Triclabendazole disrupts mitochondrial electron transport in vitro.

Mitochondrial respiration, which relies on succinate dehydrogenase (SDH), among other factors, is essential for cellular energy metabolism. This study shows that triclabendazole and its primary metabolites inhibit SDH in mitochondria of the cestode Echinococcus multilocularis, while other benzimidazoles do not. Similar effects were observed in mitochondria from additional helminths (trematodes, nematodes) and mammalian cells. These findings indicate a shared mode of action and highlight potential safety risks associated with long-term triclabendazole treatment in mammals.