| Bioactivity | Tivantinib is a highly selective c-Met tyrosine kinase inhibitor with a Ki of 355 nM. | ||||||||||||
| Invitro | Tivantinib (ARQ 197) selectively inhibits c-Met activity in cell-free and cell-based assays. c-Met-expressing cancer cell lines treated with Tivantinib display either a dose-dependent loss of proliferative capacity or caspase-dependent apoptosis that positively correlates with either ligand-dependent c-Met activity or constitutively active c-Met. To examine the biochemical mode of inhibition of Tivantinib, kinetic analyses are done using recombinant human c-Met in a filtermat-based assay. The Km of ATP is 50.5±2.2 μM, which is similar to the Km value of ATP. In these kinetic studies, Tivantinib inhibits human recombinant c-Met with a calculated inhibitory constant (Ki) of ~355 nM. In vitro exposure to Tivantinib inhibits constitutive c-Met phosphorylation in HT29 and MKN-45 cells, and HGF-induced c-Met phosphorylation in MDA-MB-231 and NCI-H441 cells with an IC50 of 100 to 300 nM[1]. Tivantinib is a low-molecular-weight compound, and is the first in class orally available selective inhibitor of c-Met[2]. | ||||||||||||
| Name | Tivantinib | ||||||||||||
| CAS | 905854-02-6 | ||||||||||||
| Formula | C23H19N3O2 | ||||||||||||
| Molar Mass | 369.42 | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
|