CYP2C9*2 — slower warfarin and NSAID metabolism
One copy of the CYP2C9*2 reduced-function variant detected.
You have one working copy and one less-active copy of the CYP2C9 gene.
Intermediate warfarin sensitivity. If warfarin is ever prescribed, dose adjustment is typical. NSAIDs and several other drugs are cleared more slowly.
You're modestly more sensitive than average to the blood-thinner warfarin. If you ever need warfarin, your doctor will likely use a lower dose. Common painkillers (NSAIDs) and a few other drugs also leave your system more slowly.
What this means
CYP2C9 metabolises warfarin (Coumadin), several NSAIDs (celecoxib, ibuprofen at the margin), phenytoin, and sulfonylureas. *2 reduces enzyme activity. Combined with VKORC1 variants, CYP2C9 genotype is the most validated pharmacogenetic predictor of warfarin dosing — though the move toward direct-acting oral anticoagulants has reduced warfarin use in many patient groups.
CYP2C9 is an enzyme in your liver that breaks down the blood-thinner warfarin (Coumadin), some painkillers like celecoxib and ibuprofen, the anti-seizure drug phenytoin, and some diabetes medicines (sulfonylureas). The *2 version of the gene makes a less-active enzyme, so these drugs hang around in your system longer. Combined with the VKORC1 gene, this is the best-validated genetic predictor for warfarin dosing — although many people are now prescribed newer blood-thinners (apixaban, rivaroxaban) instead, where this gene matters less.
Caveats
- Most relevant if warfarin or related drugs are prescribed.
- Combining CYP2C9 and VKORC1 genotype gives a much better warfarin starting-dose estimate than either alone.
- Many people now receive DOACs (apixaban, rivaroxaban) instead of warfarin; CYP2C9 has limited relevance to those drugs.