TPP-IOA

TPP-IOA (0-10 μM) physically interacts with cytochrome c, dose-dependently inhibiting both ascorbate-mediated cytochrome c reduction and the rate of resorufin formation in cytochrome c/cardiolipin solution^[1].
TPP-IOA (0.5-10 μM) suppresses resorufin formation in isolated mitochondria, with significant inhibition at 5 μM, which is due to its imidazole-containing oleic acid moiety^[1].
TPP-IOA (0-10 μM) exhibits IC₅₀ values of 0.65 nmol per nmol cytochrome c for peroxidase activity and 5.28 nmol per nmol cytochrome c for reduction activity^[1].
TPP-IOA (0.5-10 μM) dose-dependently reduces the respiratory control ratio and oxidative phosphorylation coupling efficiency in rat liver mitochondria^[1].
TPP-IOA (1 μM, 3 h) reduces mitochondrial membrane potential, disrupts mitochondrial reticulum morphology, decreases mitochondrial content, and inhibits FCCP-uncoupled respiration while maintaining basal oxygen consumption in SH-SY5Y cells^[1].
TPP-IOA (0.25-5 μM) inhibits H2O2-induced total death & caspase-3 activity in SH-SY5Y cells in glucose but not galactose medium^[1][2].
TPP-IOA (2.5-5 μM, 48 h) shows radiation mitigating effects on mouse embryonic cells in a model of intrinsic apoptosis induced in mouse embryonic cells by γirradiation as evidenced by PS externalization, caspase 3/7 activation and cyt c release^[2].

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