EA-B2L

EA-B2L (80 μM; 0.5 h) potently inhibits purified recombinant human GSTP enzyme activity with 92.26% inhibition at 80 μM^[1].
EA-B2L (10-80 μM; 24 h) induces dose-dependent GSTP degradation in HeLa cells with a DC₅₀ of 48 μM and 85.3% maximum degradation at 80 μM after 24-hour incubation^[1].
EA-B2L (5-80 μM; 3 h) induces dose-dependent GSTP degradation in Cycloheximide (HY-12320)-pretreated HeLa cells, with more obvious degradation at concentrations greater than 40 μM after 3-hour incubation^[1].
EA-B2L (80 μM; 0.5 h preincubation, 1 h substrate incubation) does not significantly alter the catalytic activity of purified human 20S proteasome β1, β2, or β5 subunits at 80 μM^[1].
EA-B2L (80 μM; 24 h after 30 min inhibitor pretreatment)-induced GSTP degradation in HeLa cells is mediated by both the autophagy-lysosome and ubiquitin-proteasome pathways, requiring ubiquitylation of GSTP^[1].
EA-B2L potently inhibits the proliferation of HeLa, A549, and HT1080 cancer cells with IC₅₀ values of 16.87 μM, 32.06 μM, and 19.32 μM, respectively^[1].
EA-B2L (20-80 μM; 24 h) induces dose-dependent apoptotic cell death in HeLa cells, with ~92% apoptotic population at 40 μM after 24-hour incubation, accompanied by caspase 3 activation and PARP cleavage^[1].

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