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Cytochrome P450 family 3 subfamily A member 11 (CYP3A11) is the primary mouse ortholog of the human CYP3A4 enzyme and plays a central role in the phase I metabolism of xenobiotics and endogenous compounds [1, 2]. It is highly expressed in the liver and intestinal mucosa, where it facilitates the detoxification and clearance of a diverse range of lipophilic substances, including over 50% of marketed pharmaceuticals [9, 11]. The expression of CYP3A11 is tightly regulated by nuclear receptors, most notably the Pregnane X Receptor (PXR), which mediates its induction in response to various drugs and environmental chemicals [1, 5]. Consequently, CYP3A11 is a major site for drug-drug interactions, as its induction or inhibition can significantly alter the pharmacokinetics and toxicity profiles of co-administered medications [10, 15]. Beyond drug metabolism, it is involved in the homeostasis of steroid hormones and bile acids, and its dysregulation is associated with conditions such as cholestasis and inflammation-induced metabolic changes [4, 10]. Understanding CYP3A11 activity is essential in preclinical drug development for predicting human metabolic profiles and assessing safety risks associated with metabolic liabilities [3, 12].
Catalyzes the oxidative metabolism of lipophilic substrates, including hydroxylation, N-demethylation, O-dealkylation, and epoxidation, using molecular oxygen and electrons from NADPH-cytochrome P450 reductase.
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