摘要
Hydroxamic acid is an excellent metal ion chelating group and is used commonly in the design of histone deacetylase (HDAC) inhibitors. Despite its utility, the hydroxamic acid group suffers from poor metabolic stability and undergoes rapid conversion to carboxylic acid, a process that has generally been described as hydrolytic metabolism. By using the HDAC inhibitor, bisthianostat as a model drug, this study provided novel insights into the role of cytochrome P450 (P450) enzymes in the metabolism of the hydroxamic acid group into the carboxylic acid metabolite (M351). The primary formation of M351 was observed in liver microsomes after incubating bisthianostat with different human liver, intestinal and plasma fractions. Chemical inhibition experiments further indicated that P450 enzyme-mediated oxidation was the main pathway for generation of M351, with hydrolysis making a minor contribution. 18 O-labeling isotope experiments and Griess assays demonstrated that the peroxoferric species of P450 enzymes acted as a nucleophile, attacking the carbonyl carbon of hydroxamic acid, leading to the formation of carboxylic acid and reactive nitrogen species. The metabolism of eight hydroxamic acid derivatives in human liver microsomes indicated that P450 enzymes exhibited substrate specificity in catalyzing the conversion of hydroxamic acids to carboxylic acids. Molecular docking results further revealed that oxidative metabolism occurred when the hydroxamic acid group was in appropriate proximity to the P450 catalytic center. Overall, this study demonstrated the important role of P450 enzymes in hydroxamic acid metabolism and provided valuable insights for future rational design and clinical applications of hydroxamic acid-based drugs.
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