Your patient's genotype will predict a metabolizer phenotype for each of these enzymes. Poor Metabolizers (PMs) and Ultrarapid Metabolizers (UMs) are likely to have the most significant clinical effects from their genetic make-up (see the table below). The effect of the metabolizer phenotype will be different based on whether the drug is an active or prodrug.
Possible Consequences of the Metabolizer Phenotypes
| Metabolizer Phenotype | Enzyme Activity | Active Drug | Prodrug |
| Extensive Metabolizer (EM) | Normal | Normal response. | Normal response. |
| Poor Metabolizer (PM) | Inactive | Slower metabolism, overdose, and increased side effects. | Decreased levels of active metabolite with reduced or absent response. |
| Intermediate Metabolizer (IM) | Diminished | Potential for similar, but more mild, effects of poor metabolizers. | Potential for similar, but more mild, effects of poor metabolizers. |
| Ultrarapid Metabolizer (UM) | Increased | Faster metabolism, lower concentration, reduced efficacy. | Increased levels of active metabolite may lead to toxicity. |
Because genotypes don't change, it should only be necessary to test your patients for metabolizer status for these three genes once in a lifetime. New information about specific gene-drug interactions is being accumulated at a rapid rate. Once the metabolizer phenotype for these enzymes has been determined for your patient, you can use that information, together with what is currently known about a specific drug, any time a new drug therapy is being considered.
It is possible that other significant variants will be found in these or other CYP450 genes that warrant follow-up testing based on the clinical circumstances.