TPP-IOA is a cytochrome c peroxidase inhibitor. It prevents apoptosis by blocking cardiolipin oxidation and the release of cytochrome c into the cytosol. TPP-IOA interferes with oxidative phosphorylation in isolated mitochondria. It inhibits cell death of SH-SY5Y cells in glucose medium but is ineffective in galactose medium. Additionally, TPP-IOA induces mitochondrial depolarization and network fragmentation, and it reduces radiation-induced mortality in mice.

TPP-IOA (0-10 μM) interacts physically with cytochrome c, inhibiting ascorbate-mediated cytochrome c reduction in a dose-dependent manner and reducing the formation rate of resorufin in cytochrome c/cardiolipin solutions. At concentrations of 0.5-10 μM, TPP-IOA suppresses resorufin formation in isolated mitochondria, with significant inhibition observed at 5 μM due to its imidazole-containing oleic acid moiety. It inhibits cytochrome c peroxidase and reductase activities with IC50 values of 0.65 nmol and 5.28 nmol, respectively, per nmol of cytochrome c. In a dose-dependent fashion, TPP-IOA (0.5-10 μM) also reduces the respiratory control ratio and oxidative phosphorylation coupling efficiency in rat liver mitochondria. At 1 μM for 3 hours, TPP-IOA decreases the mitochondrial membrane potential of SH-SY5Y cells, disrupts mitochondrial networks, reduces mitochondrial content, and inhibits FCCP-stimulated respiration while maintaining basal oxygen consumption. In SH-SY5Y cells, TPP-IOA (0.25-5 μM) inhibits H2O2-induced cell death and caspase-3 activity in glucose, but not in galactose, medium.

TPP-IOA (5 mg/kg, intraperitoneal injection, once daily for 52 days) demonstrated significant radioprotective effects in C57BL/6NTac female mice exposed to 9.25 Gy of whole-body radiation.