Aim:To investigate the in vitro metabolism of imrecoxib in rat liver microsomesand to identify the cytochrome P450(CYP)forms involved in its metabolism.Methods:Liver microsomes of Wistar rats were prepared using an ultracentrifuge.The in vitro metabolism of imrecoxib was studied by incubation with rat livermicrosomes.To characterize the CYP forms involved in the 4’-methyl hydroxyla-tion of imrecoxib,the effects of typical CYP inducers(such as dexamethasone,isoniazid and β-naphthoflavone)and of CYP inhibitors(such as ketoconazole,quinine,α-naphthoflavone,methylpyrazole,and cimetidine)on the formation rateof 4’-hydroxymethyl imrecoxib were investigated.Results:Imrecoxib was me-tabolized to 3 metabolites by rat liver microsomes:4’-hydroxymethyl imrecoxib(M4),4’-hydroxymethyl-5-hydoxyl imrecoxib(M3),and 4’-hydroxymethyl-5-car-bonyl imrecoxib(M5).Over the imrecoxib concentration range studied(5-600μmol/L),the rate of 4’-methyl hydroxylation conformed to monophasic Michaelis-Menten kinetics.Dexamethasone significantly induced the formation of M4.Ketoconazole markedly lowered the metabolic rate of imrecoxib in a concentra-tion-dependent manner.Moreover,a significant inhibitory effect of quinine onthe formation of M4 was observed in microsomes obtained from control rats,isoniazid-induced rats,and β-naphthofiavone-induced rats.In contrast,α-naphthoflavone,cimetidine,and methylpyrazole had no inhibitory effects on thismetabolic pathway.Conclusion:Imrecoxib is metabolized via 4’-methyl hydroxy-lation in rat liver microsomes,The reaction is mainly catalyzed by CYP 3A.CYP2D also played a role in control rats,in isoniazid-induced rats and in β-naphthoflavone-induced rats. Aim: To investigate the in vitro metabolism of imrecoxib in rat liver microsomesand identify the cytochrome P450 (CYP) forms involved in its metabolism. Methods: Liver microsomes of Wistar rats were prepared using an ultracentrifuge. The in vitro metabolism of imrecoxib was studied by incubation with rat liver microorganisms. To characterize the CYP forms involved in the 4’-methyl hydroxyla tion of imrecoxib, the effects of typical CYP inducers (such as dexamethasone, isoniazid and β-naphthoflavone) and of CYP inhibitors (such as ketoconazole, quinine , α-naphthoflavone, methylpyrazole, and cimetidine) on the formation rate of 4’-hydroxymethyl imrecoxib were investigated. Results: Imrecoxib was me-tabolized to 3 metabolites by rat liver microsomes: 4’-hydroxymethyl imrecoxib -5-hydoxyl imrecoxib (M3), and 4’-hydroxymethyl-5-carbinol imrecoxib (M5). Over the imrecoxib concentration range studied (5-600 μmol / L), the rate of 4’-methyl hydroxylation conformed to monophasic Michaelis-Menten kineti dexamethasone significantly induced the formation of M4.Ketoconazole markedly lowered the metabolic rate of imrecoxib in a concentration-dependent manner. Moreover, a significant inhibitory effect of quinine on the formation of M4 was observed in microsomes obtained from control rats, isoniazid- induced rats, and β-naphthofiavone-induced rats. In contrast, α-naphthoflavone, cimetidine, and methylpyrazole had no inhibitory effects on this metabolic pathway. Confluence: Imrecoxib is metabolized via 4’-methyl hydroxy-lation in rat liver microsomes, The reaction is mainly catalyzed by CYP 3A. CYP2D also played a role in controlling rats, in isoniazid-induced rats and in beta-naphthoflavone-induced rats.