Successful, we will reply to you quickly.

OK

Please select the quantity.

OK

Your message is being sent, please wait.

Close

test

Close

Send mail failed, please send again!

Close

Products are for research use only. Not for human use. We do not sell to patients.

Signaling Pathway

Tivantinib

HY-50686

(ARQ197; ARQ-197; ARQ 197)

Tivantinib

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.

Size Price Stock Quantity
Free sample   Apply now  
10 mM * 1 mL in DMSO $66 In-stock
5 mg $60 In-stock
10 mg $90 In-stock
50 mg $255 In-stock
100 mg $405 In-stock
200 mg Get quote
500 mg Get quote
Size Price Stock Quantity
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
200 mg Get quote
500 mg Get quote

* Please select Quantity before adding items.

Bulk Inquiry

Inquiry Information
Product name: Tivantinib
Cat. No.: HY-50686

Tivantinib Data Sheet

  • View current batch:

    Purity: 98.51% ee.:99.94%

  • Pdf Version Network Version

    DataSheet

    Pdf Version Network Version

    MSDS

    Pdf Version

    COA

Customer View

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)

More

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

Related c-Met/HGFR Products

  • Altiratinib

    Altiratinib(DCC-2701) is a novel c-MET/TIE-2/VEGFR inhibitor; effectively reduce tumor burden in vivo and block c-MET pTyr(1349)-mediated signaling, cell growth and migration as compared with a HGF antagonist in vitro.

  • AMG-208

    AMG-208 is a potent small molecular c-Met inhibitor with an IC50 of 9.3 nM.

  • AMG-337

    AMG-337 is a potent and highly selective small molecule ATP-competitive MET kinase inhibitor. AMG 337 inhibits MET kinase activity with an IC50 of < 5nM in enzymatic assays.

  • BMS 777607

    BMS-777607 is a Met-related inhibitor for c-Met, Axl, Ron and Tyro3 with IC50 of 3.9 nM, 1.1 nM, 1.8 nM and 4.3 nM, 40-fold more selective for Met-related targets versus Lck, VEGFR-2, and TrkA/B, and more than 500-fold greater selectivity versus all other receptor and non receptor kinases.

  • BMS-794833

    BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7/15 nM; also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378.

  • c-Met inhibitor 1

    c-Met inhibitor 1 is an inhibitor of the c-Met receptor signaling pathway useful for the treatment of cancer including gastric, glioblastoma, and pancreatic cancer.

  • E-7050

    E7050(Golvatinib) is a dual c-Met and VEGFR-2 inhibitor with IC50 of 14 nM and 16 nM.

  • EMD-1214063

    EMD 1214063 is a potent and selective c-Met inhibitor with IC50 of 4 nM, >200-fold selective for c-Met than IRAK4, TrkA, Axl, IRAK1, and Mer.

  • Foretinib

    Foretinib (GSK1363089; XL880; EXEL-2880; GSK089) is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met and KDR with IC50 of 0.4 nM and 0.9 nM. Less potent against Ron, Flt-1/3/4, Kit, PDGFR(alpha)/(beta) and Tie-2, and little activity to FGFR1 and EGFR.

  • Glesatinib hydrochloride

    Glesatinib hydrochloride is an inhibitor of the MET and Axl receptor tyrosine kinase pathways, which drive tumour growth when altered.

MORE