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Signaling Pathway



(ARQ197; ARQ-197; ARQ 197)


Tivantinib Chemical Structure

Tivantinib (ARQ 197) is the first non-ATP-competitive c-Met inhibitor with Ki of 0.355 μM, little activity to Ron, and no inhibition to EGFR, InsR, PDGFRα or FGFR1/4.

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10 mM * 1 mL in DMSO $66 In-stock
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Free sample   Apply now  
10 mM * 1 mL in DMSO €65 In-stock
5 mg €59 In-stock
10 mg €88 In-stock
50 mg €250 In-stock
100 mg €397 In-stock
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Product name: Tivantinib
Cat. No.: HY-50686

Tivantinib Data Sheet

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    Purity: 98.51% ee.:99.94%

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Related Compound Libraries

Biological Activity of Tivantinib

Tivantinib (ARQ 197) is the first non-ATP-competitive c-Met inhibitor with Ki of 0.355 μM, little activity to Ron, and no inhibition to EGFR, InsR, PDGFRα or FGFR1/4.
IC50 value: 0.355 μM(Ki)
Target: c-Met
in vitro: ARQ-197 has been shown to prevent HGF/c-met induced cellular responses in vitro. ARQ-197 possesses antitumor activity; inhibiting proliferation of A549, DBTRG and NCI-H441 cells with IC50 of 0.38, 0.45, 0.29 μM. Treatment with ARQ-197 results in a decrease in phosphorylation of the MAPK signaling cascade and prevention of invasion and migration. In addition, ectopic expression of c-Met in NCI-H661, a cell line having no endogenous expression of c-Met, causes it to acquire an invasive phenotype that is also suppressed by ARQ-197. Although the addition of increasing concentrations of ARQ-197 does not significantly affect the Km of ATP, exposure of c-Met to 0.5 μM ARQ-197 decreased the Vmax of c-Met by approximately 3-fold. The ability of ARQ-197 to decrease the Vmax without affecting the Km of ATP confirmed that ARQ-197 inhibits c-Met through a non–ATP-competitive mechanism and may therefore account for its high degree of kinase selectivity. ARQ-197 prevents human recombinant c-Met with a calculated inhibitory constant Ki of approximately 355 nM. Although the highest concentration of ATP used is 200 μM, the potency of ARQ-197 against c-Met is not reduced by using concentrations of ATP up to 1 mM. ARQ-197 blocks c-Met phosphorylation and downstream c-Met signaling pathways. ARQ-197 suppresses constitutive and ligand-mediated c-Met autophosphorylation and, by extension, c-Met activity, in turn leading to the inhibition of downstream c-Met effectors. ARQ-197 induction of caspase-dependent apoptosis is increased in c-Met–expressing human cancer cells including HT29, MKN-45, and MDA-MB-231 cells [1][2].
in vivo: All three xenograft models treated with ARQ-197 display reductions in tumor growth: 66% in the HT29 model, 45% in the MKN-45 model, and 79% in the MDA-MB-231 model. In these xenograft studies, no significant body weight changes following oral administration of ARQ-197 at 200 mg/kg are observed. Pharmacodynamically, the phosphorylation of c-Met in human colon xenograft tumors (HT29) is strongly inhibited by ARQ-197, as assessed by a dramatic reduction of c-Met autophosphorylation 24 hours after a single oral dose of 200 mg/kg of ARQ-197. This same dosage in mice exhibits that tumor xenografts are exposed to sustained plasma levels of ARQ-197, consistent with the observed pharmacodynamic inhibition of c-Met phosphorylation and inhibition of proliferation of c-Met harboring cancer cell lines. Plasma levels of ARQ-197 10 hours after dosing are determined to be 1.3 μM, more than 3-fold above the biochemical inhibitory constant of ARQ-197 for c-Met. Therefore, ARQ-197 is able to suppress its target in vivo in the xenografted human tumor tissue. In conclusion, ARQ-197 inhibits the growth of c-Met-dependent xenografted human tumors [1].

Protocol (Extracted from published papers and Only for reference)


Chemical Information

M.Wt 369.42 Storage Please store the product under the recommended conditions in the Certificate of Analysis.
Formula C23H19N3O2
CAS No 905854-02-6
Solvent & Solubility

200 mM in DMSO

Preparing Stock Solutions

1 mg 5 mg 10 mg
1 mM 2.7069 mL 13.5347 mL 27.0695 mL
5 mM 0.5414 mL 2.7069 mL 5.4139 mL
10 mM 0.2707 mL 1.3535 mL 2.7069 mL

Clinical Information of Tivantinib

Product Name Sponsor Only Condition Start Date End Date Phase Last Change Date
Tivantinib Daiichi Sankyo Co Ltd Metastatic non small cell lung cancer 30-NOV-10 31-JUL-13 Phase 3 07-OCT-13
Daiichi Sankyo Inc Hepatocellular carcinoma 31-DEC-12 31-DEC-15 Phase 3 16-OCT-13
Istituto Clinico Humanitas Metastatic colorectal cancer 31-MAR-13 30-JUN-15 Phase 2 08-JUL-13
Kyowa Hakko Kirin Co Ltd Metastatic non small cell lung cancer 31-JUL-11 Phase 3 26-MAR-13
National Cancer Institute Mesothelioma 31-JAN-13 28-FEB-15 Phase 2 23-OCT-13

References on Tivantinib

Inhibitor Kit

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