In vitro metabolic study identifies 18 tuxobertinib metabolites across mammalian liver microsomes, highlighting CYP3A4-driven biotransformation without human-specific products.
Tuxobertinib is an EGFR tyrosine kinase inhibitor, which was undergoing clinical development for the treatment of non-small cell lung cancer (NSCLC). The aim of this study was to characterize the metabolites of tuxobertinib in liver microsomes and recombinant cytochrome P450 enzymes and to propose the metabolic pathways. The metabolites were generated by individually incubating tuxobertinib (5 μM) with rat, dog, monkey, and human liver microsomes, NADPH, and at 37°C for 60 min. The samples were analyzed by ultra-high-performance liquid chromatography-quadrupole/orbitrap mass spectrometry (UPLC-Q/Orbitrap-MS) using electrospray ionization in positive ion mode. The metabolites were characterized and identified by their accurate MS and MS/MS data. Totally, 18 metabolites were detected, and their structure was characterized. All these metabolites were -NADPH-dependent. The metabolic pathways of tuxobertinib included O-dealkylation, hydroxylation, oxidative deamination, dehydrogenation, and the opening of morpholine. M4 (O-dealkylation) was the major metabolite in all species. No human specific metabolite was observed. In human recombinant CYP3A4, 13 metabolites were detected, and CYP3A4 was the primary enzyme responsible for tuxobertinib metabolism. This is the first report on the metabolism of tuxobertinib, which provided an overview of the metabolism profiles of tuxobertinib in vitro, which is helpful in understanding its safety and action.
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