Abstract
The cytochrome P450 2D6 enzyme contributes to the metabolism of approximately one-quarter of all clinically prescribed drugs, and its gene is among the most polymorphic in the human pharmacogenome, with allelic variants ranging from complete loss of function to markedly increased activity relative to the reference allele. Genotype-based classification of patients into poor, intermediate, normal, and ultrarapid metabolizer phenotypes has become a well-established framework for anticipating altered drug exposure, yet a growing body of evidence indicates that genotype alone is insufficient to predict an individual's actual metabolic phenotype at the point of prescribing [1].
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