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Venlafaxine oxidation in vitro is catalysed by CYP2D6.
TLDR
In vitro findings predict phenotypic differences in the kinetics of venlafaxine in vivo, although the clinical importance of this is unclear as O-demethylvenlafxine is pharmacologically similar to the parent drug. Expand
Interactions of amphetamine analogs with human liver CYP2D6.
TLDR
It is suggested that phenylisopropylamines as a class interact with CYP2D6 as substrates and/or inhibitors, and the potential for polymorphic oxidation via CYP 2D6 may be a source of interindividual variation in their abuse liability and toxicity. Expand
Use of quinidine inhibition to define the role of the sparteine/debrisoquine cytochrome P450 in metoprolol oxidation by human liver microsomes.
TLDR
The hypothesis that cytochrome P450-SP/DB catalyzes the formation of alpha-hydroxylation but is only partially responsible for metoprolol O-demethylation is supported, which could explain the previously reported inability to detect polymorphism in the O- Demethylation pathway in vivo. Expand
Inhibition by fluoxetine of cytochrome P450 2D6 activity
TLDR
Inhibition of CYP2D6 activity in patients undergoing treatment with fluoxetine or other serotonin uptake inhibitors could contribute to toxicity or attenuated response from concurrent medications that are substrates of this enzyme. Expand
Effect of cytochrome P450 2D1 inhibition on hydrocodone metabolism and its behavioral consequences in rats.
TLDR
Data suggest that differences in CYP2D6 phenotype will have limited influence on the drug response to hydrocodone after nonoral administration, verified in a study showing that inhibition of hydrocODone biotransformation to hydromorphone does not affect measures of abuse liability. Expand
Competitive inhibition of sparteine oxidation in human liver by beta-adrenoceptor antagonists and other cardiovascular drugs.
TLDR
In vitro competitive inhibition of sparteine oxidation by a drug indicates that this drug is capable of occupying the same enzymatic site as spartanine and may mean that the competing drug is also metabolized at that site and thereby subject to the same genetic variation as spartein's oxidation. Expand
CYP2D6 phenotype determines the metabolic conversion of hydrocodone to hydromorphone
TLDR
The data establish the importance of CYP2D6 in the formation of hydromorphone from hydrocodone and suggest that the activity of this enzyme may limit the abuse liability of hydrocODone. Expand
Pharmacokinetics of dextromethorphan and metabolites in humans: influence of the CYP2D6 phenotype and quinidine inhibition.
TLDR
It is demonstrated that the CYP2D6 phenotype and the concurrent administration of quinidine significantly affect the disposition of dextromethorphan and the formation of the active metabolite dextrorphan and are important factors to be considered in studies of the pharmacologic and behavioral effects of dexfinity. Expand
Effects of route of administration on dextromethorphan pharmacokinetics and behavioral response in the rat.
TLDR
The present studies demonstrate the route-specific effects on the disposition of dextromethorphan and dextrorphan in rat plasma and brain, as well as the behavioral consequence of the difference. Expand
Inhibition of human cytochrome P450 2D6 (CYP2D6) by methadone.
TLDR
In microsomes prepared from three human livers, methadone competitively inhibited the O-demethylation of dextromethorphan, a marker substrate for CYP2D6, suggesting inhibition of CYP6 activity in these patients might contribute to exaggerated response or unexpected toxicity from drugs that are substrates of this enzyme. Expand
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