle group. Both Selumetinib and AZD-0364 ethanesulfonic acid reduce tumor growth relative to vehicle only control. The combination of Selumetinib and AZD-0364 ethanesulfonic acid results in a reduction in tumor growth[1].

Name: GDC-0927 SRN-927, CAS: 1642297-01-5, stock 19.3g, assay 99%, MWt: 461.52, Formula: C28H28FNO4, Solubility: DMSO : 83.33 mg/mL (180.56 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: GDC-0927 (SRN-927) is a novel, potent, non-steroidal, orally bioavailable, selective estrogen receptor antagonist.
IC50 & Target: Estrogen receptor[1]
In Vivo: GDC-0927 is a novel, potent, non-steroidal, orally bioavailable, selective ER antagonist/ER degrader (SERD) that induces tumor regression in estrogen receptor (ER)+breast cancer (BC) patient-derived xenograft models[1].

Name: INCB-057643, CAS: 1820889-23-3, stock 17.5g, assay 98.6%, MWt: 415.46, Formula: C20H21N3O5S, Solubility: DMSO : 62.5 mg/mL (150.44 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Apoptosis;Epigenetics, Target: Apoptosis;Epigenetic Reader Domain, Biological_Activity: INCB-057643 is a novel, orally bioavailable BET inhibitor.
IC50 & Target: BET[1]
In Vitro: INCB-057643 is a novel, orally bioavailable BET inhibitor. INCB-057643 inhibits binding of BRD2/BRD3/BRD4 to an acetylated histone H4 peptide in the low nM range, and is selective against other bromodomain containing proteins. In vitro analyses show that INCB-057643 inhibits proliferation of human AML, DLBCL, and multiple myeloma cell lines, with a corresponding decrease in MYC protein levels. Cell cycle analyses indicate that G1 arrest and a concentration-dependent increase in apoptosis are seen within 48 hours of treatment with INCB-057643[1].
In Vivo: Production of several cytokines, including IL-6, IL-10 and MIP-1α, is repressed by INCB-057643 in human and mouse whole blood stimulated ex vivo with LPS. Oral administration of INCB-057643 results in significant anti-tumor efficacy in xenograft models of AML, myeloma, and DLBCL. Additionally, combining INCB-057643 with standard of care agents used for the treatment of DLBCL including rituximab and bendamustine results in enhanced anti-tumor efficacy relative to that achieved with single agent therapies at doses that are well tolerated[1].

Name: LSZ-102, CAS: 2135600-76-7, stock 30.9g, assay 98.7%, MWt: 470.46, Formula: C25H17F3O4S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (212.56 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: LSZ-102 is a potent, orally bioavailable selective estrogen receptor degrader with an IC50 of 0.2 nM.
IC50 & Target: estrogen receptor[1]
In Vitro: LSZ-102 is a potent, orally bioavailable selective estrogen receptor degrader with an IC50 of 0.2 nM and currently in Phase I/Ib trials for the treatment of ERα positive breast cancer. LSZ-102 induces significant degradation of ERα after 24 h, when given as a 10 μM solution to MCF-7 cells. Robust inhibition of cell proliferation in MCF-7 cells is observed upon incubation with LSZ-102 with a half inhibitory concentration of 1.7 nM. Results demonstrate that LSZ-102 effectively inhibits the estrogen-induced activation of the ERE-luciferase reporter using charcoal-stripped serum treated with E2 with IC50 of 0.3 nM[1].
In Vivo: Treatment of the mice with LSZ-102 once daily at 20 mg/kg results in significant tumor growth inhibition as compare to the control group treated with vehicle alone, resulting in tumor stasis (mean change in tumor volume of LSZ-102 vs control=%ΔT/ΔC of 2.4% on day 48, p<0.05). Dosing of 3 mg/kg solution of LSZ-102 in male Sprague-Dawley rats results in 33% bioavailability and a dose-normalized exposure of 620 nM•h[1].

Name: Vildagliptin dihydrate LAF237 dihydrate;NVP-LAF 237 dihydrate, CAS: 2133364-01-7, stock 35.2g, assay 98.6%, MWt: 339.43, Formula: C17H29N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease;Apoptosis, Target: Dipeptidyl Peptidase;Ferroptosis, Biological_Activity: Vildagliptin (LAF237 dihydrate;NVP-LAF 237 dihydrate) is a dipeptidyl peptidase 4 (DPP4) inhibitor that delays the degradation of glucagon-like peptide-1 (GLP-1).
IC50 & Target: Target: Dipeptidyl Peptidase 4 (DPP4)[1]
In Vivo: Treatment of obese diabetic mice with 1 mg/kg/day Vildagliptin or with 10 mg/kg/day valsartan for 8 weeks increases pancreatic islet β-cell density and stimulates islet β-cell proliferation while preventing apoptosis and islet fibrosis and decreasing superoxide production and nitrotyrosine formation. The combination of both compounds significantly magnifies the beneficial effect of either monotherapy[1]. Valsartan or Vildagliptin pretreatment significantly increases plasma GLP-1 expression, reduces apoptosis of endothelial cells isolated from diabetic mice aorta. The expression of NADPH oxidase subunits also significantly decreases resulting in decreased superoxide production and ICAM-1 (fold change: valsartan : 7.5±0.7, P<0.05; LAF237: 10.2±1.7, P<0.05), VCAM-1 (fold change: valsartan : 5.2±1.2, P<0.05; LAF237: 4.8±0.6, P<0.05), and MCP-1 (fold change: valsartan: 3.2±0.6, LAF237: 4.7±0.8; P<0.05) expression. Moreover, the combination treatment with valsartan and Vildagliptin results in a more significant increase of GLP-1 expression. The decrease of the vascular oxidative stress and inflammation reaction is also higher than monotherapy with valsartan or Vildagliptin[2]. Daily oral administration of Vildagliptin (5 mg/kg) alone or in combination with Pioglitazone (20 mg/kg) for 7 weeks significantly reduces blood glucose levels and HbA1c. It increases serum insulin levels and decreases serum glucagon. It also shows a strong anti-oxidant activity[3].

Name: Desisobutyryl-ciclesonide CIC-AP;Ciclesonide active principle, CAS: 161115-59-9, stock 18.7g, assay 98.5%, MWt: 470.60, Formula: C28H38O6, Solubility: DMSO : ≥ 50 mg/mL (106.25 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: Desisobutyryl-ciclesonide is the active metabolite of Ciclesonide. Desisobutyryl-ciclesonide has affinity for the glucocorticoid receptor.
IC50 & Target: Glucocorticoid receptor[1]
In Vitro: Ciclesonide, an inhaled corticosteroid with almost no affinity for the glucocorticoid receptor, is highly effective in downregulating in vitro pro-inflammatory activities of airway parenchymal cells when converted into the active metabolite Desisobutyryl-ciclesonide. Peripheral blood mononuclear cell proliferation to C. albicans is dose-dependently inhibited by 0.3-3.0 μM Ciclesonide and Desisobutyryl-ciclesonide but inhibition by Desisobutyryl-ciclesonide is higher. A significant proliferation to PhlP5 is observed only in cultures from atopic subjects: an effective downregulation is already detected at 0.03 μM Ciclesonide and 0.003 μM Desisobutyryl-ciclesonide (complete inhibition at 3 μM Ciclesonide and 0.03 μM Desisobutyryl-ciclesonide). 3 μM Ciclesonide and Desisobutyryl-ciclesonide reduce the PhlP5-specific T-cell blast proliferation and interleukin 4-producing cell proportion. In PBMCs cultures from atopic patients, both Ciclesonide (CIC) and Desisobutyryl-ciclesonide (des-CIC) induce a dose-dependent downregulation of PhlP5-induced proliferation. The effect is already significantat 0.03 μM Ciclesonide and at 0.003 μM Desisobutyryl-ciclesonide (p<0.001, each comparison),with an early complete inhibition observed at 3μM Ciclesonide and at 0.03 μM Desisobutyryl-ciclesonide. The inhibitory activity toward PhlP5-induced PBMC proliferation is higher for Desisobutyryl-ciclesonide than for Ciclesonide at 0.003 μM (p<0.05), 0.03 μM (p<0.001) and 0.3 μM (p<0.05)[1].

Name: Salsolidine 6,7-Dimethoxy-1-methyl-1,2,3,4-tetrahydroisoquinoline, CAS: 5784-74-7, stock 27.3g, assay 98.5%, MWt: 207.27, Formula: C12H17NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: Salsolidine is a tetrahydroisoquinoline alkaloid, acts as a stereoselective competitive MAO A inhibitor.
IC50 & Target: MAO A[1]
In Vitro: Salsolidine is a tetrahydroisoquinoline alkaloid, acts as a stereoselective competitive MAO A inhibitor. The R-salsolidine is more active against MAO A than S-salsolidine (Ki, 6 μM and 186 μM)[1]. Salsolidine weakly inhibits the binding of δ-receptor, with a Ki of >100 μM[2]. Salsolidine has the potential of inhibiting Acetylcholinestearse and butyrylcholinesterase[3].

Name: DIM-C-pPhOCH3, CAS: 33985-68-1, stock 36.6g, assay 98.1%, MWt: 352.43, Formula: C24H20N2O, Solubility: DMSO : ≥ 33.3 mg/mL (94.49 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DIM-C-pPhOCH3 is a Nur77 agonist. Nerve growth factor-induced Bα (NGFI-Bα, Nur77) is an orphan nuclear receptor.
IC50 & Target: Nur77[1]
In Vitro: DIM-C-pPhOCH3 decreases survival and induces apoptosis in RKO colon cancer cells, and this is accompanied by induction of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) protein. DIM-C-pPhOCH3 also induces Nur77-independent apoptosis. DIM-C-pPhOCH3 (10 μM) inhibits cell growth after treatment for 24, 48, or 72 h, and the maximum inhibitory response is observed after 72 h, where there is considerable cell detachment and dead cells. The growth-inhibitory effects observed for DIM-C-pPhOCH3 after 72 h are also accompanied by several markers of apoptosis, including PARP cleavage and cleavage of caspase-3, caspase-9, and caspase-8. PARP cleavage is also observed after treatment of RKO cells for 48 h with DIM-C-pPhOCH3[1].
In Vivo: DIM-C-pPhOCH3 (25 mg/kg/d) also inhibits tumor growth in athymic nude mice bearing RKO cell xenografts. The effects of DIM-C-pPhOCH3 (25 mg/kg/d) on colon tumor growth are also investigated in athymic nude mice bearing RKO cell xenografts. Treatment with the DIM-C-pPhOCH3 significantly decreases tumor volumes and final tumor weights compared with corn oil controls[1].

Name: LRRK2 inhibitor 1, CAS: 1802525-61-6, stock 18.5g, assay 98.7%, MWt: 397.43, Formula: C20H23N5O4, Solubility: DMSO : 62.5 mg/mL (157.26 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: LRRK2, Biological_Activity: LRRK2 inhibitor 1 is a potent, selective and oral LRRK2 inhibitor with an pIC50 of 6.8 nM.
IC50 & Target: pIC50: 6.8 nM (LRRK2)[1]

Name: RGX-104, CAS: 610318-03-1, stock 17.6g, assay 98.3%, MWt: 632.54, Formula: C34H34Cl2F3NO3, Solubility: DMSO : 150 mg/mL (237.14 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: LXR, Biological_Activity: RGX-104 is a small-molecule LXR agonist that modulates innate immunity via transcriptional activation of the ApoE gene.
IC50 & Target: LXR[1]
In Vivo: Oral administration of GW3965 or RGX-104 to animals bearing palpable tumors significantly suppresses the growth of multiple cancer types. Strong tumor growth suppression is also observed in animals bearing large tumors. In some instances, the treatment causes partial or complete tumor regression. Responses are seen across a wide spectrum of malignancies, including lung cancer, melanoma, glioblastoma, and ovarian, renal cell, triple-negative breast, and colon cancer[1].

Name: Y06036, CAS: 1832671-96-1, stock 4.4g, assay 98.6%, MWt: 427.27, Formula: C16H15BrN2O5S, Solubility: DMSO : 130 mg/mL (304.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: Y06036 is a potent and selective BET inhibitor, which binds to the BRD4(1) bromodomain with Kd value of 82 nM[1]. Antitumor activity[1].
In Vitro: Y06036 (0.001-100 nM, 96 hours for LNCaP, C4-2B, and 22Rv1 cells; 144 hours for VCaP cells) exhibits low micromolar or nanomolar potencies (IC50: 0.29-2.6 μΜ) in the four androgen receptor (AR)-positive prostate cancer cell lines LNCaP, C4-2B, 22Rv1, and VCaP. Treatment of 22Rv1 cells with Y06036 (1, 2, 4, 8, and 16 μM, 48 hours) results in significant down-regulation of both full-length (AR-fl) and AR variants levels[1].
In Vivo: Y06036 (50 mg/kg, i.p. injection, 5 times per week, 25 days) demonstrates therapeutic effects in a C4-2B CRPC xenograft tumor model in mice. Y06036 is well tolerated in the treated mice, based on the weight of the animal body and their general behavior[1].

Name: Y06137, CAS: 2226534-49-0, stock 38.2g, assay 99%, MWt: 444.57, Formula: C27H32N4O2, Solubility: DMSO : 62.5 mg/mL (140.59 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: Y06137 is a potent and selective BET inhibitor for treatment of castration-resistant prostate cancer (CRPC). Y06137 binds to the BRD4(1) bromodomain with a Kd of 81 nM[1].
In Vitro: Y06137 (0.001-100 nM, 96 hours for LNCaP, C4-2B, and 22Rv1 cells; 144 hours for VCaP cells) exhibits low micromolar or nanomolar potencies (IC50: 0.29-2.6 μΜ) in the four androgen receptor (AR)-positive prostate cancer cell lines LNCaP, C4-2B, 22Rv1, and VCaP. Treatment of 22Rv1 cells with Y06137 (1, 2, 4, 8, and 16 μM, 48 hours) results in significant down-regulation of both full-length (AR-fl) and AR variants levels[1].
In Vivo: Y06137 (50 mg/kg, i.p. injection, 5 times per week, 25 days) demonstrates therapeutic effects in a C4-2B CRPC xenograft tumor model in mice. Y06137 is well tolerated in the treated mice, based on the weight of the animal body and their general behavior[1].

Name: NAcM-OPT, CAS: 2089293-61-6, stock 6.4g, assay 98.4%, MWt: 434.40, Formula: C23H29Cl2N3O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (287.75 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: E1/E2/E3 Enzyme;NEDD8-activating Enzyme, Biological_Activity: NAcM-OPT is an orally bioavailable cullin neddylation 1 (DCN1) inhibitor, which potently inhibits the DCN1-UBE2M interaction[1].
IC50 & Target: DCN1[1]
In Vitro: NAcM-OPT (Compound 67) is orally bioavailable, well tolerated in mice, and currently used to study the effects of acute pharmacologic inhibition of the DCN1-UBE2M interaction on the NEDD8/CUL pathway[1].

Name: PDGFRα kinase inhibitor 1, CAS: 2209053-93-8, stock 3.2g, assay 98.3%, MWt: 586.69, Formula: C34H34N8O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: PDGFR, Biological_Activity: PDGFRα kinase inhibitor 1 is a highly selective type II PDGFRα kinase inhibitor with IC50s of 132 nM and 6115 nM for PDGFRα and PDGFRβ, respectively[1].
In Vitro: PDGFRα kinase inhibitor 1 (CHMFL-PDGFR-159, Compound 15i) exhibits weak inhibition to DDR1 kinase (IC50: 2462±126 nM)[1].

Name: PI3K/mTOR Inhibitor-2, CAS: 1848242-58-9, stock 39.5g, assay 98.1%, MWt: 478.86, Formula: C20H13ClF2N4O4S, Solubility: DMSO : 8.33 mg/mL (17.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR, Target: PI3K;mTOR, Biological_Activity: PI3K/mTOR Inhibitor-2 is a potent dual pan-PI3K/mTOR inhibitor with IC50s of 3.4/34/16/1 nM for PI3Kα/PI3Kβ/PI3Kδ/PI3Kγ and 4.7 nM for mTOR[1]. Antitumor activity[1].
In Vitro: PI3K/mTOR Inhibitor-2 (Compound 31) inhibits p-AKT and p-p70s6k in MCF-7 cells with IC50s of 11.6 and 89.2 nM, respectively[1].

Name: IPI-3063, CAS: 1425043-73-7, stock 36.1g, assay 98.6%, MWt: 455.51, Formula: C25H25N7O2, Solubility: DMSO : ≥ 83.33 mg/mL (182.94 mM), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: IPI-3063 is a potent and selective PI3K p110δ inhibitor with an IC50 of 2.5 ± 1.2 nM.
IC50 & Target: IC50: 2.5±1.2 nM (p110δ), 1171±533 nM (p110α), 1508±624 nM (p110β), 2187±1529 nM (p110γ)[1]
In Vitro: IPI-3063 inhibits p110α, p110β, and p110γ with IC50s of 1171±533 nM, 1508±624 nM, and 2187±1529 nM, respectively. IPI-3063 potently reduces mouse B cell proliferation, survival, and plasmablast differentiation while increasing antibody class switching to IgG1. IPI-3063 is a p110δ selective compound with an IC50=0.1 nM in p110δ-specific cell-based assays and cellular IC50 values for the other class I PI3K isoforms are at least 1,000-fold higher (IC50=1901±1318 nM for p110α, IC50=102.8±35.7 nM for p110β, IC50=418.8±117.2 nM for p110γ). IPI-3063 is very potent in reducing p-AKT (significant effect at 1 nM). IPI-3063 also reduces p-ERK1/2 with a significant effect at 10 nM. IPI-3063 is very potent, achieving a significant decrease in B cell survival when present at 10 nM[1].

Name: 4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine, CAS: 566169-98-0, stock 8.6g, assay 98.7%, MWt: 319.22, Formula: C14H11BrN2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: 4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine is a potent amyloid imaging agent which binds to Amyloid-β (1-40) with a KD of 1.7 nM.
IC50 & Target: Ki: 1.7 nM (Amyloid-β)[1]
In Vivo: Alzhermer's Disease (AD) is a neurodegenerative illness characterized by memory loss and other cognitive deficits. The ability to quantify amyloid load before treatment is critical to the efficient development of this class of drugs[2]. Brain entry in control mice and baboons is high for 4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine. Staining of AD frontal cortex tissue sections with 4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine indicates the selective binding of the compound to amyloid plaques and cerebrovascular amyloid. The encouraging properties of the compound support the choice of this derivative for further evaluation in human subject studies of brain Amyloid-βdeposition. The brain radioactivity concentrations (%ID-kg/g) of 4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine is remarkably similar in mice and baboons (0.21 vs 0.27). The rate of clearance of radioactivity is considerably slower from baboon brain than from mouse brain, although the rank order of clearance rate is similar in mice and baboons. The tissue staining findings utilizing nonradiolabeled, fluorescent 4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine are similar to those reported for BTA-1. Both amyloid plaques and cerebrovascular amyloid are stained by 4-(6-Bromo-2-benzothiazolyl)-N-methylbenzenamine in a manner similar to serial sections stained with an antibody to Amyloid-β, and relatively little tissue background staining is observed[1].

Name: 4-(6-Bromo-2-benzothiazolyl)benzenamine, CAS: 566169-97-9, stock 21g, assay 98.6%, MWt: 305.19, Formula: C13H9BrN2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: 4-(6-Bromo-2-benzothiazolyl)benzenamine is a β-amyloid PET (positron emission tomography) tracer that can be used in the diagnosis of neurological diseases, such as Alzheimer's and Down's syndrome.
IC50 & Target: β-amyloid[1]
In Vitro: 4-(6-Bromo-2-benzothiazolyl)benzenamine (compound 6l) plus ultraviolet A (UVA) can induce caspase-3 activity, poly(ADP-ribose)polymerase cleavage, M30 positive CytoDeath staining, and subsequent apoptotic cell death. Treatment of A375 cells with 4-(6-Bromo-2-benzothiazolyl)benzenamine plus UVA results in a decrease in mitochondrial membrane potential (ΔΨmt), oxidative phosphorylation system (OXPHOS) subunits, and adenosine triphosphate (ATP) but an increase in mitochondrial DNA 4977-bp deletion via reactive oxygen species (ROS) generation. Transmission electron microscopy (TEM) observations also show major ultrastructural alterations of mitochondria[2].
In Vivo: 4-(6-Bromo-2-benzothiazolyl)benzenamine plus UVA is shown to reduce murine melanoma size in a mouse model. 4-(6-Bromo-2-benzothiazolyl)benzenamine-PDT may serve as a potential ancillary modality for the treatment of melanoma[2].

Name: BAY-678 racemate, CAS: 675103-35-2, stock 16.3g, assay 98.1%, MWt: 400.35, Formula: C20H15F3N4O2, Solubility: DMSO : ≥ 150 mg/mL (374.67 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Elastase, Biological_Activity: BAY-678 racemate is a racemate of BAY-678. BAY-678 is an orally bioavailable, highly potent, selective and cell-permeable inhibitor of human neutrophil elastase (HNE), with an IC50 of 20 nM. BAY-678 is also nominated as a chemical probe to the public via the Structural Genomics Consortium (SGC).

Name: dTRIM24, CAS: 2170695-14-2, stock 1.7g, assay 98.3%, MWt: 1113.30, Formula: C55H68N8O13S2, Solubility: Ethanol : < 1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: dTRIM24 is a selective bifunctional degrader of TRIM24 based on PROTAC.
IC50 & Target: TRIM24[2].
In Vitro: dTRIM24 is a degrader of TRIM24 bromodomain. Recruitment of the VHL E3 ubiquitin ligase by dTRIM24 elicits potent and selective degradation of TRIM24. The anti-proliferative consequences of chemical degradation versus inhibition of TRIM24 are assessed. Growth over time is determined for MOLM-13 cells treated with dTRIM24, IACS-9571, VL-269, and eTRIM24. dTRIM24 suppresses growth to a greater extent than does IACS-9571, accompanied by apoptosis measured as enhanced PARP cleavage. In agreement with a sustained proliferative defect observed following dTRIM24 treatment, near-complete degradation of TRIM24 is observed in dTRIM24-treated cells throughout the duration of the experiment[2].

Name: (+)-Tetrabenazine D6, CAS: 1977511-05-9, stock 23g, assay 98.7%, MWt: 323.46, Formula: C19H21D6NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Monoamine Transporter, Biological_Activity: (+)-Tetrabenazine D6 is the deuterium labeled (+)-Tetrabenazine. (+)-Tetrabenazine is a reversible inhibitor of vesicular monoamine transporter 2 (VMAT-2).

Name: (S,R,S)-AHPC (TFA) MDK7526 (TFA);VH032-NH2 (TFA);VHL ligand 1 (TFA), CAS: 1631137-51-3, stock 22.7g, assay 98.3%, MWt: 544.59, Formula: C24H31F3N4O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for E3 Ligase, Biological_Activity: (S,R,S)-AHPC TFA (MDK7526 TFA) is the VH032-based VHL ligand used in the recruitment of the von Hippel-Lindau (VHL) protein. (S,R,S)-AHPC TFA (MDK7526 TFA) can be connected to the ligand for protein (e.g., BCR-ABL1) by a linker to form PROTACs (e.g., GMB-475). GMB-475 induces the degradation of BCR-ABL1 with an IC50 of 1.11 μM in Ba/F3 cells[1].
IC50 & Target: E3 ligase VHL[1]

Name: Tafenoquine WR 238605, CAS: 106635-80-7, stock 11.2g, assay 98.3%, MWt: 463.49, Formula: C24H28F3N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Tafenoquine (WR 238605) 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: GSTO1-IN-1, CAS: 568544-03-6, stock 26g, assay 98.6%, MWt: 311.18, Formula: C10H12Cl2N2O3S, Solubility: DMSO : ≥ 300 mg/mL (964.07 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Gutathione S-transferase, Biological_Activity: GSTO1-IN-1 is a potent glutathione S-transferase omega 1 (GSTO1) inhibitor with an IC50 of 31 nM.
IC50 & Target: IC50: 31 nM (GSTO1)[1]
In Vitro: GSTO1-IN-1 (C1-27) potently inhibits GSTO1 enzyme activity with an IC50 value of 31 nM. GSTO1-IN-1 also potently competes with 5-chloromethylfluorescein diacetate (CMFDA) for binding to recombinant protein, as well as endogenous GSTO1 in the milieu of a soluble proteome. HCT116 cells treated with GSTO1-IN-1 also show a decrease in cell viability in a dose-dependent manner. GSTO1-IN-1 inhibits the clonogenic survival of HCT116 cells at sub-micromolar concentrations[1].
In Vivo: To test whether GSTO1-IN-1 had in vivo efficacy, its effects are evaluated in a human colon cancer cell line xenograft model. GSTO1-IN-1 (20-45 mg/kg) is administered as a single agent to nude mice bearing HCT116 xenografts. After 5 weeks of treatment, tumor growth is significantly inhibited in GSTO1-IN-1-treated mice compared with the vehicle-treated group (P<0.05). GSTO1-IN-1 treatment is generally well tolerated by mice up to 45 mg/kg, with no overt signs of toxicity and no significant variations in average body weights throughout the duration of the study[1].

Name: Capzimin, CAS: 2084868-04-0, stock 27g, assay 98.2%, MWt: 628.81, Formula: C30H24N6O2S4, Solubility: DMSO : ≥ 55.67 mg/mL (88.53 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Proteasome, Biological_Activity: Capzimin is a potent and moderately specific proteasome isopeptidase Rpn11 inhibitor.
IC50 & Target: Target: Rpn11[1]
In Vitro: Capzimin (3027) shows 80-fold selectivity for Rpn11 over Csn5, 10-fold over AMSH and 6-fold over BRCC36 (IC50=30 μM, 4.5 μM and 2.3 μM respectively. Capzimin is screened against the NCI panel of 60 cancer cell lines. The median GI50 is 3.3 μM. Capzimin exhibits promising activity in leukemia cells including the SR and K562 cell lines (GI50 values of 0.67 μM and 1 μM respectively), as well as several solid tumor cell lines including NCI-H460 (non-small cell lung cancer; GI50= 0.7 μM) and MCF7 (breast cancer; GI50=1.0 μM). Immunoblotting for the processed form of caspase 3 and caspase-cleaved poly ADP-ribose polymerase in HCT116 cells confirm that Capzimin not only blocks cell growth, but also induces apoptosis[1].

Name: IACS-10759, CAS: 1570496-34-2, stock 32.2g, assay 98.7%, MWt: 562.56, Formula: C25H25F3N6O4S, Solubility: DMSO : 62.5 mg/mL (111.10 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: IACS-10759 is a potent inhibitor of complex I of oxidative phosphorylation (OXPHOS).
IC50 & Target: OXPHOS[1]
In Vitro: IACS-10759 inhibits the conversion of NADH to NAD+ in an immunoprecipitated complex I assay at low nM concentrations[1].
In Vivo: IACS-10759 is orally bioavailable with excellent physicochemical properties in preclinical species and achieves significant in vivo efficacy with daily oral dosing of 10-25 mg/kg. There is a >50 day extension of median survival in an orthotopic AML cell line xenograft and robust regression in DLBCL and GBM xenograft models[1].

Name: GSK2983559 (free acid), CAS: 1579965-12-0, stock 34.9g, assay 98.2%, MWt: 538.53, Formula: C21H23N4O7PS2, Solubility: DMSO : 5 mg/mL (9.28 mM; ultrasonic and warming and heat to 80°C), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: RIP kinase, Biological_Activity: GSK2983559 free acid (compound 3) is a potent, specific and oral bioavailable receptor interacting protein 2 (RIP2) kinase inhibitor. GSK2983559 free acid has excellent activity in blocking many proinflammatory cytokine responses in vivo and in human inflammatory bowel disease explant samples[1].
IC50 & Target: RIP2[1]

Name: PTC596, CAS: 1610964-64-1, stock 12.5g, assay 98.4%, MWt: 420.34, Formula: C19H13F5N6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: PTC596 is an orally active and selective B-cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) inhibitor. PTC596 targets BMI1 expressed by both tumor cells and cancer stem cells (CSCs), and induces hyper-phosphorylation of BMI1, leading to its degradation. PTC596 downregulates MCL-1 and induces p53-independent mitochondrial apoptosis in acute myeloid leukemia progenitor cells[1][2].
IC50 & Target: BMI-1[1]

Name: Chlorotoxin, CAS: 163515-35-3, stock 31g, assay 98.2%, MWt: 3995.71, Formula: C158H249N53O47S11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Chloride Channel, Biological_Activity: Chlorotoxin is a 36 amino-acid peptide from the venom of the Israeli scorpion Leiurus quinquestriatus with anticancer activity. Chlorotoxin is a chloride channel blocker.
IC50 & Target: Target: Chloride Channel[1]
In Vitro: Chlorotoxin (Chlorotoxin) preferentially binds to tumor cells and has been harnessed to develop an imaging agent to help visualize tumors during surgical resection. In addition, chlorotoxin has potential as a vehicle to deliver anti-cancer drugs specifically to cancer cells. Chlorotoxin is shown to bind glioma cells, but is unable to bind normal rat astrocytes and Te671, a human rhabdomyosarcoma cell line. Chlorotoxin inhibits the migration of U251MG (glioma) cells, with an IC50 of 600 nM[2]. Chlorotoxin binds to glioma cells is specific and involves high affinity (Kd=4.2 nM) and low affinity (Kd=660 nM) binding sites[3].Small conductance chloride channels are shown to be potently blocked by Chlorotoxin. Chlorotoxin has been used as a general pharmacological tool to investigate the function of chloride channels[4].
In Vivo: Chlorotoxin shows insecticidal activity on insects and other invertebrates. After the administration of I-Chlorotoxin to tumor-bearing mice, the peptides accumulated within the tumor[2].Chlorotoxin selectively accumulates in the brain of tumor-bearing mice with calculated brain: muscle ratios of 36.4% of injected dose/g (ID/g), as compared to 12.4%ID/g in control animals[3].

Name: CU-CPT-8m TLR8-specific antagonist, CAS: 125079-83-6, stock 10.7g, assay 98.4%, MWt: 252.27, Formula: C14H12N4O, Solubility: DMSO : 30 mg/mL (118.92 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: CU-CPT-8m is a specific TLR8 antagonist, with an IC50 of 67 nM.
IC50 & Target: IC50: 67 nM (TLR8)[1].
In Vitro: CU-CPT-8m is a specific TLR8 antagonist, with an IC50 of 67±10 nM and negligible cytotoxicity. The Kd value of CU-CPT-8m is determined to be 220 nM. CU-CPT-8m only reduces the proinflammatory response in the TLR8-overexpressing cells strongly supports that CU-CPT-8m directly recognizes TLR8 in cells. It is particularly notable that TLR7 signaling is not affected at concentrations up to 75 μM. TLR7 and TLR8 are closely related and share many common ligands. Treatment of 1 μM CU-CPT-8m completely abolishes the elevation of TNF-α and IL-8 mRNA levels induced by R848. CU-CPT-8m inhibits R848-induced TNF-α production in the differentiated THP-1 monocytes cells in a dose-dependent manner with an IC50 of 90±10 nM, which is in good agreement with its IC50 value determined in HEK-Blue TLR8 cells[1].

Name: CU-CPT9b, CAS: 2162962-69-6, stock 23.2g, assay 99%, MWt: 251.28, Formula: C16H13NO2, Solubility: DMSO : 100 mg/mL (397.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: CU-CPT9b is a specific TLR8 antagonist, with an IC50 of 0.7 nM. CU-CPT9b shows high binding affinity towards TLR8 with a Kd of 21 nM[1].
IC50 & Target: IC50: 0.7 nM (TLR8)[1]. 
Kd: 21 nM[1].
In Vitro: CU-CPT9b is a specific TLR8 antagonist, with an IC50 of 0.7±0.2 nM. ITC experiments have confirmed the strong binding of CU-CPT9b with a Kd of 21 nM. It is shown that CU-CPT-9b binds to the inactive TLR8 dimer in a similar way to CU-CPT8m. CU-CPT9b utilizes hydrogen bonds with G351 and V520*, which are conserved among TLR8/antagonist structures. Additionally, CU-CPT9b forms water-mediated contacts with S516* and Q519*, which are not observed in TLR8/CU-CPT8m structure, suggesting that the enhanced potency of CU-CPT9b derives from the new interactions with these polar residues. The orientation of Y567* also changes to facilitate van der Waals interactions with CU-CPT9b as compared to TLR8/CU-CPT8m[1].

Name: Aminomalonic acid, CAS: 1068-84-4, stock 11.9g, assay 98.3%, MWt: 119.08, Formula: C3H5NO4, Solubility: H2O : 8.33 mg/mL (69.95 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Aminomalonic acid is an amino endogenous metabolite, acts as a strong inhibitor of L-asparagine synthetase from Leukemia 5178Y/AR (Ki= 0.0023 M) and mouse pancreas (Ki= 0.0015 M) in vitro. Aminomalonic acid is a potential biomarker to discriminate between different stages of melanoma metastasis[1][2][3].
IC50 & Target: Ki: 0.0023 M (L-asparagine synthetase from Leukemia 5178Y/AR), 0.0015 M (L-asparagine synthetase from mouse pancreas)[2]

Name: DPPH 2,2-Diphenyl-1-picrylhydrazyl, CAS: 1898-66-4, stock 10.6g, assay 98.3%, MWt: 394.32, Formula: C18H12N5O6, Solubility: DMSO : 62.5 mg/mL (158.50 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DPPH (2,2-Diphenyl-1-picrylhydrazyl) is a stable free radical that can be used to measure the radical scavenging activity of antioxidants. The odd electron of nitrogen atom in DPPH is reduced by receiving a hydrogen atom from antioxidants to the corresponding hydrazine. DPPH method may be utilized in aqueous and nonpolar organic solvents and can be used to examine both hydrophilic and lipophilic antioxidants[1].
In Vitro: DPPH shows a strong absorption band at 517 nm due to its odd electron and solution appears a deep violet colour, the absorption vanishes as the electron pairs off. The resulting decolorization is stoichiometric with respect to the number of electrons taken up. The alcoholic solutions of 0.5 mM are densely colored and at this concentration, the Lambert-Beer law is obeyed over the useful range of absorption[1]. 
DPPH assay is a rapid, simple, inexpensive and widely used method to measure the ability of compounds to act as free radical scavengers or hydrogen donors, and to evaluate antioxidant activity of foods. It can also be used to quantify antioxidants in complex biological systems, for solid or liquid samples. This method is easy and applies to measure the overall antioxidant capacity and the free radical scavenging activity of fruit and vegetable juice. This assay has been successfully utilized for investigating antioxidant properties of wheat grain and bran, vegetables, conjugated linoleic acids, herbs, edible seed oils, and flours in several different solvent systems including ethanol, aqueous acetone, methanol, aqueous alcohol and benzene. It is a convenient method for the antioxidant assay of cysteine, glutathione, ascorbic acid, tocopherol and polyhydroxy aromatic compounds, for olive oil, fruits, juices and wines[1].

Name: DIM-C-pPhOH, CAS: 151358-47-3, stock 26.6g, assay 98.6%, MWt: 338.40, Formula: C23H18N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: DIM-C-pPhOH is a nuclear receptor 4A1 (NR4A1) antagonist. DIM-C-pPhOH inhibits cancer cell growth and mTOR signaling, induce apoptosis and cellular stress. DIM-C-pPhOH reduces cell proliferation with IC50 values of 13.6 μM and 13.0 μM for ACHN cells and 786-O cells, respectively[1].
IC50 & Target: Nuclear receptor 4A1 (NR4A1)[1]
In Vitro: DIM-C-pPhOH (7.5-20 μM; 24 hours; ACHN and 786-O cells) treatment significantly decreases cell proliferation[1]. 
DIM-C-pPhOH (20 μM; 24 hours; ACHN and 786-O cells) treatment induces Annexin V staining in ACHN and 786-O cells, confirming that DIM-C-pPhOH induce apoptosis, and also induces cleavage of caspases 7 and 8[1]. 
DIM-C-pPhOH (15-20 μM; 24 hours; ACHN and 786-O cells) treatment inhibits NR4A1-regulated expression of survivin, bcl-2 and EGFR in ACHN and 786-O cells. And also induces sestrin 2, activates AMPKα and inhibits activation of mTOR and downstream kinases[1]. 
DIM-C-pPhOH decreases expression of β1-integrin protein and mRNA and β1-integrin-dependent responses in MCF7, MDA-MB-231, and SKBR3 cells and also inhibits migration of the latter two cell lines[2].
In Vivo: DIM-C-pPhOH (30 mg/kg; oral gavage; daily; for 50 days; male athymic nude mice) treatment results in a significant inhibition of tumor growth[1].

Name: DIM-C-pPhCO2Me, CAS: 151358-48-4, stock 20g, assay 98.3%, MWt: 380.44, Formula: C25H20N2O2, Solubility: DMSO : ≥ 125 mg/mL (328.57 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DIM-C-pPhCO2Me is a nuclear receptor 4A1 (NR4A1) antagonist[1]. Antineoplastic activity[1].
IC50 & Target: Nuclear receptor 4A1 (NR4A1)[1]

Name: Afatinib BIBW 2992, CAS: 850140-72-6, stock 21.3g, assay 98.4%, MWt: 485.94, Formula: C24H25ClFN5O3, Solubility: DMSO : ≥ 100 mg/mL (205.79 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Autophagy, Target: EGFR;EGFR;Autophagy, Biological_Activity: Afatinib is an irreversible, dual EGFR/HER2 inhibitor, shows potent activity against wild-type and mutant forms of EGFR and HER2, with IC50 of 0.5 nM, 0.4 nM, 10 nM and 14 nM for EGFRwt, EGFRL858R, EGFRL858R/T790M and HER2, respectively.
IC50 & Target: IC50: 0.5 nM (EGFRwt), 0.4 nM (EGFRL858R), 10 nM (EGFRL858R/T790M), 14 nM (HER2)[1]
In Vitro: In cell-free in vitro kinase assays, Afatinib (BIBW2992) dimaleate shows potent activity against wild-type and mutant forms of EGFR and HER2, similar to Gefitinib in potency for L858R EGFR, but about 100-fold more active against the Gefitinib-resistant L858R-T790M EGFR double mutant, with an IC50 of 10 nM. BIBW2992 is furthermore comparable to Lapatinib and Canertinib for in vitro potency against HER2, with an IC50 of 14 nM. The most sensitive kinase in this evaluation is lyn with an IC50 of 736 nM[1]. Afatinib is an irreversible inhibitor of these ErbB family receptors. Esophageal squamous cell carcinoma (ESCC) cell lines are sensitive to Afatinib with IC50 concentrations at lower micro-molar range (at 48 hour incubation: HKESC-1=78 nM, HKESC-2=115 nM, KYSE510=3.182 μM, SLMT-1=4.625 μM and EC-1=1.489 μM; and at 72 hour incubation: HKESC-1=2 nM, HKESC-2=2 nM, KYSE510=1.090 μM, SLMT-1=1.161 μM and EC-1=109 nM) with a maximum growth inhibition over 95%. Afatinib can strongly induce G0/G1 cell cycle arrest in HKESC-2 and EC-1 in a dose- and time-dependent manner[2].
In Vivo: Afatinib (15 mg/kg) strongly inhibits the growth of HKESC-2 tumor once the treatment began. Average tumor sizes of vehicle and treatment at end point are 348±24 mm3 and 108±36 mm3 respectively, showing significantly difference between them. And apparently tumor size does not bounce back in a short period of time after the end of Afatinib administration. Without rapid change of body weight throughout the treatment shows that the toxicity of Afatinib is minimal and this drug is well tolerated[2].

Name: DMTr-LNA-5MeU-3-CED-phosphoramidite, CAS: 206055-75-6, stock 25.1g, assay 98.8%, MWt: 772.82, Formula: C41H49N4O9P, Solubility: DMSO : 250 mg/mL (323.49 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Nucleoside Antimetabolite/Analog, Biological_Activity: DMTr-LNA-5MeU-3-CED-phosphoramidite is a nucleoside derivative[1].

Name: Saccharin 1-methylimidazole, CAS: 482333-74-4, stock 33.7g, assay 98.7%, MWt: 265.29, Formula: C11H11N3O3S, Solubility: DMSO : 100 mg/mL (376.95 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: Saccharin 1-methylimidazole is an activator for DNA/RNA Synthesis.
IC50 & Target: Target: DNA/RNA Synthesis[1]
In Vitro: Exposure to certain concentrations of the entirely different promoters phenobarbital and the calcium and sodium salts of saccharin (22, 23, 25, 29, 38) stimulates calcium-deprived T51B cells to initiate DNA synthesis as rapidly and as effectively, or nearly as effectively, as raising the extracellular calcium concentration to 1.25 mM[1].

Name: 8-OH-DPAT 8-Hydroxy-DPAT, CAS: 78950-78-4, stock 12.2g, assay 98.8%, MWt: 247.38, Formula: C16H25NO, Solubility: DMSO : ≥ 155 mg/mL (626.57 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: 8-OH-DPAT is a potent and selective 5-HT agonist, with a pIC50 of 8.19 for 5-HT1A and a Ki of 466 nM for 5-HT7; 8-OH-DPAT weakly binds to 5-HT1B (pIC50, 5.42), 5-HT (pIC50 <5).
IC50 & Target: pIC50: 8.19 (5-HT1A)[1] 
Ki: 466 nM (5-HT7)[2]
In Vitro: 8-OH-DPAT is a potent and selective 5-HT agonist, with a pIC50 of 8.19 for 5-HT1A; weakly binds to 5-HT1B (pIC50, 5.42), 5-HT (pIC50 <5)[1]. 8-OH-DPAT has high affinity at 5-HT7 with a Ki of 466 nM, and does not bind to 5-HT6 or 5-HT4[2].
In Vivo: 8-OH-DPAT (1 mg/kg) normalizes hypolocomotion, significantly increases wakefulness and reduces the duration of REM sleep without effect on the duration of non-REM sleep in the dark period in orexin knockout (KO) mice. 8-OH-DPAT shows no obvious effect on wakefulness or the duration of either REM sleep or non-REM sleep in WT mice. 8-OH-DPAT (1 mg/kg, s.c.) activates 5-HT1A receptor in orexin knockout mice[3].

Name: SBI-115, CAS: 882366-16-7, stock 27.9g, assay 98.2%, MWt: 340.78, Formula: C14H13ClN2O4S, Solubility: DMSO : 150 mg/mL (440.17 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPCR19, Biological_Activity: SBI-115 is a TGR5 (GPCR19) antagonist. SBI-115 decreases hepatic cystogenesis with polycystic liver diseases via inhibiting TGR5[1].
In Vitro: SBI-115 (100-200 µM, 24 hours) inhibits proliferation triggered by pre-treatment of cystic cholangiocytes with Taurolithocholic acid (TLCA) in shRNA-transfected ADPKD cholangiocytes[1].

Name: Mitochonic acid 5 MA-5, CAS: 1354707-41-7, stock 6g, assay 98.2%, MWt: 329.30, Formula: C18H13F2NO3, Solubility: DMSO : ≥ 106.66 mg/mL (323.90 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Mitochondrial Metabolism, Biological_Activity: Mitochonic acid 5 binds mitochondria and ameliorates renal tubular and cardiac myocyte damage. Mitochonic acid 5 modulates mitochondrial ATP synthesis.
IC50 & Target: Mitochondrial Metabolism[1]
In Vitro: Mitochonic acid 5 (MA-5) modulates mitochondrial ATP synthesis independently of oxidative phosphorylation and the electron transport chain. Mitochondrial dysfunction causes increased oxidative stress and depletion of ATP, which are involved in the etiology of a variety of renal diseases[1]. Mitochonic acid 5 (MA-5), which is derived from the plant growth hormone indole-3-acetic acid, can protect mitochondrial function by regulating energy metabolism and reducing mitochondrial oxidative stress. To observe the protective role of Mitochonic acid 5 in microglia under inflammatory conditions, TNFα is applied. Subsequently, the MTT assay is used to evaluate cell viability. In response to the TNFα treatment, cell viability significantly decreases. However, this effect is dose-dependently inhibited by Mitochonic acid 5 treatment[2].
In Vivo: Administration of Mitochonic acid 5 (MA-5) to an ischemia-reperfusion injury model and a cisplatin-induced nephropathy model improved renal function. To examine the tissue-protective effect of Mitochonic acid 5, the oral bioavailability is examined. Oral administration of Mitochonic acid 5 increases the plasma concentration in a dose-response manner at the peak time of 1 hour[1].

Name: CIL56, CAS: 300802-28-2, stock 14.1g, assay 98.8%, MWt: 489.61, Formula: C23H27N3O5S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (102.12 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Ferroptosis, Biological_Activity: CIL56 is a potent and selective ferroptosis inducer. Ferroptosis is an iron-dependent form of regulated cell death (RCD).
In Vitro: Ferroptosis is a non-apoptotic form of regulated cell death observed in cancer cells, kidney cells and neurons.CIL56 induces iron-dependent reactive oxygen species (ROS). Antioxidants and iron chelators only suppress the lethality of low concentrations of CIL56[1]. CIL56 triggers cell death dependent upon the rate-limiting de novo lipid synthetic enzyme ACC1.Using mass spectrometry, the metabolome of HT-1080 cells treated with CIL56 (6.5 μM)±TOFA (4 μM) is analyzed, compared to vehicle-treated controls. Among the 298 polar and nonpolar metabolites identified in this analysis, the levels of 141 metabolites are significantly altered by CIL56 treatment, with 82 metabolites significantly increased and 59 significantly decreased (FDR q<0.01). CIL56 triggers the striking TOFA-sensitive accumulation of all detectable long chain saturated and monounsaturated fatty acids and all detectable polyunsaturated fatty acids. A plausible model to account for the accumulation of both nonessential and essential fatty acids species is that CIL56 inhibits the normal breakdown of fatty acids by mitochondrial β-oxidation. CIL56 accelerates the ACC1-dependent production of malonyl-CoA, a metabolite that acts as a negative regulator of this process[2].

Name: PF-06869206, CAS: 2227425-05-8, stock 20.3g, assay 98.8%, MWt: 374.75, Formula: C15H14ClF3N4O2, Solubility: DMSO : ≥ 125 mg/mL (333.56 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: PF-06869206 is an orally bioavailable selective inhibitor of the sodium-phosphate cotransporter NaPi2a (SLC34A1) with an IC50 of 380 nM.
IC50 & Target: IC50: 380 nM (NaPi2a/SLC34A1)[1]
In Vitro: PF-06869206 shows a balance of attributes with 380 nM NaPi2a inhibition potency, excellent subtype selectivity, and acceptable aqueous solubility (46 μM). PF-06869206 is profiled for potency in the rodent NaPi2a and NaPi2c cell lines. PF-06869206 shows comparable submicromolar activity for the human, rat, and mouse NaPi2a isoforms with IC50s of 0.4±0.047 μM and 0.54±0.099 μM for rat NaPi2a and mouse NaPi2a, respectively[1].
In Vivo: PF-06869206 is evaluated in rodent PK studies to determine suitability for in vivo pharmacology exploration. Results show moderate clearance in both rat and mouse. Oral bioavailability at 5 mg/kg is good in rat and moderate in mouse. At higher oral doses of 50 mg/kg, supraproportional increases in exposure are observed in both species, suggestive of saturation of clearance. PF-06869206 has moderate terminal elimination half-life (t1/2=1.35 h, and 0.75 h for Wistar-Han rats (10 mg/kg, iv), and C57BL6 mice (1 mg/kg, iv)). Furthermore, permeability is good (14×10-6 cm/s), and rat liver microsome (RLM) clearance is low (<14 μL/min/mg; HLM=39 μL/min/mg)[1].

Name: SHIN1 RZ-2994, CAS: 2146095-85-2, stock 18.9g, assay 98.8%, MWt: 400.47, Formula: C24H24N4O2, Solubility: DMSO : ≥ 50 mg/mL (124.85 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SHIN1 (RZ-2994) is a human serine hydroxymethyltransferse 1 and 2 (SHMT1/2) inhibitor with IC50s of 5 and 13 nM, respectively, in an in vitro assay.
IC50 & Target: IC50: 5 nM (SHMT1), 13 nM (SHMT1)[1]
In Vitro: SHIN1 (RZ-2994) inhibits human SHIN1 SHMT1/2 with IC50s of 5 and 13 nM, respectively in an in vitro assay. SHIN1 inhibits the growth of SHMT2 deletion HCT-116 cells with an IC50 of 10 nM. SHIN1 (RZ-2994) inhibits SHMT1/2 in HCT-116 cells. SHIN1 (RZ-2994) is particularly active against B-cell malignancies. SHIN1 blocks cell growth through a progressive depletion of purines, leading to loss of nucleotide triphosphates[1].

Name: Lidoflazine, CAS: 3416-26-0, stock 32g, assay 98.6%, MWt: 491.62, Formula: C30H35F2N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Potassium Channel;Calcium Channel, Biological_Activity: Lidoflazine is a high affinity blocker of the HERG (human ether-a-go-go-related gene) K+ channel. Lidoflazine is an antianginal calcium channel blocker that carries a significant risk of QT interval prolongation and ventricular arrhythmia[1].
In Vitro: Lidoflazine inhibits potently HERG current (IHERG) recorded from HEK 293 cells stably expressing wild-type HERG (IC50 of ~16 nM).

Name: Atropine methyl bromide Methylatropine bromide, CAS: 2870-71-5, stock 33.6g, assay 98.1%, MWt: 384.31, Formula: C18H26BrNO3, Solubility: DMSO : 150 mg/mL (390.31 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Atropine methyl bromide, a muscarinic receptor (mAChR) antagonist, is a quaternary ammonium salt of atropine and a mydriatic for dilation of the pupil during ophthalmic examination. It is introduced for relieving pyloric spasm in infants for its highly polar nature. It penetrates less readily into the central nervous system than atropine[1][2].

Name: 13-cis-N-[4-(Ethoxycarbonyl)phenyl]retinamide Ethyl 4-((2Z,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohex-1-en-1-yl)nona-2,4,6,8-tetraenamido)benzoate, CAS: 251441-94-8, stock 12.5g, assay 98.1%, MWt: 447.61, Formula: C29H37NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 13-cis-N-[4-(Ethoxycarbonyl)phenyl]retinamide is a derivative of Retinoic acid.

Name: (S,R,S)-AHPC-Me VHL ligand 2;E3 ligase Ligand 1A, CAS: 1948273-02-6, stock 24.8g, assay 98.9%, MWt: 444.59, Formula: C23H32N4O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for E3 Ligase, Biological_Activity: (S,R,S)-AHPC-Me (VHL ligand 2) is the (S,R,S)-AHPC-based VHL ligand used in the recruitment of the von Hippel-Lindau (VHL) protein[1]. (S,R,S)-AHPC-Me can be used to synthesize ARV-771, a von Hippel-Landau (VHL) E3 ligase-based BET PROTAC degrader. ARV-771 potently degrades BET protein in castration-resistant prostate cancer (CRPC) cells with a DC50 <1 nM[2].
IC50 & Target: Ligand for E3 Ligase

Name: BAY885, CAS: 2307249-33-6, stock 8.7g, assay 99%, MWt: 515.53, Formula: C25H28F3N7O2, Solubility: DMSO : 16.67 mg/mL (32.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway, Target: ERK;ERK, Biological_Activity: BAY885 is a novel ERK5 inhibitor.

Name: N-Bis(2-hydroxypropyl)nitrosamine DHPN;Di(2-hydroxypropyl)nitrosamine;Diisopropanolnitrosamine, CAS: 53609-64-6, stock 38g, assay 98.7%, MWt: 162.19, Formula: C6H14N2O3, Solubility: DMSO : ≥ 125 mg/mL (770.70 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Bis(2-hydroxypropyl)nitrosamine is an agent with carcinogenic activity.
In Vitro: N-Bis(2-hydroxypropyl)nitrosamine is an agent with carcinogenic activity[1].
In Vivo: N-Bis(2-hydroxypropyl)nitrosamine causes the tumors to develop in the lung, liver, and thyroid of rats at a dose of 100 ppm, in the lung, liver thyroid, esophagus, kidney, and urinary bladder of rats at a dose of 500 ppm, and in the lung, liver thyroid, esophagus, kidney, and urinary bladder of rats at both doses[1]. Bisphenol A (BPA) enhances the susceptibility to thyroid carcinoma stimulated by N-Bis(2-hydroxypropyl)nitrosamine (DHPN; 2800 mg/kg) in rats[2].

Name: AZD4573, CAS: 2057509-72-3, stock 39.2g, assay 98.9%, MWt: 429.94, Formula: C22H28ClN5O2, Solubility: DMSO : ≥ 125 mg/mL (290.74 mM), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: AZD4573 is a potent and highly selective CDK9 inhibitor (IC50 of <4 nM) that enables transient target engagement for the treatment of hematologic malignancies[1].
IC50 & Target: IC50: <3 nM (CDK9)[1]
In Vitro: Short-term treatment with AZD4573 led to a rapid dose- and time-dependent decrease in cellular pSer2-RNAPII, resulting in activation of caspase 3 and cell apoptosis in a broad range of haematological cancer cell lines (e.g. caspase activation EC50 13.7 nM in an acute myeloid leukemia model MV4-11) [1].
In Vivo: AZD4573 exhibits a short half-life in multiple species (less than one hour in rat, dog and monkey) and good solubility for intravenous administration[1].

Name: LXH254, CAS: 1800398-38-2, stock 34.4g, assay 99%, MWt: 502.49, Formula: C25H25F3N4O4, Solubility: DMSO : ≥ 83.3 mg/mL (165.77 mM), Clinical_Informat: Phase 1, Pathway: MAPK/ERK Pathway, Target: Raf, Biological_Activity: LXH254 is a potent B/C RAF inhibitor extracted from patent WO2018051306A1, Compound A.
IC50 & Target: CRAF, BRAF[1]
In Vitro: LXH254 (Compound A) is an adenosine triphosphate (ATP)-competitive inhibitor of BRAF (also referred to herein as b-RAF or b-Raf) and CRAF (also referred to herein as c-RAF or c- Raf) protein kinases. Throughout the present disclosure, LXH254 is also referred to as a c-RAF (or CRAF) inhibitor or a C-RAF/c-Raf kinase inhibitor. In cell-based assays, LXH254 has demonstrated anti-proliferative activity in cell lines that contain a variety of mutations that activate MAPK signaling. Moreover, LXH254 is a Type 2 ATP -competitive inhibitor of both B-Raf and C-Raf that keeps the kinase pocket in an inactive conformation, thereby reducing the paradoxical activation seen with many B-Raf inhibitors, and blocking mutant RAS-driven signaling and cell proliferation[1].
In Vivo: Treatment with LXH254 (Compound A) generates tumor regression in several KRAS-mutant models including the NSCLC-derived Calu-6 (KRAS Q61K) and NCI-H358 (KRAS G12C). LXH254 exhibits efficacy in numerous MAPK-driven human cancer cell lines and in xenograft tumors representing model tumors harboring human lesions in KRAS, NRAS and BRAF oncogenes[1].

Name: ABBV-744, CAS: 2138861-99-9, stock 13.2g, assay 98.9%, MWt: 491.55, Formula: C28H30FN3O4, Solubility: DMSO : 37.14 mg/mL (75.56 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Epigenetics;Anti-infection, Target: Epigenetic Reader Domain;HIV, Biological_Activity: ABBV-744 is a highly BDII-selective BET bromodomain inhibitor, used in the research of inflammatory diseases, cancer, and AIDS.
IC50 & Target: BET bromodomain[1]
In Vitro: ABBV-744 is a highly BDII-selective BET bromodomain inhibitor, used in the research of inflammatory diseases, cancer, and AIDS[1].

Name: GSK2200150A, CAS: 1443138-53-1, stock 27.8g, assay 98.1%, MWt: 357.47, Formula: C20H23NO3S, Solubility: DMSO : ≥ 83.33 mg/mL (233.11 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: GSK2200150A, identified by high-throughput screening (HTS) campaign, is an anti-tuberculosis (TB) agent.
IC50 & Target: MIC: 0.38 μM (M.tuberculosis strain H37Rv)[1]
In Vitro: GSK2200150A is a novel antimycobacterial agent against Mycobacterium tuberculosis.The activities of GSK2200150A containing the spirocycle core are determined against the virulent M.tuberculosis strain (H37Rv) with MIC of 0.38 μM[1].

Name: WNK-IN-11, CAS: 2123489-30-3, stock 26.9g, assay 98.7%, MWt: 462.40, Formula: C21H21Cl2N5OS, Solubility: DMSO : 150 mg/mL (324.39 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: WNK-IN-11 is an allosteric With-No-Lysine (WNK) kinase inhibitor, with an IC50 of 4 nM for WNK1.
IC50 & Target: IC50: 4 nM (WNK1)[1].
In Vitro: WNK-IN-11 (compound 11) shows IC50<2 μM in the cellular OSR1 phosphorylation assay with reasonable aqueous solubility, albeit with still rather high microsomal clearance. WNK-IN-11 shows ATP noncompetitive inhibition. When tested against a panel of 440 human kinases at 10 μM concentration, 2500-fold above enzyme IC50 value, WNK-IN-11 shows excellent selectivity with only a few significant off-target kinase inhibitions, most notably BTK and feline encephalitis virus-related (FER) kinase, neither of which are implicated for blood pressure regulation. This excellent selectivity profile is consistent with the predicted allosteric binding mode outside the highly conserved ATP-pocket[1].

Name: eCF506, CAS: 1914078-41-3, stock 27g, assay 98%, MWt: 510.63, Formula: C26H38N8O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (122.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Src, Biological_Activity: eCF506 is a highly potent and orally bioavailable inhibitor of the non-receptor tyrosine kinase Src with an IC50 of less than 0.5 nM.
IC50 & Target: IC50: less than 0.5 nM (Src)[1]
In Vitro: eCF506 induces a very potent antiproliferative effect in both MCF7 and MDA-MB-231 cells. eCF506 inhibits phosphorylation of SRC and FAK at low nanomolar levels, with complete inhibition observed at 100 nM. eCF506 significantly reduces cell motility at 10 nM as early as 6 h into the study, with equivalent efficacy to dasatinib. eCF506 exclusively inhibits SFK, with subnanomolar IC50 values against SRC and YES (IC50=0.5, 2.1 nM). It is important to highlight that eCF506 displays a vast difference in activity (>950-fold difference) between ABL and its primary target SRC[1].
In Vivo: eCF506 shows a moderate oral bioavailability (25.3%). A significant reduction of phospho-SRCY416 is observed in the xenograft sections from mice treated with eCF506 relative to the untreated animal controls[1].

Name: E260, CAS: 1241537-79-0, stock 35.4g, assay 98.9%, MWt: 438.63, Formula: C24H34N6S, Solubility: DMSO : 1 mg/mL (2.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: E260 is a Fer/FerT kinase inhibitor.
IC50 & Target: Fer/FerT kinase[1]
In Vitro: E260 is a Fer and FerT inhibitor, which selectively evokes metabolic stress in cancer cells by imposing mitochondrial dysfunction and deformation, and onset of energy-consuming autophagy which decreases the cellular ATP level. To demonstrate that E260 directly targets Fer and FerT, an in vitro kinase assay is performed using a purified kinase domain (KD)-containing fragment of these enzymes. This analysis demonstrates the direct inhibitory effect of E260 on this domain as reflected by the significantly decreased auto-phosphorylation level of the Fer/FerT KD when incubated with ATP and increasing concentrations of E260. Moreover, computational analysis of E260 docking in the modeled whole Fer protein reveals that the highest scored binding mode of E260 to Fer falls in the ATP-binding pocket of the enzyme’s KD. To measure the dissociation constant (Kd) of E260 from Fer/FerT KD, a microscale thermophoresis (MST) test is performed using ascending concentrations of E260. This analysis corroborates the direct binding of E260 to Fer/FerT KD and determines a Kd of 0.85 µM. To examine the effect of the E260 micellar formulation on Fer in malignant cells, the kinase is immunoprecipitated from untreated and from E260-treated SW620 CC cells. When applied to metastatic grade IV SW620 CC cells, which are serum starved for 16 h and treated with 3 mM H2O2 to activate Fer, E260 exhibits inhibitory effects on the Fer-kinase activity as is reflected by suppressed auto-phosphorylation activity of the enzyme. To characterize the effect of E260 on malignant cells, metastatic SW620 cells are treated with E260 followed by analysis of viability. Onset of death is observed in the E260-treated cells, with an EC50 value of 400 nM after 24 h of treatment and an EC50 of 300 nM after 48 h. E260 exhibits an EC50 of 3.2 µM after 72 h treatment of non-metastatic PANC-1 cells, which are derived from a primary pancreatic ductal carcinoma. Moreover, the maximum death level of these cells after 72 h of treatment with E260 is about 70% following treatment with 4 µM E260. In comparison, SU.86.86 which are metastatic ductal carcinoma cells, prove to be more susceptible to E260 with an EC50 of 1.1 µM after 72 h of treatment and 100% death level imposed by 2 µM E260[1].
In Vivo: E260 suppresses xenografts progression in vivo. The pharmacokinetic (PK) profile of E260 is determined in mice. E260 exhibits a T1/2 of 175 min in the blood, and a volume of distribution of 4244 mL/kg suggesting an efficient distribution of the compound in the animal tissues. To evaluate the efficacy of E260 on tumor growth, SW620 cells are subcutaneously introduced into immuno-compromised “Nude” mice. Administration of E260 leads to a significant attenuation of tumor progression throughout the experiment, and to a 10-fold decrease in average tumor volume after 22 days of treatment. To further demonstrate the anti-cancer activity of E260 in vivo, mice bearing SW48 cells derived xenografts are treated with E260 and the tumor progression profiles are determined. Mice treated with E260 demonstrate a 5-6-fold attenuation in tumors progression when compared to the control treated group[1].

Name: PAC, CAS: 2158322-33-7, stock 7.6g, assay 98.3%, MWt: 1674.93, Formula: C94H107N13O16, Solubility: DMSO : 100 mg/mL (59.70 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others;Antibody-drug Conjugate/ADC Related;PROTAC, Target: Estrogen Receptor/ERR;PROTAC-linker Conjugate for PAC;PROTAC-linker Conjugate for PAC, Biological_Activity: PAC, consists the ADCs linker and PROTACs, conjugated to an antibody. PAC extracts from patent WO2017201449A1, compound LP2. PAC conjugated to an antibody is a more marked estrogen receptor-alpha (ERα) degrader compared to PROTAC (without Ab).
IC50 & Target: Estrogen receptor-alpha (ERα)[1]
In Vitro: Treatment of HER2 expressing cells with HER2 antibody containing PAC Anti-HER2(Endox-XIAP) results in a marked decreased Estrogen Receptor-alpha (ERα) levels with an IC50 of 132 ng/mL. The PROTAC-Antibody Conjugate (PAC) molecules comprise an antibody conjugated via a linker (L1) to a PROTAC, wherein the PROTAC comprises an ubiquitin E3 ligase binding group (“E3LB”), a linker (“L2”) and a protein binding group (“PB”). The following sections describe the components that comprise the PAC. To obtain a PAC having potent efficacy and a desirable therapeutic index, the following components are provided. 1. Antibody (Ab): The antibody portion of a PAC can target a cell that expresses an antigen whereby the antigen specific PAC is delivered intracellularly to the target cell, typically through endocytosis While PACs that comprise an antibody directed to an antigen that is not found on the cell surface may result in less specific intracellular delivery of the PROTAC portion into the cell, the PAC may still undergo pinocytosis. 2. Linkers (L1): A“linker” (L1) is a bifunctional or multifunctional moiety that can be used to link one or more PROTAC moieties (D) to an antibody (Ab) to form a PAC. In some embodiments, PACs can be prepared using a L1 having reactive functionalities for covalently attaching to the PROTAC and to the antibody. 3. PROTAC(D) [1].

Name: Prohydrojasmon racemate Propyl dihydrojasmonate, CAS: 158474-72-7, stock 1.5g, assay 98.5%, MWt: 254.37, Formula: C15H26O3, Solubility: DMSO : ≥ 54 mg/mL (212.29 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Prohydrojasmon racemate is a synthesized plant gowth regulator.
In Vitro: Prohydrojasmon racemate (n-propyl dihydrojasmonate, PDJ) is a functional analogue of Jasmonic acid (JA) [1]. Prohydrojasmon racemate (n-propyl dihydrojasmonate, PDJ) is a plant growth promoter[2].

Name: 6-(γ,γ-Dimethylallylamino)purine N6-(2-lsopentenyl)adenine, CAS: 2365-40-4, stock 15.9g, assay 98.3%, MWt: 203.24, Formula: C10H13N5, Solubility: DMSO : 60 mg/mL (295.22 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-(γ,γ-Dimethylallylamino)purine is a plant growth substance.
In Vitro: Derivative UV spectroscopic data show that the plant growth substances 6-(γ,γ-Dimethylallylamino)purine (N6-(delta 2-isopentenyl) adenine, i6Ade)and indolylacetic acid (IAA) can bind to the yeast alcohol dehydrogenase (ADH) and affect coenzyme-enzyme binding. At fixed ethanol concentrations (27.8 and 111.1 mM) and varying NAD+ concentrations (0.033-2 mM), as well as at fixed levels of coenzyme (0.67 and 2 mM), and at varying concentrations of ethanol (1.4-111.1 mM), the rate of ethanol oxidation is significantly inhibited by i6Ade and IAA. The kinetics of the ADH reaction is affected by two inhibition constants (Ki and Ki') which correspond to the dissociation constants of complexes EI and ESI, respectively. For i6Ade the Ki=0.52±0.06 mM and Ki'=0.74±0.07 mM, and for IAA the Ki=0.88±0.03 mM and Ki'=0.99±0.02 mM[1].

Name: Meta-Topolin m-Topolin, CAS: 75737-38-1, stock 13.7g, assay 98.6%, MWt: 241.25, Formula: C12H11N5O, Solubility: DMSO : ≥ 60 mg/mL (248.70 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Meta-Topolin (m-Topolin) is a highly active aromatic cytokinin.
In Vitro: Meta-Topolin is first isolated from poplar leaves. Meta-Topolin is a natural constituent of plant tissues, together with its 9-β-D-ribofuranosyl and 9-β-v-glucopyranosyl derivatives. Meta-topolin is more active than zeatin and benzyladenine in the promotion of shoot formation in plant tissue cultures[1]. In Spathiphyllum floribundum, shoot production in media with BAP and meta-topolin is very similar[2].

Name: Folcisteine 3-Acetylthiazolidine-4-carboxylic acid, CAS: 5025-82-1, stock 32.5g, assay 98.8%, MWt: 175.21, Formula: C6H9NO3S, Solubility: DMSO : ≥ 160 mg/mL (913.19 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Folcisteine is a plant growth regulator.
In Vivo: Folcisteine has radio-protective effect when administered before radiation with 700 rads.

Name: Chitosan oligosaccharide COS, CAS: 148411-57-8, stock 7.1g, assay 98.1%, MWt: 1000, Formula: N/A, Solubility: H2O : 50 mg/mL (Need ultrasonic); DMSO : 50 mg/mL (Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: Chitosan oligosaccharide (COS) is an oligomer of β-(1→4)-linked D-glucosamine. Chitosan oligosaccharide (COS) activates AMPK and inhibits inflammatory signaling pathways including NF-κB and MAPK pathways.
IC50 & Target: AMPK[1]
In Vitro: Chitosan oligosaccharide (COS) represents a class of natural polymers that holds therapeutic promise in several diseases due to not only its physiochemical properties including water-solubility and low viscosity but also its favorable pharmacological properties including good pharmacokinetics and safety profiles and diverse beneficial biological activities. Activation of AMPK and inhibition of inflammatory signaling pathways including NF-κB and MAPK pathways are recognized as major mechanisms responsible for several effects of Chitosan oligosaccharide (COS) including anti-inflammation, anti-cancer, and anti-diabetes. COS can interrupt cancer progression at multiple stages by modulating several signaling proteins/pathways including NF-κB, AMPK, mTOR, caspase-3, CD147, MMP-2, MMP-9, and VEGF. In vitro experiments have demonstrated that Chitosan oligosaccharide (COS) induced the death of several cancer cell types including ascites, bladder cancer, prostate cancer, lung cancer, liver cancer, leukemia, cervical cancer and colorectal cancer. The values of IC50 of Chitosan oligosaccharide (COS) in inducing cytotoxicity are 25 μg/mL-50 μg/mL depending on types of cancer cells[1].
In Vivo: The oral administration of Chitosan oligosaccharide (16 mg/kg/day) suppresses the production of the proinflammatory cytokines involved in allergic reactions, i.e., IL-4, IL-13 and TNF-α, in the lung tissues and bronchoalveolar lavage fluid of the mice. Last, an anti-inflammatory effect of Chitosan oligosaccharide (COS) on lymphocyte activation has been documented in a rat model of autoimmune anterior uveitis induced by immunization with bovine melanin-associated antigen[1]. Chitosan oligosaccharide (COS) inhibits UV-induced macroscopic appearance in mice skin. Compared with healthy dorsal skin with smoothness and some shallow wrinkles of hairless mice in normal control group, UV exposure for 10 weeks triggers skin erythema, dry, thickening, sagging and coarse wrinkles, and even leathery appearance and slight flesh-colored lesion in the model mice, the visual score of which is markedly higher than that of the normal control group (p<0.05), indicating that UV induces photoaging in skin surface[2].

Name: SLV-2436 SEL201-88;SEL-201, CAS: 2095704-43-9, stock 17.4g, assay 98.3%, MWt: 350.80, Formula: C19H15ClN4O, Solubility: DMSO : ≥ 100 mg/mL (285.06 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MNK, Biological_Activity: SLV-2436 is a highly potent and ATP-competitive inhibitor of MNK1 and MNK2 with IC50s of 10.8 nM and 5.4 nM, respectively.
IC50 & Target: IC50: 5.4 nM (MNK2),10.8 nM (MNK1)[1]
In Vitro: To confirm the kinome selectivity of SLV-2436 (SEL201), the broad KINOMEscan competitive binding assay is performed at 1 μM, which includes 450 distinct kinases. The observed binding profile for SLV-2436 is significantly concentrated in the CAMK family of kinases that comprises MNK1 and MNK2. SLV-2436-treated KIT-mutant melanoma cells have lower oncogenicity and reduced metastatic ability[1].
In Vivo: To investigate the pharmacodynamic properties of SLV-2436 (SEL201), 5 consecutive oral doses of 10, 25, and 50 mg/kg are administered to mice every 12 hours (twice-daily schedule). At the 10 mg/kg twice-daily dosage, 4 hours after the fifth administration, a low plasma concentration of 125 ng/mL SLV-2436 is determined. However, dosing at 25 and 50 mg/kg twice daily, equivalent to 50 and 100 mg/kg/d of SLV-2436, yields substantially increased dose-dependent plasma exposure, reaching an average level of 1,299 ng/mL and 2,075 ng/mL, respectively. At the 24-hour time point, SLV-2436 is still detectable in the plasma, with dose-dependent concentrations of 9, 73, and 124 ng/mL in the 10, 25, and 50 mg/kg twice-daily treatment groups. Oral (p.o.) administration of SLV-2436 at the dosage of 50 mg/kg twice daily, that is, 100 mg/kg/d, for 37 days is well tolerated in mice[1].

Name: KRN2, CAS: 248260-75-5, stock 26.6g, assay 98.7%, MWt: 479.93, Formula: C27H23ClFNO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KRN2 is a selective inhibitor of nuclear factor of activated T cells (NFAT5), with an IC50 of 100 nM. KRN2 has potential to treat NFAT5-mediated Chronic Arthritis[1].
IC50 & Target: IC50: 100 nM (NFAT5)[1].
In Vitro: KRN2 selectively suppresses the expression of pro-inflammatory genes, including Nos2 and Il6, without hampering high-salt-induced NFAT5 and its target gene expressions[1]. 
KRN2 dose-dependently inhibits the NF-κB p65 binding to Nfat5 promoter 1 and directly blocks the interaction between NF-κB p65 and its DNA binding sequence in the upstream site (base pairs -3000 to +1) of Nfat5 exon 1[1].
In Vivo: KRN2 (3 mg/kg, i.p., daily for 2 weeks) effectively suppresses AIA in which innate immune cells play a predominant role[1]. 
KRN2 (3 mg/kg, i.p., daily) effectively suppresses CIA as well as AIA in mice, decreasing the production of pro-inflammatory cytokines and autoantibodies as well as macrophage infiltration[1].

Name: KRN5, CAS: 1800465-47-7, stock 33.9g, assay 98%, MWt: 459.47, Formula: C27H22FNO5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 6 mg/mL (13.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KRN5, a derivative of KRN2, is an oral active Nuclear factor of activated T cells 5 (NFAT5) suppressor, with an IC50 of 750 nM. KRN5 has potential to treat NFAT5-mediated Chronic Arthritis[1].
IC50 & Target: IC50: 750 nM (NFAT5)[1].
In Vitro: KRN5 is less toxic than BBR as determined by a cytotoxicity assay, hERG K+ channel assay, cytochrome inhibition assay, and liver microsomal metabolic stability test, which makes it a potential drug candidate[1]. 
KRN5 at a concentration of 1 μM inhibits the expressions of NFAT5, IL-6,MCP-1, and GM-CSF,which are NFAT5 target molecules, in RAW264.7 macrophages stimulated with LPS[1]. 
In Vivo: Oral feeding of KRN5 (15 mg/kg and 60 mg/kg) every other day for 3 weeks from day 21 dose-dependently mitigates arthritis severity[1]. 
The concentration of serum anti-type II collagen IgG also significantly decreases in the sera of KRN5-treated mice. TNF-α and IL-6 production by LPS-stimulated splenocytes are significantly lower in KRN5-treated CIA mice than in vehicle-treated mice[1].

Name: AGI-24512, CAS: 2201066-53-5, stock 38.2g, assay 98.3%, MWt: 400.47, Formula: C24H24N4O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (312.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AGI-24512 is a methionine adenosyltransferase 2A (MATA2 ) inhibitors useful for treatment of cancer. AGI-24512 blocks growth of MTAP-deleted cancer cells in vitro.
IC50 & Target: MATA2[1]

Name: MAT2A inhibitor 1, CAS: 2201057-10-3, stock 12.5g, assay 98.3%, MWt: 526.61, Formula: C31H22N6OS, Solubility: DMSO : 5 mg/mL (9.49 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MAT2A inhibitor 1 is a methionine adenosyltransferase 2A (MATA2) inhibitor with an IC50 less than l00 nM[1].
IC50 & Target: MATA2[1]
In Vitro: MAT2A inhibitor 1 (Compound 196) is a safe and effective compound that prevents and manages cancers while reducing or avoiding the toxicities and/or side effects associated with the conventional therapies. The cancers include those that are refractory to standard treatments, such as surgery, radiation therapy, chemotherapy and hormonal therapy[1].

Name: Palmitodiolein Triglyceride POO; Glycerol dioleate palmitate; 1,2-Dioleoyl-3-palmitoylglycerol, CAS: 2190-30-9, stock 3.7g, assay 98.3%, MWt: 859.39, Formula: C55H102O6, Solubility: DMSO : 12.5 mg/mL (14.55 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Palmitodiolein (Triglyceride POO) is a triacylglycerol which is present in vegetable oils.

Name: TAO Kinase inhibitor 1, CAS: 850467-66-2, stock 7.9g, assay 98.6%, MWt: 384.47, Formula: C25H24N2O2, Solubility: DMSO : 62.5 mg/mL (162.56 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TAO Kinase inhibitor 1 (compound 43) is a selective, ATP-competitive thousand-and-one amino acid kinases (TAOK) inhibitor with IC50s of 11 to 15 nM for TAOK1 and 2, respectively. TAO Kinase inhibitor 1 delays mitosis and induces mitotic cell death[1].
In Vitro: TAO Kinase inhibitor 1 delays mitosis and induces mitotic cell death in centrosome amplified breast cancer cells[1].

Name: Ensartinib hydrochloride X-396 hydrochloride, CAS: 2137030-98-7, stock 13.3g, assay 98.8%, MWt: 634.36, Formula: C26H29Cl4FN6O3, Solubility: H2O : 33.33 mg/mL (52.54 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;ALK, Biological_Activity: Ensartinib hydrochloride (X-396 hydrochloride) is a potent and dual ALK/MET inhibitor with IC50s of <0.4 nM and 0.74 nM, respectively.
IC50 & Target: IC50: <0.4 nM (ALK), 0.74 nM (MET)[1]
In Vitro: Ensartinib (X-396) is a potent and dual ALK/MET inhibitor with IC50s of <0.4 nM and 0.74 nM, respectively. Ensartinib is potent in H3122 lung cancer cells harboring EML4-ALK E13;A20 (IC50: 15 nM). Ensartinib is also potent in H2228 lung cancer cells harboring EML4-ALK E6a/b; A20 (IC50: 45 nM). Furthermore, X-376 is potent in SUDHL-1 lymphoma cells harboring NPM-ALK (IC50: 9 nM)[1].
In Vivo: Ensartinib (X-396) shows substantial bioavailability and moderate half-lives in vivo. Nude mice harboring H3122 xenografts are treated with Ensartinib at 25 mg/kg bid. Ensartinib significantly delays the growth of tumors compared to vehicle alone. In the xenograft experiments, Ensartinib appears well-tolerated in vivo. Mouse weight is unaffected by Ensartinib treatment. Drug-treated mice appear healthy and do not display any signs of compound related toxicity. To further assess potential side effects of Ensartinib, additional systemic toxicity and toxico-kinetic studies are performed in Sprague Dawley (SD) rats. Following 10 days of repeated oral administration of Ensartinib at 20, 40, 80 mg/kg in SD rats, all animals survive to study termination. The no significant toxicity (NST) levels are determined to be 80 mg/kg for Ensartinib. At NST levels, Ensartinib achieves an AUC of 66 μM×hr and a Cmax of 7.19 μM[1].

Name: JH-VIII-157-02, CAS: 1639422-97-1, stock 12.3g, assay 98.8%, MWt: 465.55, Formula: C28H27N5O2, Solubility: DMSO : ≥ 25 mg/mL (53.70 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: ALK, Biological_Activity: JH-VIII-157-02 is a structural analogue of alectinib, acts as an ALK inhibitor, and shows an IC50 of 2 nM for echinoderm microtubule-associated protein-like 4-ALK (EML4-ALK) G1202R in cells.
IC50 & Target: IC50: 2 nM (EML4-ALK G1202R, cell assay), 2 nM (EML4-ALKwt, cell assay), 2 nM (EML4-ALK C1156Y, cell assay), 2 nM (EML4-ALK F1174L, cell assay), 2 nM (EML4-ALK F1174L, cell assay)[1]
In Vitro: JH-VIII-157-02 is a structural analogue of alectinib, acts as an ALK inhibitor, and shows an IC50 of 2 nM for echinoderm microtubule-associated protein-like 4-ALK (EML4-ALK) G1202R in cells. JH-VIII-157-02 also potently inhibits EML4-ALKwt (Eawt), EAC1156Y, EAF1174L, EAS1206Y (IC50, 2 nM), EAG1269A (IC50, 3 nM), EAL1196M (IC50, 58 nM), EA1151Tins (IC50, 107 nM), and EAL1152R (IC50, 196 nM). Moreover, JH-VIII-157-02 has selectivity at other kinases, including IRAK1, CLK4, RET, RET V804L, RET V804M and IRAK 4, and the IC50s are 14 nM, 14 nM, 3 nM, 13 nM, 12 nM, and 465 nM respectively. JH-VIII-157-02 exhibits inhibitory growth of cancer cell lines, such as H3122, DFCI76 (L1152R] with EC50s of 5, 19 nM, respectively[1].
In Vivo: JH-VIII-157-02 exhibits good oral bioavailability following an oral dose of 10 mg/kg in mice. JH-VIII-157-02 also penetrates the CNS of mice[1].

Name: AB-423, CAS: 1572510-80-5, stock 38g, assay 98.6%, MWt: 386.39, Formula: C17H17F3N2O3S, Solubility: DMSO : 83.3 mg/mL (215.59 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HBV, Biological_Activity: AB-423 is an inhibitor of HBV capsid assembly, and potent inhibits HBV replication with EC50/EC90 of 0.08-0.27 μM/0.33-1.32 μM in cells.
IC50 & Target: HBV capsid[1]
In Vitro: AB-423 is an inhibitor of HBV capsid assembly. AB-423 shows inhibitory effect on rcDNA production in AML12-HBV10 and HepDE19 cells with EC50s of ∼0.260 μM. AB-423 also suppresses cccDNA formation-dependent HBeAg production in the HepBHAe82 assay with an EC50 of 0.267 μM and inhibits HBV DNA levels in culture supernatants of HepG 2.2.15 cells with an EC50 of 0.134 μM. However, AB-423 has no cytotoxicity in any of the three cell lines[1].
In Vivo: AB-423 (30 and 100 mg/kg, p.o. bid) blocks HBV replication in a mouse model of HBV. AB-423 (100 mg/kg, p.o. bid) with entecavir (ETV, 100 ng/mg, qd, p.o.) or 0.1 mg/kg dose of ARB-1467 potently inhibits serum HBV DNA in an HDI model of HBV in immunodeficient NOD-SCID mice[1].

Name: TP0463518, CAS: 1558021-37-6, stock 30.1g, assay 98.8%, MWt: 431.83, Formula: C20H18ClN3O6, Solubility: DMSO : ≥ 125 mg/mL (289.47 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIF/HIF Prolyl-Hydroxylase, Biological_Activity: TP0463518 is a potent hypoxia-inducible factor prolyl hydroxylases (PHDs) inhibitor with a Ki value of 5.3 nM for human PHD2. TP0463518 also inhibits human PHD1/PHD3 with IC50s of 18 and 63 nM as well as monkey PHD2 with an IC50 value of 22 nM[1].

Name: ZL0420, CAS: 2230496-80-5, stock 13.4g, assay 98.8%, MWt: 296.32, Formula: C16H16N4O2, Solubility: DMSO : 125 mg/mL (421.84 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: ZL0420 is a potent and selective bromodomain-containing protein 4 (BRD4) inhibitor with IC50 values of 27 nM against BRD4 BD1 and 32 nM against BRD4 BD2.
IC50 & Target: IC50: 27 nM (BRD4 BD1), 32 nM (BRD4 BD2)[1]
In Vitro: ZL0420 is well docked into the acetyl-lysine (KAc) binding pocket of BRD4, forming key interactions including the critical hydrogen bonds with Asn140 directly and Tyr97 indirectly via a H2O molecule. ZL0420 exhibits submicromolar potency of inhibiting the TLR3-dependent innate immune gene program, including ISG54, ISG56, IL-8, and Groβ genes in cultured human small airway epithelial cells (hSAECs) with IC50s of 0.49-0.86 µM[1].
In Vivo: ZL0420 demonstrates potent efficacy reducing airway inflammation in a mouse model with low toxicity. ZL0420 displays high efficacy and almost completely blocks the profound accumulation of neutrophils around the small and medium sized airways induced by poly(I:C) administration[1].

Name: MS4078, CAS: 2229036-62-6, stock 13.6g, assay 98.6%, MWt: 914.47, Formula: C45H52ClN9O8S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 250 mg/mL (273.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;PROTAC, Target: ALK;PROTAC, Biological_Activity: MS4078 is an anaplastic lymphoma kinase (ALK) PROTAC (degrader) with a Kd of 19 nM for binding affinity to ALK[1].
IC50 & Target: Kd: 19±3 nM (ALK)[1] 
PROTAC[1]
In Vitro: MS4078 effectively inhibits cancer cell proliferation. MS4078 (10-3, 10-2.5, 10-2, 10-1.5, 10-1, 10-0.5, 1 μM; 3 days) concentration-dependently inhibits proliferation of SU-DHL-1 cells with an IC50 of 33±1  nM. In comparison with SU-DHL-1 cells, the proliferation of NCI-H2228 cells is less sensitive to MS4078(10-2, 10-1.5, 10-1, 10-0.5, 1, 100.5 μM; 3 days)[1]. 
MS4078 potently reduces the ALK fusion protein levels and inhibits the ALK auto-phosphorylation and down-steam STAT3 phosphorylation in both SU-DHL-1 and NCI-H2228 cells in a concentration-dependent manner. In SU-DHL-1 cells, MS4078 reduces the NPM-ALK protein levels with impressive DC50 (50% degradation) value of 11±2 nM after 16-hour treatment. Over 90% of inhibition of both ALK Y1507 and STAT3 Y705 phosphorylation is achieved at the 100 nM concentration. In NCI-H2228 cells, MS4078 reduces the EML4-ALK protein levels with similar DC50 value of 59 ± 16 nM after 16-hour treatment. At the 100 nM concentration, NCI-H2228 cells reduces more than 90% of EML4-ALK protein levels[1].

Name: PF-06751979, CAS: 1818339-66-0, stock 4.4g, assay 98.8%, MWt: 455.50, Formula: C18H19F2N5O3S2, Solubility: Ethanol : 50 mg/mL (109.77 mM; Need ultrasonic); DMSO : 150 mg/mL (329.31 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Neuronal Signaling, Target: Beta-secretase, Biological_Activity: PF-06751979 is a potent, brain penetrant, β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor with an IC50 of 7.3 nM in BACE1 binding assay.
IC50 & Target: IC50: 7.3 nM (BACE1), 194 nM (BACE2)[1]
In Vitro: PF-06751979 shows improved selectivity over BACE2 (IC50=194 nM) in binding (27-fold) relative to the literature examples and across multiple chemical series in BACE1 program. PF-06751979 also inhibits BACE1 and BACE2 in a fluorescent polarization (FP) assay with IC50s of 26.9 nM and 238 nM, respectively. PF-06751979 has excellent potency at BACE1 in binding or FP assay formats along with cellular activity looking at production of sAPPβ in H4 cells with an IC50 of 5 nM[1].
In Vivo: PF-06751979 displays excellent brain penetration, potent in vivo efficacy, and broad selectivity over related aspartyl proteases including BACE2. Acute administration of PF-06751979 yields a robust dose-responsive and time-dependent reduction of cerebral spinal fluid (CSF) Aβx-40 with peak inhibition at 3 h of >77%. To determine if the reduction in brain and CSF Aβ is maintained during sustained exposure to PF-06751979, a 5 day subchronic study is executed, dosing once daily by subcutaneous (SC) administration (10 or 50 mg/kg/day). Brain and CSF samples are collected on day 5, following the last dose. PF-06751979 produces a dose-responsive and time-dependent inhibition of Aβ42 in mouse brain. At the 50 mg/kg/day dose, maximal brain lowering is 63% at 7 to 9 h. Administration of PF-06751979 (10 or 50 mg/kg/day for 5 days) produces a dose-responsive and time-dependent inhibition of Aβx-40 in mouse CSF resulting in 77% inhibition of CSF at 3 h post-final 50 mg/kg dose[1].

Name: NSC139021 ERGi-USU, CAS: 1147-56-4, stock 25.6g, assay 98.5%, MWt: 255.30, Formula: C13H9N3OS, Solubility: DMSO : ≥ 62 mg/mL (242.85 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NSC139021 (ERGi-USU) is a highly selective inhibitor for the growth of ERG-positive cancer cells with IC50s ranging from 30 to 400 nM.
IC50 & Target: IC50: 30 to 400 nM (ERG-positive cancer cells)[1]
In Vitro: NSC139021 selectively inhibits growth of ERGpositive cancer cell lines with minimal effect on normal prostate or endothelial cells or ERG-negative tumor cell lines. The IC50 of NSC139021 for cell growth inhibition of responsive cell lines range between 30 nM to 400 nM. Combination of NSC139021 with enzalutamide shows additive effects in inhibiting growth of VCaP cells. A screen of kinases reveal that NSC139021 directly bound the ribosomal biogenesis regulator atypical kinase RIOK2 and induces ribosomal stress signature[1].
In Vivo: NSC139021 treatment inhibits growth of ERG-positive VCaP tumor xenografts with no apparent toxicity. Significant (P<0.05, P<0.005) inhibition of tumor growth is noted at day 26 in treatment groups indicating 44% (100 mg/kg) and 65% (150 mg/kg) reduction of tumor burden. At 100 mg/kg and 150 mg/kg, no apparent toxicity including weight loss, lethargy, diarrhea, loss of appetite, respiratory distress, or overall drug related toxicity is observed. [1].

Name: Branebrutinib BMS-986195, CAS: 1912445-55-6, stock 27.6g, assay 98.9%, MWt: 370.42, Formula: C20H23FN4O2, Solubility: DMSO : ≥ 100 mg/mL (269.96 mM), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: Branebrutinib (BMS-986195) is a highly potent, selective covalent, irreversible inhibitor of Bruton’s tyrosine kinase (BTK), with an IC50 of 0.1 nM[1][2].
IC50 & Target: IC50: 0.1 nM (BTK)[1].
In Vitro: BMS-986195 is a potent and highly selective inhibitor of BTK, which acts by covalently modifying an active-site cysteine residue. BMS-986195 is more than 5000-fold selective for BTK over all kinases outside of the Tec family, and selectivity ranges from 9- to 1010-fold within the Tec family. BMS-986195 inactivates BTK in human whole blood with a rapid rate of inactivation (3.5×10-4nM-1•min-1) and potently inhibits antigen-dependent interleukin-6 production, CD86 expression and proliferation in B cells (IC50<1 nM) without effect on antigen-independent measures in the same cells. A similar potency is measured against FcγR-dependent TNF-α production in human cells[1].
In Vivo: In mice, BMS-986195 demonstrates robust efficacy in murine models of RA including CIA and CAIA, protecting against clinically evident disease, histologic joint damage and bone mineral density loss. In both mice and monkeys, maximal efficacy is observed at doses ≤0.5 mg/kg PO QD, which achieves ≥95% inactivation of BTK in vivo. At similar doses, BMS-986195 is also highly protective against nephritis in the NZB/W mouse model of lupus. To investigate the dynamics of BTK inactivation and resynthesis of BTK, cynomolgus monkeys are given single or multiple doses of BMS-986195. 100% peak inactivation of BTK is obtained with a single administration of BMS-986195 at 0.5 mg/kg PO[1].

Name: BOS-172722, CAS: 1578245-44-9, stock 27g, assay 98.2%, MWt: 446.55, Formula: C24H30N8O, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Mps1;Mps1, Biological_Activity: BOS-172722 is an inhibitor of monopolar spindle 1 (MPS1) checkpoint with an IC50 of 2 nM.
IC50 & Target: 2 nM (MPS1)[1].
In Vitro: BOS-172722 is an inhibitor of monopolar spindle 1 (MPS1) checkpoint with an IC50 of 2 nM. BOS-172722 also has potential for the treatment of various forms of breast cancer[1].

Name: IACS-8968 IDO/TDO Inhibitor, CAS: 2144425-14-7, stock 13.8g, assay 98.5%, MWt: 381.35, Formula: C17H18F3N5O2, Solubility: DMSO : 50 mg/mL (131.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Indoleamine 2,3-Dioxygenase (IDO), Biological_Activity: IACS-8968 (IDO/TDO Inhibitor) is a dual IDO and TDO inhibitor, with pIC50s of 6.43 for IDO and <5 for TDO, respectively.
IC50 & Target: pIC50: 6.43 (IDO), <5 (TDO)[1].

Name: PRN1008, CAS: 1575596-29-0, stock 2.1g, assay 98.7%, MWt: 665.76, Formula: C36H40FN9O3, Solubility: DMSO : ≥ 130 mg/mL (195.27 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: PRN1008 is a reversible covalent, selective and oral active inhibitor of Bruton’s Tyrosine Kinase (BTK), with an IC50 of 1.3 nM.
IC50 & Target: 1.3 nM (BTK)[1][2].
In Vitro: PRN1008 is a reversible covalent inhibitor of Bruton’s Tyrosine Kinase (BTK), with an IC50 of 1.3±0.5 nM. PRN1008 is also found to be highly selectively when tested in a panel of 251 other kinases. Cysteine targeting of BTK by PRN1008 results in a slow off-rate demonstrated by retention of 79±2% of binding to BTK in PBMC 18 hours after washing away the compound in vitro. The covalent cysteine binding is completely reversible after denaturation of the target. Anti-IgM induces human B cell proliferation (10% serum) and B cell CD69 expression are inhibited by PRN1008 with IC50 of 5±2.4 nM and 123±38 nM, respectively[2].
In Vivo: In vivo PRN1008 demonstrates enduring pharmacodynamic effects after the compound has cleared from circulation, consistent with extended target residence time. PRN1008 also reverses and completely suppresses collagen-induced arthritis in rats in a dose dependent manner which allows correlation of target occupancy and disease modification[2].

Name: GDC-0575 ARRY-575;RG7741, CAS: 1196541-47-5, stock 20.8g, assay 98.7%, MWt: 378.27, Formula: C16H20BrN5O, Solubility: DMSO : ≥ 50 mg/mL (132.18 mM), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: Checkpoint Kinase (Chk), Biological_Activity: GDC-0575 (ARRY-575, RG7741) is a highly-selective oral small-molecule Chk1 inhibitor with an IC50 of 1.2 nM.
IC50 & Target: 1.2 nM (Chk1)[1]
In Vitro: GDC-0575 is significantly more potent in promoting DNA damage, replication stress and cell death than V158411, LY2603618, and MK-8776 in a panel of melanoma cell lines[1]. GDC-0575 abrogates DNA damage-induced S and G2–M checkpoints, exacerbates DNA double-strand breaks and induces apoptosis in STS cells. GDC-0575 has a synergistic or additive effect together with gemcitabine[2]. CHK1 inhibitor GDC-0575 in combination with AraC enhances the killing of primary acute myeloid leukemia cells ex vivo by inducing apoptosis[3].
In Vivo: GDC-0575 is active at 25 mg/kg as a single agent, but the efficacy is improved at the higher drug dose. GDC-0575 effectively blocks tumor growth in the D20 and C002 xenografts, and the effect is maintained for at least 10 days after the final dose is administered[1].

Name: γ-L-Glutamyl-L-alanine, CAS: 5875-41-2, stock 31.3g, assay 98.7%, MWt: 218.21, Formula: C8H14N2O5, Solubility: H2O : ≥ 50 mg/mL (229.14 mM); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: γ-L-Glutamyl-L-alanine, composed of gamma-glutamate and alanine, is a proteolytic breakdown product of larger proteins.

Name: Tenalisib R Enantiomer RP6530 R Enantiomer, CAS: 1639417-54-1, stock 4.2g, assay 98.2%, MWt: 415.42, Formula: C23H18FN5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tenalisib R Enantiomer is an R enantiomer of Tenalisib.

Name: Prolylleucine ((Benzyloxy)carbonyl)-L-prolyl-D-leucine, CAS: 61596-47-2, stock 35g, assay 98.8%, MWt: 362.42, Formula: C19H26N2O5, Solubility: DMSO : ≥ 100 mg/mL (275.92 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Prolylleucine is a dipeptide containing branched-chain amino acids.
In Vitro: The addition of specific dipeptide containing branched-chain amino acids, such as Prolylleucine, to the growth medium negatively affects cell envelope-associated proteinase (CEP) activity, whereas dipeptides without branched-chain amino acids had no effect on the enzyme's production. To determine if certain peptides are involved in the regulation of CEP biosynthesis, eight specific dipeptides, one tripeptide, and two peptide fractions (LMMP and HMMP) from Casitone are evaluated. The CEP activity levels of L. delbrueckii subsp. lactis CRL 581 grown in MDM supplemented with LMMP are similar to those obtained in cells grown in minimal defined medium (MDM) supplemented with Casitone (99-fold reduction). The addition of leucylglycylglycine (LGG), leucylleucine (LL), leucylproline (LP), or Prolylleucine (PL) (final concentration, 1 mM) to MDM leads to a 6.5-, 7-, 4-, or 3.5-fold reduction in CEP activity, respectively. An increase of up to 5 mM in the concentration of these dipeptides results in a further two- or threefold reduction of CEP activity compared to the activity obtained in the presence of 1 mM of the peptide mentioned above. LGG, LL, LP, and Prolylleucine contain leucine as a branched-chain amino acid (BCAA). In contrast, no effect on CEP activity is observed by the supplementation of MDM with 1 to 5 mM of GT, PA, TG, GM, GP (dipeptides without BCAA), or HMMP. No inhibitory effect on proteinase activity from the presence of high concentrations (10-fold increase) of each of the 20 amino acids in the growth medium is observed. However, a 50-fold increase in BCAA concentration in MDM leads to a repression of proteinase synthesis of 40%. L. delbrueckii subsp. lactis is auxotrophic for BCAA[1].

Name: UDP-GlcNAc Disodium Salt UDP-α-D-N-Acetylglucosamine Disodium Salt, CAS: 91183-98-1, stock 30.3g, assay 99%, MWt: 651.32, Formula: C17H25N3Na2O17P2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: UDP-GlcNAc Disodium Salt (UDP-α-D-N-Acetylglucosamine Disodium Salt) is a donor substrate of O-GlcNAc transferase (OGT).
In Vitro: OGT is a nucleocytoplasmic glycosyltransferase (uridine diphospho-N--acetylglucosamine:polypeptide β-N-acetylglucosaminyltransferase or O-GlcNAc transferase) assigned to the GT41 family in the CAZY (Carbohydrate-Active enZYme) database. Using UDP-GlcNAc Disodium Salt (UDP-GlcNAc) as the donor substrate, this enzyme modifies thousands of proteins by adding a unique N-acetylglucosamine residue onto acceptor substrates mainly confined within cytosol and nucleus[1].

Name: N-Acetylhistamine N-Omega-acetylhistamine, CAS: 673-49-4, stock 23.6g, assay 98.2%, MWt: 153.18, Formula: C7H11N3O, Solubility: DMSO : ≥ 100 mg/mL (652.83 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: N-Acetylhistamine is a histamine metabolite. N-acetylhistamine can be used as a potential biomarker of histidine metabolism for anaphylactoid reactions.
In Vitro: N-Acetylhistamine is an important indice for anaphylactoid reactions[1].

Name: Dianemycin Nanchangmycin (free acid), CAS: 35865-33-9, stock 5.7g, assay 98.9%, MWt: 867.11, Formula: C47H78O14, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 155 mg/mL (178.75 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Dianemycin (Nanchangmycin free acid), produced by Streptomyces nanchangensis NS3226, inhibits gram-positive bacteria[1]. Dianemycin is a broad spectrum antiviral active against Zika virus[2].
IC50 & Target: Bacteria[1] 
Zika virus[2]
In Vitro: Dianemycin (Nanchangmycin) can be used as a growth promotant in poultry and to cure coccidiosis in chickens. Dianemycin is active against drug resistant strains of malaria[1]. 
Dianemycin (Nanchangmycin) as a potent inhibitor of Zika virus (ZIKV) entry across all cell types tested including physiologically relevant primary cells. Dianemycin potently reduces infection of all three strains of ZIKV across all three cell types. The IC50s for infection are between 0.1 and 0.4 μM while Dianemycin has low toxicity in these ranges. In addition, DENV is inhibited by Dianemycin across cell types[2].

Name: JNJ-678 JNJ-53718678, CAS: 1383450-81-4, stock 24.7g, assay 98.8%, MWt: 500.92, Formula: C21H20ClF3N4O3S, Solubility: DMSO : 65 mg/mL (129.76 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: RSV, Biological_Activity: JNJ-678 (JNJ-53718678) is a novel fusion protein inhibitor in clinical trials for the treatment of respiratory syncytial virus (RSV).
IC50 & Target: Fusion protein[1]
In Vitro: JNJ-678 (JNJ-53718678) is a small-molecule respiratory syncytial virus (RSV) fusion inhibitor currently under clinical evaluation in infants hospitalized for RSV infection. JNJ-678 (JNJ-53718678) binds to RSV F protein in its prefusion conformation. JNJ-678 (JNJ-53718678) displays very potent antiviral activity and low cytotoxicity. In addition to its activity against the RSV A2 strain, JNJ-678 (JNJ-53718678) is also highly active against a number of RSV strains from both A and B subtypes. The EC50 in an RSV infection assay using HeLa cells is 460 pM[1].
In Vivo: Oral treatment of neonatal lambs with JNJ-678 (JNJ-53718678), or with an equally active close analog, efficiently inhibits established acute lower respiratory tract infection in the animals, even when treatment is delayed until external signs of respiratory syncytial virus illness have become visible[1].

Name: KO-947, CAS: 1695533-89-1, stock 18.2g, assay 98.5%, MWt: 355.39, Formula: C21H17N5O, Solubility: DMSO : 62.5 mg/mL (175.86 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway, Target: ERK;ERK, Biological_Activity: KO-947 is a potent and selective inhibitor of ERK1/2 kinases with potential clinical utility in MAPK pathway dysregulated tumors.
IC50 & Target: ERK1/2[1]
In Vitro: KO-947 is a 10 nM inhibitor of ERK with at least 50-fold selectivity against a panel of 450 kinases. KO-947 blocks ERK signaling and proliferation of tumor cells exhibiting dysregulation of MAPK pathway signaling, including mutations in BRAF, NRAS or KRAS, at low nanomolar concentrations[1].
In Vivo: In cell-line derived xenograft studies, KO-947 profoundly suppresses ERK signaling for up to five days after a single dose and induces regressions in RAS- and RAF-mutant melanoma, NSCLC and pancreatic cancer models on administration schedules ranging from daily to weekly. Intermittent dosing enables comparable antitumor activity at reduced dose-intensity[1].

Name: UM-164 DAS-DFGO-II, CAS: 903564-48-7, stock 33.3g, assay 98.5%, MWt: 640.68, Formula: C30H31F3N8O3S, Solubility: DMSO : 5 mg/mL (7.80 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;MAPK/ERK Pathway;Autophagy, Target: Src;p38 MAPK;Autophagy, Biological_Activity: UM-164 (DAS-DFGO-II) is a highly potent inhibitor of c-Src with a Kd of 2.7 nM. UM-164 also potently inhibits p38α and p38β.
IC50 & Target: Kd: 2.7 nM (c-Src)[1] 
p38α, p38β[1]
In Vitro: In biochemical assays, UM-164 is a highly potent inhibitor of c-Src with a binding constant comparable with Dasatinib (UM-164 Kd=2.7 nM, Dasatinib Kd=0.7 nM). To confirm that UM-164 is capable of inhibiting the activation of c-Src in vitro, the effect of UM-164 is examined on the c-Src autophosphorylation in two TNBC cell lines (MDA-MB 231 and SUM 149). Inhibition of c-Src autophosphorylation is detected in a concentration- and a time-dependent manner. At 120 minutes, complete abrogation of c-Src autophosphorylation is observed at 50 nM, demonstrating that UM-164 is a potent c-Src inhibitor in vitro. Flow cytometry experiments demonstrate that UM-164 treatment of MDA-MB 231 and SUM 149 increased the proportion of G0-G1 cells by 25% and 28%, respectively, and concurrently decreased the fraction of S cells by 16% and 19%, respectively[1].
In Vivo: A xenograft study is performed using NCr/nude mice implanted with MDA-MB 231 and SUM 149 cell lines. Once the tumors become palpable, the mice are randomized into control and treatment groups. Mice are injected intraperitoneally with either drug (10 and 20 mg/kg in both xenograft studies; a 15 mg/kg dose is added to the SUM 149 xenograft studies) or vehicle every other day (n=5 for each group). At the selected doses of UM-164, there is no significant weight loss or gross abnormalities observed in the treated animals, even after 52 days of treatment. However, tumor growth is significantly inhibited in both the 10 mg/kg and 20 mg/kg dose groups compared with the vehicle-treated group (P<0.026 and P<0.004, respectively)[1].

Name: GLP-1 receptor agonist 1, CAS: 2212020-52-3, stock 2.5g, assay 98.1%, MWt: 882.96, Formula: C48H48F2N10O5, Solubility: DMSO : 125 mg/mL (141.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucagon Receptor, Biological_Activity: GLP-1 receptor agonist 1 is a glucagon-like peptide-1 (GLP-1) receptor agonist extracted from patent WO2018056453A1, Compound 67.
IC50 & Target: GLP-1 receptor[1]

Name: Interferon receptor inducer-1, CAS: 2215120-36-6, stock 1.1g, assay 98.3%, MWt: 254.33, Formula: C12H22N4O2, Solubility: DMSO : ≥ 55 mg/mL (216.25 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: IFNAR, Biological_Activity: Interferon receptor inducer-1 (compound 6) is an interferon (IFN) receptor inducer. Used accordingly in the treatment of a disorder in which the induction of interferon is involved[1].

Name: Adrenomedullin (AM) (1-52), human Human adrenomedullin-(1-52)-NH2, CAS: 148498-78-6, stock 22.3g, assay 98.7%, MWt: 6028.82, Formula: C264H406N80O77S3, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Adrenomedullin (AM) (1-52), human is a 52-amino acid peptide, which affects cell proliferation and angiogenesis in cancer.
In Vitro: To explore the effect of Adrenomedullin (AM) (1-52), human on astroglioma cells, CRT-MG cells are incubated in the absence or presence of Adrenomedullin (AM) (1-52), human (ADM1-52) for 48 h in a medium containing 1% FBS, and wound-healing assay is performed. The number of cells migrating to the wound region significantly increases in the ADM1-52-treated cells, in a dose-dependent manner, compared to the untreated cells[1].

Name: Adipokinetic Hormone (AKH) (24-32), locust, CAS: 53027-55-7, stock 30.9g, assay 98.9%, MWt: 1159.27, Formula: C54H74N14O15, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Adipokinetic Hormone (AKH) (24-32), locust is a peptide hormone isolated from locusts.
In Vitro: Adipokinetic Hormone (AKH) function is pleiotropic, generally involved in energy metabolism. Adipokinetic Hormone (AKH) increases drosophila mortality elicited by entomopathogenic nematodes and affects drosophila locomotion[1].

Name: Adrenomedullin (AM) (13-52), human, CAS: 154765-05-6, stock 31.8g, assay 98.1%, MWt: 4533.10, Formula: C200H308N58O59S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Adrenomedullin (AM) (13-52), human is a 40 amino acid peptide, which acts as an endothelium-dependent vasodilator agent.
In Vitro: The effects of Adrenomedullin (AM) (13-52), human [hADM-(13-52)] are investigated in the rat pulmonary vascular bed and in isolated rings from the rat pulmonary artery (PA). Under conditions of controlled blood flow and constant left atrial pressure when tone is increased with U-46619, injection of hADM-(13-52) produces dose-related decreases in lobar arterial pressure. hADM-(13-52) modulates receptor-mediated, but not voltage-dependent, pulmonary vascular contraction by influencing Ca2+ influx[1].

Name: Glucagon-Like Peptide (GLP) I (7-36), amide, human Human GLP-1-(7-36)-amide, CAS: 107444-51-9, stock 7.5g, assay 98.5%, MWt: 3297.68, Formula: C149H226N40O45, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucagon Receptor, Biological_Activity: Glucagon-Like Peptide (GLP) I (7-36), amide, human is a physiological incretin hormone that stimulates insulin secretion.
In Vitro: The sequence of Glucagon-Like Peptide after residue 7 shows similarities to glucagon and to other biologically active members of the secretin peptide family, particularly glucose-dependent insulinotropic peptide (GIP). This sequence has been especially well preserved, showing 66% nucleotide homology with GLP-1 in the proglucagon of the very primitive anglerfish. This 7-36 sequence of GLP-1 is a potent insulin-releasing peptide in vitro[1]. Glucagon-Like Peptide (GLP) I (7-36), amide is a product of the tissue-specific post-translational processing of the glucagon precursor. It is released postprandially from intestinal endocrine L cells and stimulates insulin secretion. DPP IV is the main degradation enzyme for GLP-l(7 - 36)amide in human serum. Dipeptidyl-peptidase IV can initiate the metabolism of GIP and GLP-1(7-36)amide in human serum[2].
In Vivo: Glucagon-Like Peptide (GLP) I (7-36), amide is a physiological incretin hormone that is released after nutrient intake from the lower gut and stimulates insulin secretion at elevated plasma glucose concentrations. Exogenous GLP-1 (7-36 amide) is an effective means of normalizing fasting plasma glucose concentrations in poorly-controlled Type 2 diabetic subjects[3]. Exogenously administered GLP-1-(7–36)amide is extremely labile in vivo, with more than 80% being cleaved into GLP-1-(9–36)amide after sc or iv administration[4].

Name: PKG drug G1, CAS: 374703-78-3, stock 37.6g, assay 98.4%, MWt: 257.31, Formula: C13H11N3OS, Solubility: DMSO : ≥ 103 mg/mL (400.30 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PKG drug G1 targets C42 of PKG Iα. PKG drug G1 can couple to vasodilation and blood pressure lowering by a C42 PKG Iα-independent mechanism.
IC50 & Target: PKG Iα[1]
In Vivo: PKG drug G1 induces vasodilation of isolated resistance blood vessels and blood pressure lowering in a mouse model of angiotensin II–induced hypertension. PKG drug G1 efficiently relaxes WT but not knockin (KI) vessels, which is then assessed in a murine model of hypertension. PKG drug G1 lowers blood pressure in hypertensive WT, but not KI, mice in vivo. PKG drug G1 is tested in vivo in healthy mice implanted with telemetric devices that allow blood pressure and heart rate to be constantly monitored. PKG drug G1 or vehicle control is administrated by intraperitoneal injection, and the acute impact on hemodynamics assessed. PKG drug G1 administered at 7.4 mg/kg does not decrease blood pressure, but there is a concomitant reflex tachycardia. When this is repeated using 14.8 mg/kg dose of PKG drug G1, again blood pressure is not altered-but this higher dose induces a potentiated increase in heart rate[1].

Name: GSK1904529A, CAS: 1089283-49-7, stock 30.9g, assay 98.4%, MWt: 851.96, Formula: C44H47F2N9O5S, Solubility: DMSO : 50 mg/mL (58.69 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: IGF-1R, Biological_Activity: GSK1904529A is a selective inhibitor of IGF-1R and IR with IC50 of 27 nM and 25 nM, >100-fold more selective for IGF-1R/InsR than Akt1/2, Aurora A/B,B-Raf, CDK2, EGFR etc.
IC50 value: 27/25 nM (IGF1R/IR) [1]
Target: IGF1R/IR
in vitro: GSK1904529A is a reversible, ATP-competitive inhibitor and has enzyme-inhibitor binding values against IGF-1R and IR with Ki of 1.6 nM and 1.3 nM, respectively. GSK1904529A potently inhibits the ligand-induced phosphorylation of IGF-1R and IR at concentrations above 0.01 μM, followed by blocking downstream signaling (AKT, IRS-1, and ERK). GSK1904529A potently inhibits NIH-3T3/LISN, TC-71, SK-N-MC, SK-ES RD-ES cells with IC50 of 60 nM, 35 nM, 43 nM, 61 nM and 62 nM, respectively. GSK1904529A also inhibits other multiple myeloma and Ewing's sarcoma cell lines including NCI-H929, MOLP-8, LP-1 and KMS-12-BM etc. GSK1904529A induces cell cycle arrest at the G1 phase in cell lines COLO 205, MCF-7, and NCI-H929, which are sensitive to GK1904529A [1].
in vivo: GSK1904529A indicates 98% tumor growth inhibition in NIH-3T3/LISN tumor-bearing mice at a dose of 30 mg/kg (orally, twice-daily) and 75% in COLO 205 xenografts mice (once daily). Among HT29 and BxPC3 xenografts, GSK1904529A produces moderate tumor growth inhibition with no side effects at a dose of 30 mg/kg. Meanwhile, GSK1904529A shows minimal effects on blood glucose levels. GSK1904529A (~3.5 μM in blood) completely inhibits IGF-1R phosphorylation. GSK1904529A has been implicated in treatment of various IGF-1R-dependent tumors including prostate, colon, breast, pancreatic, ovarian, and sarcomas [1].

Name: (R)-3-Hydroxybutanoic acid, CAS: 625-72-9, stock 20.6g, assay 98.9%, MWt: 104.10, Formula: C4H8O3, Solubility: H2O : ≥ 25 mg/mL (240.15 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (R)-3-Hydroxybutanoic acid is a metabolite, and converted from acetoacetic acid catalyzed by 3-hydroxybutyrate dehydrogenase.
In Vitro: (R)-3-Hydroxybutanoic acid (D-3-Hydroxybutyric acid) is a metabolite, and converted from acetoacetic acid. Enhanced hepatic fatty acid oxidation results in the increased production of acetoacetic acid which is in turn converted to (R)-3-Hydroxybutanoic acid by a reaction catalyzed by 3-hydroxybutyrate dehydrogenase[1].

Name: VU0467154, CAS: 1451993-15-9, stock 4.7g, assay 98.4%, MWt: 444.45, Formula: C17H15F3N4O3S2, Solubility: DMSO : ≥ 125 mg/mL (281.25 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: VU0467154 is a positive allosteric modulator of the M4 muscarinic acetylcholine receptor (mAChR), potentiating the response to ACh with pEC50s of 7.75, 6.2 and 6 for rat, human and cynomolgus monkey M4 receptor, respectively.
IC50 & Target: pEC50: of 7.75 (Rat M4 receptor), 6.2 (Human M4 receptor), 6 (Cynomolgus monkey M4 receptor)[1]
In Vitro: VU0467154 is a positive allosteric modulators of the M4 muscarinic acetylcholine receptor (mAChR), robustly potentiates the response to ACh with pEC50s of 7.75, 6.2 and 6 for rat, human and cynomolgus monkey (cyno) M4 receptor, respectively. VU0467154 does not potentiate the ACh response at rat and human M1, M2, M3, or M5[1].
In Vivo: VU0467154 (1-56.6 mg/kg, p.o. or i.p.) reverses amphetamine-induced hyperlocomotion in rats. VU0467154 (0.3-30 mg/kg, i.p.) reverses amphetamine- and MK-801-induced hyperlocomotion in wild-type but not M4 KO mice. VU0467154 alone also enhances the acquisition of both contextual and cue-mediated fear conditioning in wild-type mice[1].

Name: Shield-1, CAS: 914805-33-7, stock 23.6g, assay 98.5%, MWt: 748.90, Formula: C42H56N2O10, Solubility: DMSO : ≥ 250 mg/mL (333.82 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Apoptosis;Autophagy, Target: FKBP;FKBP;FKBP, Biological_Activity: Shield-1 is a specific, cell-permeant and high-affinity ligand of FK506-binding protein-12 (FKBP), and reverses the instability by binding to mutated FKBP (mtFKBP), allowing conditional expression of mtFKBP-fused proteins. Shield-1 can stabilize the entire fusion protein[1][2].

Name: ARQ 531, CAS: 2095393-15-8, stock 8.8g, assay 99%, MWt: 478.93, Formula: C25H23ClN4O4, Solubility: DMSO : ≥ 50 mg/mL (104.40 mM), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: ARQ 531 is a reversible non-covalent inhibitor of Bruton’s Tyrosine Kinase (BTK), with IC50s of 0.85 nM and 0.39 nM for WT-BTK and C481S-BTK, respectively.
IC50 & Target: IC50: 0.85 nM (WT-BTK), 0.39 nM (C481S-BTK)[1].
In Vitro: ARQ 531 shows strong target inhibition in TMD8 cell line. The IC50 values are 0.85 nM and 0.39 nM for WT-BTK and C481S-BTK, respectively, in biochemical assay. Additionally, ARQ 531 also shows strong inhibition of TEK kinases with IC50s of 5.23 nM (BMX), 5.80 nM (TEC), 36.4 nM (TXK). The IC50s of ARQ 531 for SRC kinases are 3.86 nM (LCK), 4.22 nM (YES), 9.71 nM (BLK), 18.3 nM (HCK), 18.8 nM (LYNa), 25.9 nM (FGR), 32.2 nM (FYN), 48.0 nM (FRK) and for TRK kinases are 11.7 nM (TrkB), 13.1 nM (TrkA), 19.1 nM (TrkC). ARQ 531 inhibits proliferation of diverse types of cell lines (TMD8: GI50=1.7 nM, REC1: GI50=0.55 nM) and shows potency in cell lines that are addict to BCR, Src-family kinase and PI3K/AKT pathways.
In Vivo: ARQ 531 is efficacious in TMD-8 tumor xenograft model. ARQ 531 causes complete tumor regression after 14 days of treatment. ARQ 531 is also efficacious in collagen induced arthritis model. ARQ 531 demonstrates potent efficacy against arthritis in mouse model. In the BTK driven TMD8 xenograft mouse model, ARQ 531 demonstrates excellent anti-tumor activity with durable response. ARQ 531 demonstrates in vivo efficacy in a mouse collagen-induced arthritis (CIA) model[1].

Name: MIK665 S-64315, CAS: 1799631-75-6, stock 30.1g, assay 98.2%, MWt: 875.41, Formula: C47H44ClFN6O6S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 125 mg/mL (142.79 mM), Clinical_Informat: Phase 1, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: MIK665 (S-64315) is a special Mcl-1 inhibitor extracted from patent WO2016207225A1, compound Preparation 13, has an IC50 of 1.81 nM[1].
IC50 & Target: IC50: 1.81 nM (Mcl-1)[1]
In Vitro: MIK665 (S-64315) inhibits H929 cell with an IC50 of 250 nM[1].

Name: O-304, CAS: 1261289-04-6, stock 5.6g, assay 98.6%, MWt: 380.25, Formula: C16H11Cl2N3O2S, Solubility: DMSO : 30 mg/mL (78.90 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: O-304 is a first-in-class, orally available pan-AMPK activator, which increases AMPK activity by suppressing the dephosphorylation of pAMPK. O-304 exhibits a great potential as a drug to treat type 2 diabetes (T2D) and associated cardiovascular complications [1][2].
IC50 & Target: AMPK[1]
In Vivo: O-304 increases glucose uptake in skeletal muscle, reduced β cell stress, and promoted β cell rest in diet-induced obese mice. O-304 reduces fasting plasma glucose levels and homeostasis model assessment of insulin resistance (HOMA-IR) in a proof-of-concept phase IIa clinical trial in type 2 diabetes (T2D) patients on Metformin[2].

Name: Diethyl aminoethyl hexanoate citrate DA-6 citrate;2-Diethylaminoethyl hexanoate citrate, CAS: 220439-24-7, stock 25.4g, assay 98.9%, MWt: 407.46, Formula: C18H33NO9, Solubility: DMSO : ≥ 125 mg/mL (306.78 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diethyl aminoethyl hexanoate citrate is a compound that is widely used as a plant growth regulator.
In Vitro: Diethyl aminoethyl hexanoate citrate is used as a plant growth regulator, stimulates the regeneration of adventitious buds[1]. Diethyl aminoethyl hexanoate (DA-6, 1 μM) with EDTA effectively causes the Cd extraction. Diethyl aminoethyl hexanoate fixes more Cd in cell walls and reduces Cd migration in shoot to reduce metal toxicity. Furthermore, Diethyl aminoethyl hexanoate/gibberellic acid 3 in combination with EDTA alleviates the adverse effect of EDTA on plant growth[2].

Name: (1R,2R)-2-PCCA(hydrochloride), CAS: 1609563-71-4, stock 28.3g, assay 98.9%, MWt: 528.56, Formula: C30H39Cl2N3O, Solubility: DMSO : 50 mg/mL (94.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (1R,2R)-2-PCCA hydrochloride is a diastereomer of 2-PCCA, and acts as a potent GPR88 receptor agonist, with an EC50 of 3 nM in cell-free assay, and 603 nM in cell assay.
IC50 & Target: EC50: 3 nM (GPR88 receptor)[1], 603 nM (GPR88 receptor, in GPR88-22F cells)[2]
In Vitro: (1R,2R)-2-PCCA (Example 3) is a potent GPR88 receptor agonist, with an EC50 of 3 nM in cell-free assay, and 603 nM in cell assay[1][2]. (1R,2R)-2-PCCA inhibits GPR88-mediated cAMP production through a Gαi-coupled pathway, with an EC50 of 56 nM in HEK293 cells stably expressing the human GPR88 receptor and the GloSensor-22F cAMP construct[2].

Name: D-Lin-MC3-DMA, CAS: 1224606-06-7, stock 1.3g, assay 98.8%, MWt: 642.09, Formula: C43H79NO2, Solubility: DMSO : ≥ 43.33 mg/mL (67.48 mM); Ethanol : 16.67 mg/mL (25.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: D-Lin-MC3-DMA, an ionizable cationic lipid, is a potent siRNA delivery vehicle.
In Vivo: Lipid nanoparticles (LNPs) containing distearoylphosphatidlycholine (DSPC), and ionizableamino-lipids such as dilinoleylmethyl-4-dimethylaminobutyrate (DLin-MC3-DMA) are potent siRNA delivery vehicles in vivo. LNP-siRNA systems optimize to achieve maximum gene silencing potency in hepatocytesfollowing IV administration in mice contain DLin-MC3-DMA (MC3), DSPC, cholesterol and a polyethyleneglycol (PEG)-lipid at mole ratios of 50/10/38.5/1.5. DLin-MC3-DMA exhibits an optimized pKa value that leads to dramatically enhanced potency[1].

Name: ZINC03129319, CAS: 1777807-64-3, stock 12.1g, assay 98.2%, MWt: 490.51, Formula: C24H14N2O6S2, Solubility: DMSO : 41.67 mg/mL (84.95 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ZINC03129319 is a dengue virus (DENV) NS2B-NS3 protease inhibitor extracted from patent US20150141521A1, has inhibition constants (Ki1) of 92±15 μM and Ki3 of 20±4 μM.
IC50 & Target: Ki1: 92±15 μM (DENV NS2B-NS3 protease)[1] 
Ki3: 20±4 μM (DENV NS2B-NS3 protease)[1]
In Vitro: ZINC03129319 inhibits DENV NS2B-NS3 protease with Ki1 of 92±15 μM and Ki3 of 20±4 μM[1].

Name: Calcitonin, eel Thyrocalcitonin eel, CAS: 57014-02-5, stock 12.3g, assay 98.2%, MWt: 3414.91, Formula: C146H241N43O47S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Calcitonin, eel is the thyroid hormone peptide that contributes to the regulation of calcium homeostasis, widely used in the research of postmenopausal osteoporosis.
In Vitro: Calcitonin, eel effectively induces a concentration-dependent stimulation of phosphoinositide hydrolysis and stimulates prolactin release compared to salmon calcitonin in cultured anterior pituitary cells. However, Calcitonin, eel is inactive on the inhibition of prolactin release under thyrotropin releasing hormone (TRH) stimulated conditions[1].

Name: Amylin, amide, rat Amylin (rat), CAS: 124447-81-0, stock 10.7g, assay 98.5%, MWt: 3920.44, Formula: C167H272N52O53S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Amylin, amide, rat is a potent and high affinity ligand of Amylin receptor AMY1 and AMY3 receptors and variably of AMY2 receptors; binding studies are generally used for the latter receptor.
IC50 & Target: Amylin receptor AMY1 and AMY3[1]
In Vitro: Amylin is an important, but poorly understood, 37 amino acid glucoregulatory hormone with great potential to target metabolic diseases. Amylin is a member of the calcitonin (CT) family of peptides, which includes CT itself, the CGRPs comprising two variants (αCGRP and βCGRP), adrenomedullin (AM) and AM2 (intermedin). Amylin is a centrally acting, neuroendocrine hormone synthesized with insulin in the beta cells of pancreatic islets. Amylin regulates glucose homeostasis by inhibiting gastric emptying, inhibiting the release of the counter-regulatory hormone glucagon and inducing meal-ending satiety. Amylin functions as a glucoregulatory and satiety-inducing hormone, which is protective against postprandial spikes in blood glucose and overeating.[1]

Name: β-Amyloid (1-16) Amyloid β-Protein (1-16), CAS: 131580-10-4, stock 28g, assay 98.3%, MWt: 1955.04, Formula: C84H119N27O28, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (1-16) is a β-Amyloid protein fragment involved in metal binding. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
IC50 & Target: Amyloid-β[1]
In Vivo: β-amyloid (1-16) fragment is considered as valid models to examine the contribution of the key histidine residues (His , His in mouse and His , His , His in human fragments) to the Ab–Cu2+ interaction. Oxidation targets for β-Amyloid (1-16) are the histidine residues coordinated to the metal ions. Copper is bound to Aβ in senile plaque of Alzheimer’s disease with β-Amyloid (1-16) taking part in the coordination of the Cu2+ ions. Cu2+ and Zn2+ are linked with the neurotoxicity of -Amyloid and free radical damage[1]. β-amyloid (1-16) is the minimal amino acidic sequence display a Cu coordination mode which involves three Histidines (His6, His13 and His14). β-amyloid (1-16) is supposed to be involved in metal binding[2]. Human β-amyloid interacts with zinc ions through its metal-binding domain 1-16. The C-tails of the two polypeptide chains of the rat Aβ(1-16) dimer are oriented in opposite directions to each other, which hinders the assembly of rat Aβ dimers into oligomeric aggregates. Thus, the differences in the structure of zinc-binding sites of human and rat β-Amyloid (1-16), their ability to form regular cross-monomer bonds, and the orientation of their hydrophobic C-tails could be responsible for the resistance of rats to Alzheimer's disease[3].

Name: [Met5]-Enkephalin, amide 5-Methionine-enkephalin amide, CAS: 60117-17-1, stock 22.7g, assay 98.6%, MWt: 572.68, Formula: C27H36N6O6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: [Met5]-Enkephalin, amide is an agonist for δ opioid receptors as well as putative ζ (zeta) opioid receptors.
IC50 & Target: δ and ζ opioid receptor[1]
In Vitro: [Met5]-Enkephalin at 0.1 nM, 10 nM, and 1 μM significantly reduces the total number of glial cells in culture[1]. [Met5]-Enkephalin, amide acts via δ-opioid receptor to inhibit pelvic nerve-evoked contractions of cat distal colon. [Met5]-enkephalin causes concentration-dependent, reversible inhibition of pelvic nerve-evoked contractions, with an IC50 value of 2.2 nM. [Met5]enkephalin at a concentration (3 nM) which produces a large inhibition of neurogenic contractions, has no effect on contractions to exogenous acetylcholine[2].

Name: ACP-105, CAS: 899821-23-9, stock 26.2g, assay 98.7%, MWt: 290.79, Formula: C16H19ClN2O, Solubility: DMSO : ≥ 103 mg/mL (354.21 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: ACP-105 is an orally available, selective amd potent androgen receptor modulator (SARM), with pEC50s of 9.0 and 9.3 for AR wild type and T877A mutant, respectively.
IC50 & Target: pEC50: 9.0 (AR wild type), 9.3 (AR T877A mutant)[1].
In Vitro: ACP-105 is an orally available, selective amd potent androgen receptor modulator (SARM), with pEC50s of 9.0 and 9.3 for AR wild type and T877A mutant, respectively. The half-lives of ACP-105 (compound 1) in human hepatocytes is measured and found to be 5.0 h[1].
In Vivo: ACP-105 enhances freezing in both sham-irradiated and irradiated mice (effect of ACP-105: F=5.44; p=0.028). For MAP-2 immunoreactivity in the cortex of sham-irradiated mice, there is a brain area×ACP-105 interaction (F=6.655; p=0.0027). While ACP-105 reduces MAP-2 immunoreactivity in the sensorymotor cortex, there is a trend towards increased MAP-2 immunoreactivity in the enthorhinal cortex[2].

Name: β-Amyloid (1-28) Amyloid β-Protein (1-28), CAS: 109770-29-8, stock 4.5g, assay 99%, MWt: 3262.51, Formula: C145H209N41O46, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (1-28) is a β-Amyloid protein fragment involved in metal binding. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
IC50 & Target: Amyloid-β[1]
In Vivo: β-Amyloid (1-28) fragment is considered as valid models to examine the contribution of the key histidine residues (His , His in mouse and His , His , His in human fragments) to the Ab–Cu2+ interaction[1]. Copper binds to β-Amyloid (1-28) at pH 7.4 with an affinity of Ka10 7 M-1[2].

Name: Bradykinin (1-6), CAS: 23815-88-5, stock 7.8g, assay 98.1%, MWt: 659.73, Formula: C30H45N9O8, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: Bradykinin (1-6) is an amino-truncated Bradykinin peptide. Bradykinin (1-6) is a stable metabolite of Bradykinin, cleaved by carboxypeptidase Y (CPY).
In Vivo: Bradykinin (1-6) is a stable metabolite of Bradykinin in rat urine. Bradykinin (BK) is very active in renal function because
it participates in increasing the renal blood flow and in diuresis and natriuresis[1].

Name: [Leu5]-Enkephalin, amide Leu-Enkephalin amide, CAS: 60117-24-0, stock 3.6g, assay 98.2%, MWt: 554.64, Formula: C28H38N6O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: [Leu5]-Enkephalin, amide is a δ opioid receptor agonist.
IC50 & Target: δ opioid receptor[1]
In Vitro: [Leu5]-Enkephalin causes concentration-dependent, reversible inhibition of pelvic nerve-evoked contractions, with an IC50 value of 2.1 nM[2].
In Vivo: Levels of [Leu5]-Enkephalin are significantly increased in the nucleus raphe magnus (NRM) of rats 2 weeks after the injection of complete Freund's adjuvant (CFA) (1.02±0.2 pmol/mg protein) as compared with saline-treated rats (0.49±0.04 pmol/mg protein; p<0.01). Tissue levels of [Leu5]-Enkephalin are uniformly increased in the caudal ventrolateral periaqueductal gray (PAG) 4 hr (1.15±0.25 pmol/mg protein), 4 d (1.16±0.18 pmol/mg protein), and 2 weeks (1.18±0.17 pmol/mg protein) after the injection of CFA as compared with saline-treated rats (0.55±0.03 pmol/mg protein; p<0.05, all times). A smaller increase in the levels of [Leu5]-Enkephalin occurred in the rostral aspect of the ventrolateral PAG at all time points. Finally, levels of [Leu5]-Enkephalin are also increased in the contralateral microcellular tegmental nucleus 4 d after the injection of CFA (0.53±0.04 pmol/mg protein) compared with levels in saline-treated rats (0.38±0.02 pmol/mg protein; p<0.05)[1].

Name: Adrenomedullin (AM) (22-52), human 22-52-Adrenomedullin (human), CAS: 159899-65-7, stock 10.9g, assay 99%, MWt: 3576.04, Formula: C159H252N46O48, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: CGRP Receptor;CGRP Receptor, Biological_Activity: Adrenomedullin (AM) (22-52), human, an NH2 terminal truncated adrenomedullin analogue, is an adrenomedullin receptor antagonist, and also antagonizes the calcitonin generelated peptide (CGRP) receptor in the hindlimb vascular bed of the cat[1][2].
IC50 & Target: Adrenomedullin receptor, CGRP receptor[1]
In Vitro: Adrenomedullin (AM) (22-52), human shows no effect on hindlimb perfusion pressure responses to adrenomedullin (ADM) at 120 nmol. However, Adrenomedullin (AM) (22-52), human selectively and reversibly decreases vasodilator responses to human calcitonin generelated peptide (hCGRP) at 30 nmol, with similar effect to that of CGRP antagonist[1]. 
Adrenomedullin (AM) (22-52), human competitively inhibits the binding of the Adrenomedullin in a dose-dependent manner, inhibits Adrenomedullin -induced cAMP accumulation in rat vascular smooth muscle cells[1].

Name: Amylin (8-37), rat Amylin (8-37) (mouse, rat), CAS: 138398-61-5, stock 1.7g, assay 98.3%, MWt: 3200.61, Formula: C140H227N43O43, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Amylin (8-37), rat is a truncated analog of native Amylin that selectively inhibits insulin-related glucose uptake and glycogen deposition in muscle tissue. Amylin (8-37), rat is a weak amylin receptor (AMY) antagonist.
IC50 & Target: Amylin receptor (AMY)[1]
In Vitro: Amylin (8-37), rat (Rat amylin-(8-37)) enhances insulin action and alters lipid metabolism in normal and insulin-resistant rats. Amylin (8-37) reduces plasma insulin (P<0.001) and enhances several measures of whole body and muscle insulin sensitivity (P<0.05) in both saline- and hGH-infused rats. Amylin-(8-37) corrects hGH-induced liver insulin resistance, increases basal plasma triglycerides and lowers plasma nonesterified fatty acids in both groups, and reduces muscle triglyceride and total long-chain acyl-CoA content in saline-treated rats (P<0.05). In isolated soleus muscle, Amylin (8-37) blocks amylin-induced inhibition of glycogen synthesis but has no effect in the absence of amylin. Thus 1) hyperamylinemia accompanies insulin resistance induced by hGH infusion; 2) Amylin (8-37) increases whole body and muscle insulin sensitivity and consistently reduces basal insulin levels in normal and hGH-induced insulin resistant rats; and 3) Amylin (8-37) elicits a significant alteration of in vivo lipid metabolism[2].

Name: β-Amyloid (22-35) Amyloid β-Protein (22-35), CAS: 144189-71-9, stock 19.7g, assay 98%, MWt: 1403.62, Formula: C59H102N16O21S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (22-35) is a 14-aa peptide, shows aggregates and induces neurotoxicity in the hippocampal cells.
IC50 & Target: Amyloid-β[1]
In Vitro: β-Amyloid (22-35) shows significant cytotoxicity on the rat hippocampal neurons at 40 μg/mL, but exhibits no cytotoxic effect on the glial cells[1].

Name: C-Peptide, dog C-Peptide (dog), CAS: 39016-05-2, stock 20.2g, assay 98.9%, MWt: 3174.47, Formula: C137H225N37O49, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: C-Peptide, dog is a component of proinsulin, released from pancreatic beta cells into blood together with
insulin.
In Vitro: C-Peptide, dog is a component of proinsulin, released from pancreatic beta cells into blood together with
insulin[1]. C-Peptide is used as a marker of insulin secretion[2].

Name: Adrenocorticotropic Hormone (ACTH) (18-39), human CLIP (human), CAS: 53917-42-3, stock 21.8g, assay 98.9%, MWt: 2465.67, Formula: C112H165N27O36, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Adrenocorticotropic Hormone (ACTH) (18-39), human is a corticotropinlike intermediate lobe peptide, which is produced in the melanotrophs of the intermediate lobe of the pituitary.
In Vitro: The ACTH family of polypeptides consists of ACTH(1-39) (adrenocorticotropin), ACTH (1-13)amide (α-melanotropin;α-MSH); and ACTH (18-39) (corticotropinlike intermediate lobe peptide, CLIP). These polypeptides are derived from a common precursor, proopiomelanocortin. In corticotropic cells of the pars distalis, proopiomelanocortin (POMC) undergoes a series of proteolytic cleavage reactions to yield ACTH (1-39) as a major end product. However, in the melanotropic cells of the pars intermedia, an additional set of proteolytic reactions results in the conversion of ACTH (1-39) to ACTH (1-13) amide and ACTH (18-39). In several species of vertebrates, ACTH (1-13) amide undergoes end product modification to yield mono- and diacetylated forms ofα-MSH as major end products in the pars intermedia[1].

Name: Adrenocorticotropic Hormone (ACTH) (1-39), rat ACTH (1-39) (mouse, rat), CAS: 77465-10-2, stock 6.7g, assay 98.2%, MWt: 4582.23, Formula: C210H315N57O57S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: Adrenocorticotropic Hormone (ACTH) (1-39), rat is a potent melanocortin 2 (MC2) receptor agonist.
IC50 & Target: Melanocortin 2 receptor[1]
In Vitro: ACTH 1-39 at concentrations of 100-400 nM has no toxic effect on neurons, while ACTH provides protection from excitotoxic neuronal death induced by glutamate (100 μM), NMDA (1 mM), AMPA (50 μM), and kainate (25 μM). ACTH at 400 nM provides substantial protection in each case. ACTH at either 200 or 400 nM protects neurons from quinolinic acid (25 μM). There is also protection by ACTH from cell death induced by 2 μM H2O2, which gives rise to reactive oxygen species (ROS), with significantly more protection at 400 nM ACTH compared to 200 nM. ACTH gives modest protection against rapid release of nitric oxide (NO) by NOC-12 but not slow release by NOC-18. ACTH (200 or 400 nM) protects neurons from cytotoxic effects of staurosporine (10-20 nM), a classic inducer of cell death via apoptosis. ACTH reduces cell death from 80% to 55%[1].
In Vivo: The icv injection of ACTH significantly reduces cumulative food intake over the observation period compared with the saline/IgG group. The injection of ACTH Ab into the PVN abolishes the anorexigenic effect of ACTH. Infusion icv of ACTH significantly decreases cumulative food intake in rats that receive α-MSH Ab into the PVN and ACTH icv, and food intake is as low as in the group treated with ACTH icv and IgG into the PVN. Injection of either ACTH Ab or α-MSH Ab into the PVN significantly increase cumulative food intake compared with IgG-treated animals; the combined application of both Ab’s do not increase food intake further[2].

Name: Adrenocorticotropic Hormone (ACTH) (4-10), human, CAS: 4037-01-8, stock 35.5g, assay 98.3%, MWt: 962.09, Formula: C44H59N13O10S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Adrenocorticotropic Hormone (ACTH) (4-10), human is a melanocortin 4 (MC4R) receptor agonist.
IC50 & Target: Melanocortin 4 receptor[1]
In Vitro: Adrenocorticotropic Hormone (ACTH) (4-10), human (ACTH (4-10)) is the core sequence of all melanocortins and binds selectively to MC4-R. In humans, ACTH (4-10) enters the cerebral fluid compartment after intranasal application and leads to a decrease in total body fat after 6 weeks of continuous treatment[1].

Name: Calmodulin-Dependent Protein Kinase II (290-309), CAS: 115044-69-4, stock 8.5g, assay 98.1%, MWt: 2273.83, Formula: C103H185N31O24S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Autophagy, Target: CaMK;Autophagy, Biological_Activity: Calmodulin-Dependent Protein Kinase II (290-309) is a potent CaMK antagonist with an IC50 of 52 nM for inhibition of Ca2+/calmodulin-dependent protein kinase II.
IC50 & Target: IC50: 52 nM (calmodulin-dependent protein kinase II)[1]
In Vitro: Peptide 290 to 309 is found to be a potent calmodulin antagonist with an IC50 of 52 nM for inhibition of Ca2+/calmodulin-dependent protein kinase. Neither truncation from the amino terminus (peptide 296-309) nor extension in the carboxyl-terminal direction (peptide 294-319) markedly affects calmodulin binding, whereas shortening the peptide from the carboxyl terminus (peptide 290-302) or from both ends (peptide 295-304) results in the elimination of this activity[1].

Name: Neuropeptide Y (13-36), amide, human Neuropeptide Y (13-36), human, CAS: 122341-40-6, stock 6.2g, assay 98.2%, MWt: 3000.40, Formula: C134H207N41O36S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Neuropeptide Y (13-36), amide, human is a neuropeptide Y receptor agonist.
IC50 & Target: Neuropeptide Y receptor[1]
In Vivo: Intraventricular injections of the Y2 neuropeptide Y receptor agonist porcine Neuropeptide Y (13-36) (25-3000 pM) produces a dose-dependent increase (up to 14%; ED50=0.3 nM for overall effects and 0.97 nM for the peak effects) in mean arterial blood pressure in the awake, unrestrains male rat without affecting heart rate. Central administration of porcine Neuropeptide Y (13-36) produces marked vasodepressor and bradycardic actions in the anaesthetized α-chloralose and in the awake unrestrained male rat[1].

Name: α-Factor Mating Pheromone, yeast Mating Factor α, CAS: 59401-28-4, stock 38g, assay 98.2%, MWt: 1684.00, Formula: C82H114N20O17S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: α-Factor Mating Pheromone, yeast is a tridecapeptide secreted by S. cerevisiae α cells via Ste2p receptor.
IC50 & Target: Ste2p[1]
In Vitro: α-Factor Mating Pheromone, yeast is synthesized constitutively by MATα cells and acting on MATa cells[1]. α-Factor Mating Pheromone, yeast inhibits the division cycle of yeast a cells, and competes for binding of 35S-α-factor to haploid a cells, with Kd of 0.3 μM, and this binding is related to five temperature-sensitive ste2 mutants, and is thermolabile. However, α-Factor Mating Pheromone, yeast binding activity of other temperature-sensitive mutants (ste4, ste5, ste7, ste11, and ste12) shows no thermolability[2].

Name: Bradykinin (1-7) Bradykinin Fragment 1-7, CAS: 23815-87-4, stock 4.6g, assay 98.9%, MWt: 756.85, Formula: C35H52N10O9, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: Bradykinin (1-7) is an amino-truncated Bradykinin peptide. Bradykinin (1-7) is a metabolite of Bradykinin, cleaved by endopeptidase.
In Vitro: The Bradykinin peptide system is a tissue-based system with potent cardiovascular and renal effects. To investigate the regulation of this system, a highly sensitive amino terminal-directed radioimmunoassay that, with high performance liquid chromatography, enables the measurement of Bradykinin-(1-7), Bradykinin-(1-8), and Bradykinin-(1-9), is developed. Together with a carboxy terminal-directed radioimmunoassay, Bradykinin peptides in rat kidney and blood are characterized. The predominant Bradykinin peptides in kidney are Bradykinin-(1-9) (~100 fmol/g wet weight of tissue) and Bradykinin-(1-7) (~70 fmol/g), with low levels of Bradykinin-(1-8) (~8 fmol/g) and Bradykinin-(4-9) (~12 fmol/g) detectable; Bradykinin-(2-9) and Bradykinin-(3-9) are below the limits of detection. In blood, the levels of Bradykinin-(1-9) are very low (~2 fmol/ml), and other Bradykinin peptides are below the limits ofdetection. Administration of the angiotensin converting enzyme (ACE) inhibitor Perindopril is associated with an approximate twofold increase in renal levels of Bradykinin-(1-8) and Bradykinin-(1-9) and a decrease in the Bradykinin-(1-7)/Bradykinin-(1-9) ratio. The amino terminal-directed radioimmunoassay is also applied to heart, aorta, brown adipose tissue, adrenal, lung, and brain. For these tissues, Bradykinin-(1-7) and Bradykinin-(1-9) are of similar abundance (16-340 fmol/g), with lower levels of Bradykinin-(1-8)[1].

Name: Substance P (1-7), CAS: 68060-49-1, stock 25.8g, assay 99%, MWt: 900.04, Formula: C41H65N13O10, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Substance P (7-11) is a fragment of the neuropeptide, substance P (SP). Substance P (7-11) gives depressor and bradycardic effects when applied to the nucleus tractus solitarius.
In Vivo: Substance P (7-11) is found to act as a very potent antagonist against the SP-induced responses and is formed locally in the nigra after SP injection. It is proposed that Substance P (7-11) is an endogenous modulator of SP actions[1]. Injection of low doses of Substance P (7-11) (1.0-4.0 pM simultaneously with SP or SP(5-11) (0.1 nM), reduce aversive behaviours induced by SP or SP(5- 11) significantly. These results indicate that SP(1-7) formed endogenously could modulate the actions of SP or SP(5-11) in the spinal cord[2].

Name: Angiotensinogen (1-14), human, CAS: 104180-23-6, stock 38.8g, assay 98.9%, MWt: 1760.04, Formula: C83H122N24O19, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angiotensinogen (1-14), human is a fragment of the renin substrate angiotensinogen, a precursor for all angiotensin peptides.
In Vitro: Angiotensinogen (AGT) is the only precursor of all angiotensin peptides. Human AGT has 485 amino acids, including a 33 amino-acid signal peptide. The 10 N-terminal amino acids are cleaved by renin to provide angiotensin I (AngI), which is the source for an array of active angiotensin peptides[1].

Name: Pressinoic Acid, CAS: 35748-51-7, stock 19.3g, assay 98.2%, MWt: 774.86, Formula: C33H42N8O10S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pressinoic Acid is a synthetic hexapeptide with potent corticotrophin-releasing activity. Pressinoic Acid is also an oxytocin inhibitor; it induces maternal behavior.
IC50 & Target: Oxytocin[1]
In Vitro: Pressinoic acid, a synthetic hexapeptide that corresponds to the ring of vasopressin, exhibits corticotrophin-releasing activity in vitro in doses of 3 and 30 ng/mL[1].

Name: Bradykinin (1-5), CAS: 23815-89-6, stock 15g, assay 98.7%, MWt: 572.66, Formula: C27H40N8O6, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: Bradykinin (1-5) is a major stable metabolite of Bradykinin, formed by the proteolytic action of angiotensin-converting enzyme (ACE).
In Vivo: Bradykinin is a short-lived vasoactive peptide, with a reported half-life in vivo of 17 s, that is rapidly metabolized in the circulation to Bradykinin (1-5). Bradykinin (1-5), the product of two sequential cleavages of Bradykinin by ACE at the Pro7-Phe8 and Phe5-Ser6bonds, has been identified as the major stable metabolite of Bradykinin in vivo in human subjects, with a terminal half-life of minutes. Both Bradykinin and Bradykinin (1-5) inhibit α- and γ-thrombin-induced platelet aggregation (P<0.01 versus baseline). Bradykinin (1-5) inhibits γ-thrombin-induced platelet aggregation 50% at a calculated dose of 183±3 pmol/min. Neither Bradykinin nor Bradykinin (1-5) affects thrombin receptor-activating peptide-induced platelet aggregation, consistent with the hypothesis that Bradykinin and Bradykinin 1-5 inhibit thrombin-induced platelet aggregation by preventing cleavage of the thrombin receptor and liberation of thrombin receptor-activating peptide. Bradykinin (1-5) significantly attenuates α-thrombin-induced platelet aggregation but not TRAP 1-6-induced platelet aggregation. Bradykinin (1-5) potently inhibits γ-thrombin (500 nM)-induced platelet aggregation with an ED50 of 183±2 pmol/min[1].

Name: OVA Peptide (257-264), CAS: 138831-86-4, stock 29g, assay 98.5%, MWt: 963.13, Formula: C45H74N10O13, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: OVA Peptide (257-264) is a class I (Kb)-restricted peptide epitope of OVA, an octameric peptide from ovalbumin presented by the class I MHC molecule, H-2Kb.
In Vitro: TAP1-I- and C57BL/6 macrophages may process Crl-OVA and full-length OVA in different cellular compartments and that the protein context of the OVA Peptide (257-264) epitope influences the extent of TAP-independent processing for MHC class I presentation. OVA Peptide (257-264) epitope is presented with a differential dependence on the TAP transporter depending on the protein context of the OVA epitope: OVA Peptide (257-264) contained within the MBPCrl-OVA or Crl-OVA bacterial fusion proteins is presented with little dependence on the TAP transporter, while OVA Peptide (257-264) contained within full-length ovalbumin is largely dependent on the TAP transporter, regardless of whether recombinant OVA is expressed in bacteria or the native protein is coupled to polystyrene beads[1].

Name: ORY-1001(trans), CAS: 1431303-72-8, stock 29.5g, assay 98.3%, MWt: 303.27, Formula: C15H24Cl2N2, Solubility: DMSO : 0.69 mg/mL (2.28 mM; Need ultrasonic and warming); H2O : 57.75 mg/mL (190.42 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: ORY-1001 trans is a selective irreversible lysine (K)-specific demethylase 1A (KDM1A/LSD1) inhibitor.
IC50 & Target: KDM1A/LSD1[1]
In Vitro: ORY-1001 trans is a KDM1A inhibitor that inactivate KDM1A by irreversible binding to the flavin adenine nucleotide (FAD) cofactor. ORY-1001 trans has very high selectivity for KDM1A over the MAO enzymes, high selectivity over KDM1B and unrivaled subnanomolar cellular activity in differentiation and colony formation assays on mixed lineage leukemia (MLL)-translocated acute myeloid leukemia (AML) cell lines. ORY-1001 provokes a time and dose-dependent induction of the Cd11b differentiation marker in MLL-AF9 cells, which interestingly preceeds changes in H3K4me2 levels. While MLL-translocated cells are especially sensitive, other acute leukemia (AL) cell lines also respond to ORY-1001 trans[1].
In Vivo: ORY-1001 trans reduces AML tumor growth in mice and rat xenografts and increases survival time in a disseminated model of T-ALL[1].

Name: Bradykinin (2-9) Des-Arg1-bradykinin, CAS: 16875-11-9, stock 15.9g, assay 98.1%, MWt: 904.02, Formula: C44H61N11O10, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: Bradykinin (2-9) is an amino-truncated Bradykinin peptide. Bradykinin (2-9) is a metabolite of Bradykinin, cleaved by Aminopeptidase P.
In Vitro: The Bradykinin peptide system is a tissue-based system with potent cardiovascular and renal effects. To investigate the regulation of this system, a highly sensitive amino terminal-directed radioimmunoassay that, with high performance liquid chromatography, enables the measurement of Bradykinin-(1-7), Bradykinin-(1-8), and Bradykinin-(1-9), is developed. Together with a carboxy terminal-directed radioimmunoassay, Bradykinin peptides in rat kidney and blood are characterized. The predominant Bradykinin peptides in kidney are Bradykinin-(1-9) (~100 fmol/g wet weight of tissue) and Bradykinin-(1-7) (~70 fmol/g), with low levels of Bradykinin-(1-8) (~8 fmol/g) and Bradykinin-(4-9) (~12 fmol/g) detectable; Bradykinin-(2-9) and Bradykinin-(3-9) are below the limits of detection. In blood, the levels of Bradykinin-(1-9) are very low (~2 fmol/ml), and other Bradykinin peptides are below the limits ofdetection. Administration of the angiotensin converting enzyme (ACE) inhibitor Perindopril is associated with an approximate twofold increase in renal levels of Bradykinin-(1-8) and Bradykinin-(1-9) and a decrease in the Bradykinin-(1-7)/Bradykinin-(1-9) ratio. The amino terminal-directed radioimmunoassay is also applied to heart, aorta, brown adipose tissue, adrenal, lung, and brain. For these tissues, Bradykinin-(1-7) and Bradykinin-(1-9) are of similar abundance (16-340 fmol/g), with lower levels of Bradykinin-(1-8)[1].

Name: Substance P (7-11), CAS: 51165-05-0, stock 3.5g, assay 98.2%, MWt: 612.78, Formula: C31H44N6O5S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Substance P (7-11) is a C-terminal fragment of Substance P which can cause an increase in the intracellular calcium concentration.
In Vitro: Substance P (7-11) increases PGE2 and collagenase production at concentrations greater than 1 μM. Substance P (7-11), but not intact SP, SP-(1-4), SP-(1-6), SP- (8-11) or SP-(9-1 1), nor the tachykinins NKA and NKB, causes an increase in the intracellular calcium concentration as measured by the fluorescent dye Fura-2. The maximal change in intracellular calcium induced by 10 μM Substance P (7-11) was 140±30 nM[1].

Name: Fibrinopeptide B, human FPB,human, CAS: 36204-23-6, stock 12.4g, assay 98.7%, MWt: 1552.56, Formula: C66H93N19O25, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fibrinopeptide B, human is a 14-aa peptide, released from the amino-terminus of β-chains of fibrinogen by thrombin.
In Vitro: Fibrinopeptide B, human is released from the amino-terminus of the B 3-chains of fibrinogen by thrombin. Fibrinopeptide B, human (hFpB, 10 nM) causes directed cell migration of neutrophils (PMN), and fibroblasts. Fibrinopeptide B, human also possesses potent chemotactic activity relative to human complement (C5a), leukotriene B4 (LTB4), and formyl-methionylleucyl-phenylalanine (fMLP), and for fibroblasts its chemotactic activity is comparable to that of platelet-derived growth factor. However, Fibrinopeptide B, human is not chemotactic for monocytes, and shows no interaction with PMN receptor for C5a, LTB4, or fMLP[1].

Name: CDK12-IN-3, CAS: 2220184-50-7, stock 32.8g, assay 98.2%, MWt: 470.52, Formula: C23H28F2N8O, Solubility: , Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CDK12-IN-3 is a potent and selective CDK12 inhibitor with an IC50 of 491 nM in enzymatic assay.
IC50 & Target: IC50: 491 nM (CDK12)[1]
In Vitro: CDK12-IN-3 is a highly selective CDK12 inhibitor profiled across a panel of 352 kinases at 0.1 µM. CDK12-IN-3 shows potent inhibition of phosphorylation of Ser2 on the CTD repeat domain of RNA Pol II as well as growth inhibition of OV90 cells and acute cytotoxicity to THP1 cells[1].

Name: Substance P (1-9), CAS: 57468-17-4, stock 16g, assay 98.4%, MWt: 1104.26, Formula: C52H77N15O12, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Substance P (1-9) is nonapeptide, which decreases the inactivation of substance P by the guinea-pig ileum and urinary bladder.
In Vitro: Substance P (1-9) is a nonapeptide, which decreases the inactivation of substance P by the guinea-pig ileum and urinary bladder, but with no significant effects on bradykinin or SP-(6-11)[1].

Name: Small Cardioactive Peptide B (SCPB), CAS: 84746-43-0, stock 23.2g, assay 98.2%, MWt: 1141.41, Formula: C52H80N14O11S2, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenylate Cyclase, Biological_Activity: Small Cardioactive Peptide B (SCPB), a neurally active peptide, stimulates adenylate cyclase activity in particulate fractions of both heart and gill tissues with EC50s of 0.1 and 1.0 μM, respectively.
IC50 & Target: EC50: 0.1 μM (adenylate cyclase, in heart tissues), 1.0 μM (adenylate cyclase, in gill tissues)[1]
In Vitro: Small cardioactive peptide B (SCPB) is a neurally active peptide endogenous to Aplysia. Small cardioactive peptide B (SCPB) possesses cardioexcitatory effects in Aplysia and reported a threshold concentration of 0.01 nM for both native and synthetic Small cardioactive peptide B (SCPB) stimulated effects on the isolated heart. Effects of Small Cardioactive Peptide B (SCPB) on the physiology of the isolated heart and gill preparations from the mollusc Aplysia californica were examined. In addition, the effects of Small Cardioactive Peptide B (SCPB) and FMRFamide (Phe-Met-Arg-Phe-NH2) on adenylate cyclase activity are compared in particulate fractions of heart and gill tissues, respectively. Small Cardioactive Peptide B (SCPB) is found to exert dose-dependent, reversible changes in cardiac activity when perfused through the isolated heart. The EC50 values effecting changes in heart rate and force of contraction are 0.03 and 0.3 nM, respectively; minimum concentrations find to effect changes in heart rate and force of contraction are normally 0.001 and 1 pM, respectively. When perfused through the isolated gill, Small Cardioactive Peptide B (SCPB) is found to suppress the gill withdrawal response amplitude with a threshold concentration of 0.01 pM and an EC50 value of 0.03 nM. Suppression of the gill withdrawal response amplitude by Small Cardioactive Peptide B (SCPB)is found to be dose dependent and reversible up to a concentration of 1nM. At higher concentrations, the suppression tended to persist irreversibly. Small Cardioactive Peptide B (SCPB) stimulates adenylate cyclase activity in particulate fractions of both heart and gill tissues with an EC50 of 0.1 and 1.0μM, respectively[1].

Name: Bradykinin (1-3), CAS: 23815-91-0, stock 21.3g, assay 98.6%, MWt: 368.43, Formula: C16H28N6O4, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: Bradykinin (1-3) is a 3-amino acid residue peptide. Bradykinin (1-3) is an amino-truncated Bradykinin peptide, cleaved by Prolyl endopeptidase.

Name: Substance P, Free Acid, CAS: 71977-09-8, stock 19.9g, assay 98.5%, MWt: 1348.61, Formula: C63H97N17O14S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Substance P, Free Acid is a native substance P analog, but shows no biological activity of substance P.

Name: Somatostatin-28 (1-14), CAS: 79243-10-0, stock 10.4g, assay 98.1%, MWt: 1528.71, Formula: C61H105N23O21S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Somatostatin-28 (1-14) is an N-terminal fragment of the neuropeptide somatostatin-28.
In Vitro: The tetradecapeptide hormone somatostatin arises from proteolytic processing of a large precursor, preprosomatostatin[1]. Somatostatin-28 (1-14) has been used to produce antibodies selective for somatostatin-28 that do not bind to the C-terminal fragment somatostatin-14[2].

Name: Luteinizing Hormone Releasing Hormone (LH-RH), human, CAS: 71447-49-9, stock 20.2g, assay 98.6%, MWt: 1302.41, Formula: C55H75N17O13.2C2H4O2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Luteinizing Hormone Releasing Hormone (LH-RH), human is hypothalamic neuropeptide which plays a key role in the control of reproductive functions.
In Vitro: Luteinizing Hormone Releasing Hormone (LH-RH), also called gonadotropin-releasing hormone (GnRH), is the primary link between the brain, the pituitary and gonadal function, and has a key role in vertebrate reproduction. The endocrine actions of Luteinizing Hormone Releasing Hormone (LH-RH) and its analogs are mediated by high-affinity membrane receptors for LHRH on pituitary gonadotrophs[1]. LHRH is expressed,together with its receptors,in hormonerelated tumors such as prostate cancer,to act as a local autocrine/paracrine growth inhibitory factor. In prostate cancer cells,the LHRH receptor is coupled to the Gi-cAMP pathway to inhibit cell proliferation[3].
In Vivo: Luteinizing Hormone Releasing Hormone treatment advances the timing of vaginal opening by 5 days, which is used as an initial indicator for the time of puberty[2].

Name: δ-Sleep Inducing Peptide Delta-Sleep Inducing Peptide, CAS: 62568-57-4, stock 4.1g, assay 98.4%, MWt: 848.81, Formula: C35H48N10O15, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: δ-Sleep Inducing Peptide is a neuropeptide, with antioxidant and anxiolytic properties.
In Vivo: In rabbit infused with δ-Sleep Inducing Peptide (DSIP), the spindle activity is increased, and heart and respiration rate are moderately decreased. δ-Sleep Inducing Peptide (DSIP) may act as a programming modulator at supra-operational level rather than as a transmitter at operational level[1]. δ-Sleep Inducing Peptide (DSIP; 40 μg/kg, i.p.) increases catalase and superoxide dismutase (SOD) activities and malonic dialdehyde (MDA) concentration in the liver homogenate of rats subjected to acute stress, but the opposite effects are observed at 120, and 360 μg/kg[2].

Name: ACTH (4-11) Adrenocorticotropic Hormone (4-11), human, CAS: 67224-41-3, stock 32.7g, assay 98.3%, MWt: 1090.26, Formula: C50H71N15O11S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ACTH (4-11), an adrenocorticotropin hormone fragment, possesses a weak α-melanocyte stimulating hormone (α-MSH) potency only at high doses (100 and 1000 nM).
In Vitro: α-melanocyte stimulating hormone (MSH) induces the differentiation of mouse epidermal melanocytes in vivo and in vitro. Adrenocorticotropic hormone (ACTH) possesses the same amino acid sequence as MSH does. α-MSH induces the differentiation of mouse epidermal melanocytes in vivo and in vitro. ACTH (4-11) loses almost all activity for the binding to melanocortin receptor 1 (MC1R)[1].

Name: β-Melanocyte Stimulating Hormone (MSH), human Beta-MSH (1-22) (human), CAS: 17908-57-5, stock 32.1g, assay 99%, MWt: 2660.92, Formula: C118H174N34O35S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: β-Melanocyte Stimulating Hormone (MSH), human, a 22-residue peptide, acts as an endogenous melanocortin-4 receptor (MC4-R) agonist[1].
IC50 & Target: Melanocortin-4 receptor (MC4-R)[1]
In Vitro: β-Melanocyte Stimulating Hormone (MSH), human (β-MSH) has high affinity at both human MC4-R transfected into CHO cells (Ki=11.4±0.4 nM) and MC4-R in rat hypothalamic homogenates (Ki=5.0±0.4 nM)[1].

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