Language

English

Publication Date

11-15-2025

Journal

Journal of Pharmaceutical and Biomedical Analysis

DOI

10.1016/j.jpba.2025.117034

PMID

40554835

PMCID

PMC12403197

PubMedCentral® Posted Date

11-15-2025

PubMedCentral® Full Text Version

Author MSS

Abstract

Pexidartinib (PEX, TURALIO®), a tyrosine kinase inhibitor, is approved for treating tenosynovial giant cell tumor in adults. However, its potential to cause fatal liver injury has prompted the U.S. FDA to issue a black box warning, and the mechanisms underlying its hepatotoxicity remain largely unknown. As biotransformation may contribute to PEX-induced hepatotoxicity, understanding its metabolism is essential. Our previous research indicated that PEX forms reactive metabolites in human and mouse liver microsomes and in human hepatocytes. We investigated PEX metabolism and liver distribution in mice with a focus on metabolite characterization. Our data shows that PEX is mainly excreted into mouse feces as an unchanged drug, in line with findings in humans. Thirty phase I metabolites reported in our previous in vitro studies were detected in mouse feces, urine, plasma, and/or liver; these include the products of unusual carbon-carbon bond cleavages. Twenty-eight phase II PEX metabolites were tentatively identified, including 12 glucuronides, 6 sulfates, 1 glucose conjugate, 2 glutathione, 1 cysteinyl-glycine, and 6 N-acetylcysteine adducts; 24 of these have not previously been reported. The detection of glutathione-PEX adducts and their degradation products indicates that reactive PEX metabolites are generated in mice, consistent with our previous findings in liver microsomes. Since glutathione-PEX adducts are also generated in human primary hepatocytes, the discovery of these new metabolites may help others to clarify the previously unknown metabolic fates of some PEX in human studies and provide starting points for investigations into PEX toxicity by further assessing the safety of its metabolites.

Keywords

Animals, Mice, Feces, Liver, Protein Kinase Inhibitors, Male, Microsomes, Liver, Humans, Pyrroles, Glutathione, Biotransformation, Aminopyridines, Mice, Inbred C57BL, pexidartinib, phase I and II metabolites, reactive metabolites, N-acetylcysteine adducts, metabolomics

Published Open-Access

yes

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