TPP-C8-CO-DSG bromide

TPP-C8-CO-DSG (bromide) (48 h) potently inhibits proliferation of PC-3, A549, MCF-7, HeLa, and HCT116 cancer cells with IC₅₀ values ranging from 0.10 to 3.1 μM, and exhibits selective toxicity with an IC₅₀ of 39.0 μM in normal L02 cells^[1].
TPP-C8-CO-DSG (bromide) (0.02-0.5 μM; 36 h) dose-dependently depolarizes the mitochondrial membrane potential in HeLa cells, with significant reductions observed at concentrations as low as 0.02 μM after 36 h of treatment^[1].
TPP-C8-CO-DSG (bromide) (0.02-0.5 μM; 36 h) dose-dependently reduces intracellular ATP production in HeLa cells, causing an 80.1% reduction at the highest tested concentration of 0.5 μM after 36 h of treatment^[1].
TPP-C8-CO-DSG (bromide) (0.02-0.5 μM; 24 h) dose-dependently induces intracellular ROS accumulation in HeLa cells, with a 28.1-fold increase observed at 0.5 μM after 24 h of treatment^[1].
TPP-C8-CO-DSG (bromide) (0.02-0.5 μM; 36 h) dose-dependently promotes apoptosis and necrosis in HeLa cells, with marked morphological changes observed at concentrations of 0.1 μM and 0.5 μM after 36 h of treatment^[1].
TPP-C8-CO-DSG (bromide) (0.02-0.5 μM; 36 h) dose-dependently induces early and late apoptosis in HeLa cells, with a combined apoptotic rate of 48.04% observed at 0.5 μM after 36 h of treatment^[1].
TPP-C8-CO-DSG (bromide) (0.02-0.5 μM; 36 h) induces apoptosis in HeLa cells via a mitochondria-associated pathway, characterized by upregulation of pro-apoptotic proteins, downregulation of anti-apoptotic Bcl-2, and activation of the caspase cascade after 36 h of treatment^[1].

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