
Keri K. answered 07/13/20
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Prodrugs (inactive parent compound) must be metabolized by the liver to become active. An example of this is clopidogrel (Plavix) being metabolized through CYP2C19. Once clopidogrel is metabolized through CYP2C19, the compound becomes active and can begin inhibiting platelets. In patients that are poor CYP2C19 metabolizers, clopidogrel cannot not be converted to the active form and thus platelet inhibition does not occur.
Depending on the pharmacogenetic test completed, the results may be reported in slightly different ways, but the most common phenotypes reported are (in order from least to most activity): Poor metabolizer -> intermediate metabolizer -> extensive metabolizer -> ultra rapid metabolizer. Extensive metabolizers are considered "normal" CYP function.
For patients that are poor or intermediate metabolizers, you would expect to see less of the parent inactive compound converted to the active compound and thus in theory would need to give either a higher dose or consider another agent. In theory, ultra rapid metabolizers would convert the parent inactive compound to the active compound more efficiently and thus a lower dose of the parent compound would be needed.