FAK-IN-32

FAK-IN-32 (compound 7g) (100 nM; 60 min) selectively inhibits FAK among 68 tyrosine kinases (in a cell-free biochemical purified enzyme system), with an inhibition rate of approximately 90%^[1].
FAK-IN-32 (0.078125-10 µM; 72 h) significantly inhibits the proliferation of HCT116 (IC₅₀ = 0.460 µM), SW620 (IC₅₀ = 3.072 µM), SW837 (IC₅₀ = 7.635 µM) and CW-2 (IC₅₀ = 0.587 µM) colon cancer cells, while having no significant effect on the proliferation of BaF3-FA (IC₅₀ = 82.39 µM) cells^[1].
FAK-IN-32 (0.125-0.5 µM; 48 h) induces morphological changes characteristic of apoptosis or necrosis in HCT116 cells. FAK-IN-32 promotes apoptosis in HCT116 cells in a dose-dependent manner^[1].
FAK-IN-32 (0.125-0.5 µM; 48 h) induces cell cycle arrest at the G2/M phase in HCT116 cells^[1].
FAK-IN-32 (0.125-0.5 µM; 48 h) inhibits the phosphorylation of FAK and its downstream target AKT in HCT116 cells in a dose-dependent manner, thereby blocking the FAK-AKT signaling pathway^[1].
FAK-IN-32 (at least 5 min until steady state) shows very weak inhibitory activity against hERG potassium channels in CHO cells stably expressing the hERG gene (indicating no significant cardiotoxicity, IC₅₀ = 12.89 µM)^[1].
FAK-IN-32 (10 µM; 48 h) significantly inhibits the proliferation of patient-derived colorectal cancer organoids (PDOs) and reduces the proportion of Ki67-positive cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.