BCS12

BCS12 (96 h) selectively inhibits the viability of triple-negative breast cancer cells MDA-MB-231 and MDA-MB-468 under hypoxic conditions (IC₅₀ = 15.49 µM and 18.81 µM), while showing extremely low toxicity toward non-tumorigenic MCF-10A cells (IC₅₀ = 121.6 µM)^[1].
BCS12 (5-10 µM; 14 days) dose-dependently inhibits the clonogenic survival capacity of MDA-MB-231 and MDA-MB-468 cells^[1].
BCS12 (20 µM) inhibits hypoxia-induced expression of HIF-1α and CAIX proteins in MDA-MB-231 and MDA-MB-468 cells^[1].
BCS12 (2-20 µM; 24 h) dose-dependently increases the ROS level in MDA-MB-231 cells, with the strongest effect observed at 20 µM^[1].
BCS12 (5-20 µM; 24 h) dose-dependently regulates the expression of apoptotic proteins in MDA-MB-231 cells, downregulates the anti-apoptotic protein Bcl-2, activates the pro-apoptotic caspase-9 and caspase-3, and induces PARP cleavage. It also induces apoptosis in MDA-MB-231 cells under hypoxic conditions, upregulates the expression of pro-apoptotic genes Bax, caspase-9, caspase-3 and caspase-7, and downregulates the anti-apoptotic gene Bcl-2 as well as hypoxia-related CA9 and HIF-1α^[1].

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