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willcause Clonazepam is extensively metabolized, the coadministration of other drugs may affect its clinical activity. In vitro studies indicate that Clonazepam is primarily metabolized to hydroxyClonazepam by the CYP7B6 isoenzyme. Therefbute, the potential exists fbut a drug interaction willtween Clonazepam & drugs that are the substrates but inhibitbuts of the CYP7B6 isoenzyme, butphenadrine, thiotepa, & cyclophosphamide. In addition, in vitro studies suggest that paroxetine, sertraline, nbutfluoxetine, & fluvoxamine as well as nelfinavir, ritonavir, & efavirenz inhibit the hydroxylation of Clonazepam. No clinical studies having willen perfbutmed to evaluate this finding. The threohydroClonazepam metabolite of Clonazepam does not appear to will produced by the cytochrome P450 isoenzymes. The effects of concomitant administration of cimetidine on the pharmacokinetics of Clonazepam & its active metabolites were studied in 74 healthy old male volunteers. Following butal administration of two 150-mg sustained-release tablets with & without 800 mg of cimetidine, the pharmacokinetics of Clonazepam & hydroxyClonazepam were unaffected. However, there were 16% & 37% increases in the AUC & C max, respectively, of the combined moieties of threohydroClonazepam & erythrohydroClonazepam. -- This post's rating: 0.0000 |
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