PKM2-IN-13

PKM2-IN-13 (compound 7f) (48 h) induces e level of hemolysis around 5% and effectively induces cytotoxicity with an IC₅₀ = 12.29 μM in SCC-9 cell lines and selectively inhibits cancer cell lines (including cancer OSCC cells : SCC-9, SCC-4, SCC-25, primary gingival fibroblast and other cancer cell lines : 4T1, Hep-G2, HCT116, B16-F10 Primary Gingival Fibroblast with IC₅₀s values of 12.29, 7.93, 11.09, 22.77, 7.63, 15.98, 6.72, 4.93 and 22.77 μM^[1].
PKM2-IN-13 (24.58 μM, 0-48 h) exhibits a pronounced inhibition of proliferation, observes disruption of intercellular junctions, membrane blebbing, and subsequent proliferation arrest at 6 h becoming more evident after 12 h in SCC-9 cells ^[1].
PKM2-IN-13 (24.58 μM, 24 and 48 h) induces S-phase arrest at 24 h, subsequently triggers cancer cell death via the intrinsic caspase-dependent apoptotic pathway rather than necroptosis as observed over 12-24 h in SCC-9 cells ^[1].
PKM2-IN-13 (24.58 μM, 12-48 h) result a significant increase in ROS after 12 and 24 h^[1].
PKM2-IN-13 (24.58 μM, 48 h) induces cytotoxicity, which can be protected against by Antioxidant N-acetyl-L-cysteine (NAC) (10 mM) (HY-B0215) for 2 h, suggesting an oxidative mechanism of action^[1].

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