Bcl-2-IN-26

Bcl-2-IN-26 (Compound 45) (72 h) exhibits potent inhibitory activity against NCI-H460 and A549 lung cancer cells with IC₅₀s of 0.66 nM and 0.73 nM, respectively^[1].
Bcl-2-IN-26 (1-5 nM; 24 h) blocks tubulin polymerization, disrupts microtubule networks and impairs mitosis in H460 cells^[1].
Bcl-2-IN-26 (2-200 nM; 24 h) induces G2/M phase arrest and apoptosis in H460 cells in a dose-dependent manner^[1].
Bcl-2-IN-26 (1-5 nM; 24 h) affects the expression of various apoptotic proteins, thereby inducing apoptosis in H460 cells^[1].
Bcl-2-IN-26 (1-5 nM; 24 h) reduces mitochondrial transmembrane potential, induces dose-dependent ROS accumulation in H460 cells^[1].
Bcl-2-IN-26 (1 nM; 48 h) triggers H460 cell death mainly by activating the p53 pathway to modulate BAX/BCL-2, with caspase activation only exerting weak auxiliary cytotoxic effects^[1].
Bcl-2-IN-26 displays optimal antitumor activity owing to synergistic fluorine and alkene-mediated binding interactions with microtubules^[1].

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