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Golvatinib

CAS No. : 928037-13-2

MCE 国际站：Golvatinib

产品活性：Golvatinib (E-7050) 是 c-Met 和 VEGFR2 的双重抑制剂，IC₅₀值分别为14 和 16 nM。

研究领域：Protein Tyrosine Kinase/RTK

作用靶点：c-Met/HGFR  |  VEGFR

In Vitro: Golvatinib (E-7050) potently inhibits phosphorylation of both c-Met and VEGFR-2. Golvatinib also potently represses the growth of both c-met amplified tumor cells and endothelial cells stimulated with either HGF or VEGF.
Golvatinib strongly inhibits the growth of MKN45, EBC-1, Hs746T, and SNU-5 tumor cells with IC₅₀ values of 37, 6.2, 23, and 24 nM, respectively. The growth of A549, SNU-1 and 0MKN74 tumor cells is inhibited by Golvatinib with much higher IC₅₀ values.
Golvatinib circumvents resistance to all of the reversible, irreversible, and mutant-selective EGFR-TKIs induced by exogenous and/or endogenous HGF in EGFR mutant lung cancer cell lines, by blocking the Met/Gab1/PI3K/Akt pathway in vitro.
Golvatinib also prevents the emergence of gefitinib-resistant HCC827 cells induced by continuous exposure to HGF.

In Vivo: Golvatinib (E-7050) shows inhibition of the phosphorylation of c-Met and VEGFR-2 in tumors, and strong inhibition of tumor growth and tumor angiogenesis in xenograft models.
Treatment of some tumor lines containing c-met amplifications with high doses of Golvatinib (50-200 mg/kg) induced tumor regression and disappearance. In a peritoneal dissemination model, Golvatinib shows an antitumor effect against peritoneal tumors as well as a significant prolongation of lifespan in treated mice.
Golvatinib (E7050) plus Gefitinib results in marked regression of tumor growth associated with inhibition of Akt phosphorylation in cancer cells.

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