Tivantinib - CAS 905854-02-6
Catalog number: 905854-02-6
Category: Inhibitor
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Tivantinib (ARQ-197) is an orally bioavailable small molecule inhibitor of c-Met with potential antineoplastic activity. c-Met inhibitor ARQ 197 binds to the c-Met protein and disrupts c-Met signal transduction pathways, which may induce cell death in tumor cells overexpressing c-Met protein or expressing consitutively activated c-Met protein. c-Met protein, the product of the proto-oncogene c-Met, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis. Check for active clinical trials or closed clinical trials using this agent
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ARQ-197; ARQ 197; ARQ197; Tivantinib
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ArQule, Inc
1.Pharmacodynamic Response of the MET/HGF-Receptor to Small Molecule Tyrosine Kinase Inhibitors Examined with Validated, Fit-for-Clinic Immunoassays.
Srivastava AK1, Hollingshead MG2, Weiner J3, Navas T3, Evrard YA4, Khin SA5, Ji JJ6, Zhang Y7, Borgel S8, Pfister TD9, Kinders R10, Bottaro DP11, Linehan WM12, Tomaszewski JE13, Doroshow JH14, Parchment RE15. Clin Cancer Res. 2016 Mar 21. pii: clincanres.2323.2015. [Epub ahead of print]
PURPOSE: Rational development of targeted MET inhibitors for cancer treatment requires a quantitative understanding of target pharmacodynamics, including molecular target engagement, mechanism of action, and duration of effect.
2.A randomized, placebo-controlled, phase 1/2 study of tivantinib (ARQ 197) in combination with irinotecan and cetuximab in patients with metas
Eng C1, Bessudo A2, Hart LL3, Severtsev A4, Gladkov O5, Müller L6, Kopp MV7, Vladimirov V8, Langdon R9, Kotiv B10, Barni S11, Hsu C12, Bolotin E13, von Roemeling R12, Schwartz B14, Bendell JC15. Int J Cancer. 2016 Jul 1;139(1):177-86. doi: 10.1002/ijc.30049. Epub 2016 Mar 22.
Cetuximab in combination with an irinotecan-containing regimen is a standard treatment in patients with KRAS wild-type (KRAS WT), metastatic colorectal cancer (mCRC). We investigated the addition of the oral MET inhibitor tivantinib to cetuximab + irinotecan (CETIRI) based on preclinical evidence that activation of the MET pathway may confer resistance to anti-EGFR therapy. Previously treated patients with KRAS WT advanced or mCRC were enrolled. The phase 1, open-label 3 + 3, dose-escalation study evaluated the safety and maximally tolerated dose of tivantinib plus CETIRI. The phase 2, randomized, double-blinded, placebo-controlled study of biweekly CETIRI plus tivantinib or placebo was restricted to patients who had received only one prior line of chemotherapy. The phase 2 primary endpoint was progression-free survival (PFS). The recommended phase 2 dose was tivantinib (360 mg/m(2) twice daily) with biweekly cetuximab (500 mg/m(2) ) and irinotecan (180 mg/m(2) ).
3.Tivantinib induces G2/M arrest and apoptosis by disrupting tubulin polymerization in hepatocellular carcinoma.
Xiang Q1,2, Zhen Z3, Deng DY4, Wang J5, Chen Y6, Li J7, Zhang Y8, Wang F9, Chen N10, Chen H11, Chen Y12. J Exp Clin Cancer Res. 2015 Oct 12;34:118. doi: 10.1186/s13046-015-0238-2.
BACKGROUND: Tivantinib has been described as a highly selective inhibitor of MET and is currently in a phase III clinical trial for the treatment of hepatocellular carcinoma (HCC). However, the mechanism of tivantinib anti-tumor effect has been questioned by recent studies.
4.Cabozantinib and Tivantinib, but not INC280, Induce Anti-Proliferative and Anti-Migratory Effects in Human Neuroendocrine Tumour Cells in vitro: Evidence for 'Off-Target' Effects not Mediated by c-M
Reuther C1, Heinzle V, Spampatti M, Vlotides G, de Toni E, Spöttl G, Maurer J, Nölting S, Göke B, Auernhammer CJ. Neuroendocrinology. 2015 Aug 25. [Epub ahead of print]
BACKGROUND/AIMS: The hepatocyte growth factor (HGF)/transmembrane tyrosine kinase receptor c-Met has been defined as a potential target in antitumoural treatment of various carcinomas. We aimed to investigate the direct effect of c-Met inhibition on neuroendocrine tumour cells in vitro.
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