In vitro study | Telatinib had 0.66, 0.17, and 2.5 times higher IC50 values for VEGFR-3, c-Kit, and PDGFR-β than VEGFR-2, respectively, while Vatalanib had 18, 20, and 16 times higher IC50 values, respectively, telatinib works better than Vatalanib. In whole cell experiments, Telatinib inhibited VEGFR-2 autophosphorylation with an IC50 of 19 nM and inhibited VEGF-dependent proliferation of human umbilical vein endothelial cells with an IC50 of 26 nM, and the growth of human aortic smooth muscle cells stimulated by PDGF was blocked, and the IC50 was 249 nM. Telatinib acts on the Raf kinase pathway, the epidermal growth factor receptor family, the fibroblast growth factor receptor (FGFR) family, and the Tie-2 receptor, with no inhibitory activity. |
In vivo study | Because tumor growth and metastasis are attributed to the loss of regulation of the VEGFR signaling pathway, Telatinib significantly inhibits tumor growth and metastasis by blocking VEGFR signaling and tumor angiogenesis. In addition to the significant inhibition of tumor angiogenesis, Telatinib treatment significantly reduced endothelial cell-dependent and independent vasodilation and also reduced capillary density, resulting in an increase in both diastolic and systolic blood pressure. Telatinib alone has potent antitumor activity in a variety of human xenograft models, including MDA-MB-231 breast, Colo-205, DLD-1, and H460 non-small cell lung cancer, as well as pancreatic and prostate cancers, this effect is dose-dependent. |