Fruquintinib (HMPL-013) acts as a potent, selective inhibitor for VEGFR 1/2/3, exhibiting IC50 values of 33 nM, 0.35 nM, and 35 nM, correspondingly[1]. Fruquintinib shows strong inhibitory effects on VEGF-A mediated KDR phosphorylation in HEK293-KDR cells and blocks VEGF-A triggered growth in primary HUVECs, with IC50 values of 0.6±0.2 nM and 1.7 nM, respectively. Fruquintinib also significantly reduces VEGFR3 activity in primary HLECs, evident from IC50s of 1.5 nM and 4.2 nM for VEGF-C induced VEGFR3 phosphorylation and proliferation, respectively. It effectively diminishes tube formation, branching, and expansion in a dose-dependent manner, reducing tubule length in primary HUVECs by 74% and 94% at concentrations of 0.03 μM and 0.3 μM, respectively. Fruquintinib's capability to inhibit tubule development and CAM angiogenesis is noted, with substantial suppression of tube formation after 18 hours at 0.3 μM[1].
体内研究
The BGC-823 gastric cancer model is notably more responsive to fruquintinib, which curbs tumor expansion by 62.3% and between 95.4～98.6% with daily dosages of 0.5 mg/kg and 2 mg/kg, respectively. Tumor regression of 24.1% and 48.6% is achieved with increased doses of 5 mg/kg and 20 mg/kg. The efficacy of fruquintinib against tumor growth shows variation across different tumor xenograft models, with a marked reduction in micro-vessel density observed even at the minimal dose of 0.8 mg/kg[1].
体外研究
Fruquintinib (HMPL-013) acts as a potent, selective inhibitor for VEGFR 1/2/3, exhibiting IC50 values of 33 nM, 0.35 nM, and 35 nM, correspondingly[1].
Fruquintinib shows strong inhibitory effects on VEGF-A mediated KDR phosphorylation in HEK293-KDR cells and blocks VEGF-A triggered growth in primary HUVECs, with IC50 values of 0.6±0.2 nM and 1.7 nM, respectively. Fruquintinib also significantly reduces VEGFR3 activity in primary HLECs, evident from IC50s of 1.5 nM and 4.2 nM for VEGF-C induced VEGFR3 phosphorylation and proliferation, respectively. It effectively diminishes tube formation, branching, and expansion in a dose-dependent manner, reducing tubule length in primary HUVECs by 74% and 94% at concentrations of 0.03 μM and 0.3 μM, respectively. Fruquintinib's capability to inhibit tubule development and CAM angiogenesis is noted, with substantial suppression of tube formation after 18 hours at 0.3 μM[1].
搜索
