What Is Cytochrome P450-2D6?


Cytochrome P450-2D6, also known as CYP-2D6, is an enzyme that is part of the cytochrome P450 family of liver/intestinal enzymes that work to metabolize medications and other drugs. Specifically, CYP-2D6 is involved in metabolizing medications such as metoprolol, propranolol, hydrocodone, meperidine, methadone, oxycodone, codeine and tramadol.

Individual genes are responsible for producing a specific enzyme. When a mutation or variation in a gene is present, it affects how the produced enzyme works. Therefore, variations in the gene that produces CYP-2D6 affect the metabolism of certain medications.

Pharmacogenetic testing for cytochrome P450 genotypes

Pharmacogenetics is the study of how an individual’s deoxyribonucleic acid, or DNA, affects the way they respond to different drugs. In 2005, a simple blood test became available to identify certain cytochrome P450 genotypes. Physicians can use this test to determine if an individual will metabolize certain medications at a different pace than expected. When an individual is tested and found to have a cytochrome P450-2D6 abnormality, they can be prescribed the appropriate dosage of pain medication rather than a typical dosage. They may also be prescribed a medication that is not metabolized by CYP-2D6, such as fentanyl, morphine, hydromorphone, oxymorphone or tapentadol.

Differences in drug metabolism

If an individual is considered a “rapid” or “ultra-rapid” CYP-2D6 metabolizer, their body metabolizes certain medications too quickly. Even a “typical” dose of opioid medication could cause high levels of toxic substances in the body, potentially causing overdose.

On the other hand, if an individual has a CYP-2D6 deficiency, they are considered a “poor metabolizer” or “non-metabolizer,” which means they do not adequately metabolize and activate certain pain medications, including codeine, hydrocodone and tramadol. An individual with this deficiency may require two to four times the typical dose of these pain medications to experience the same pain-relieving effects as an individual without the deficiency.

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