Triclabendazole disrupts mitochondrial electron transport in vitro

Antimicrobial Agents and Chemotherapy 2026 Open access

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Authors: Tobias Kämpfer, María Eugenia Ancarola, Pascal Zumstein, Alice Bernal, Trix Zumkehr, Seraina Mühlemann, Natalie Wiedemar, Britta Lundström‐Stadelmann
DOI: 10.1128/aac.01756-25
Cited by: 1
References: 27

Abstract

ABSTRACT 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.

Fields of Study & Subjects

Mitochondrial Function and Pathology Glutathione Transferases and Polymorphisms Parasites and Host Interactions

Publication details

Journal / source
Antimicrobial Agents and Chemotherapy
Publisher
American Society for Microbiology
Volume
70
Issue
6
Pages
e0175625–e0175625
Publication date
30 April 2026
Language
EN