ArticleDrug metabolism and disposition: the biological fate of chemicals2025
Impact of combined UGT2B17 and GSTA1 genotypes on exemestane pharmacogenetics.
Article in Drug metabolism and disposition: the biological fate of chemicals, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Exemestane (EXE) is an aromatase inhibitor used for the treatment of estrogen receptor-positive breast cancer. The metabolism of EXE includes reduction to form 17-β-hydroxy-EXE (17β-DHE) and subsequent UGT2B17-mediated glucuronidation to form 17-β-hydroxy-EXE-17-O-β-D-glucuronide (17β-DHE-Gluc), and GSTA1-mediated glutathione conjugation of EXE and 17β-DHE and subsequent sequential metabolism by γ-glutamyl transferases and dipeptidases to form 6-methylcysteinylandrosta-1,4-diene-3,17-dione (EXE-Cys) and 6-methylcysteinylandrosta-1,4-diene-17-β-hydroxy-3-one (17β-DHE-Cys). The aim of the present study was to determine the effects of UGT2B17 and GSTA1 genotype on the serum levels of EXE and its metabolites among subjects taking EXE. Genotypes of UGT2B17 and GSTA1 were determined by real-time polymerase chain reaction and serum EXE, 17β-DHE, 17β-DHE-Gluc, EXE-Cys, and 17β-DHE-Cys were quantified by ultra performance liquid chromatography-mass spectrometry. Shunting was observed between the 2 metabolic pathways of EXE, with serum EXE levels increased with increasing numbers of either the UGT2B17∗2 or GSTA1∗B alleles (P
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