Medications and your DNA

Each page takes one medication and sets out what published CPIC guidance says for each possible genetic result, which gene decides it, and whether the DNA file you already own can actually resolve that gene. Start from the gene instead at genes and your medications, or see the full inventory at what we analyse.

• atazanavir (UGT1A1): UGT1A1 handles atazanavir. People with the Gilbert genotype are far likelier to get harmless jaundice, and guidance weighs an alternative where that matters.
• azathioprine (NUDT15 + TPMT): Azathioprine dosing depends on TPMT and NUDT15 together. A normal result for one says nothing about the other, and either can crash blood counts.
• capecitabine and fluorouracil (DPYD): Capecitabine and fluorouracil are cleared by DPYD. Low DPYD activity risks severe, sometimes fatal toxicity, so guidance advises a lower dose or avoiding them.
• clopidogrel (CYP2C19): Clopidogrel is inactive until CYP2C19 converts it. Poor and intermediate metabolizers get less protection, and the FDA label carries a boxed warning.
• codeine and tramadol (CYP2D6): Codeine and tramadol are inactive until CYP2D6 converts them. Slow converters get no relief; fast converters can reach unsafe opioid levels.
• efavirenz (CYP2B6): CYP2B6 clears efavirenz. Slow metabolizers reach higher levels and more nervous-system side effects, and CPIC describes a reduced 400 or 200 mg daily dose.
• escitalopram and citalopram (CYP2C19): CYP2C19 clears escitalopram and citalopram. Slow metabolizers reach higher levels and more side effects; fast ones may get too little to help.
• hydralazine (NAT2): NAT2 acetylator status sets the hydralazine dose. Slow acetylators reach higher levels and start lower; faster ones often need a higher maintenance dose.
• omeprazole and lansoprazole, pantoprazole (CYP2C19): CYP2C19 clears omeprazole, lansoprazole and pantoprazole. Fast metabolizers may need a higher dose to work; slow ones can often do with less on long-term use.
• rosuvastatin (ABCG2 + SLCO1B1): Rosuvastatin levels depend on two transporters, SLCO1B1 and ABCG2. Reduced function raises muscle-symptom risk, and CPIC caps the starting dose at 20mg.
• simvastatin (SLCO1B1): SLCO1B1 moves simvastatin into the liver. A reduced-function copy raises blood levels and muscle risk, and consumer DNA files usually read it.
• tacrolimus (CYP3A5): CYP3A5 flips tacrolimus dosing: people who make the enzyme clear it fast and need a higher starting dose, not a lower one. Blood-level monitoring does the rest.
• tamoxifen (CYP2D6): Tamoxifen needs CYP2D6 to form its active metabolite endoxifen. Poor metabolizers make less, and guidance discusses whether an aromatase inhibitor fits better.
• voriconazole (CYP2C19): CYP2C19 sets voriconazole levels. Both fast and slow metabolizers sit outside the target range, and CPIC points to an alternative antifungal at either end.
• warfarin (CYP2C9): CYP2C9 changes how fast warfarin clears and VKORC1 how sensitive the target is. Together they explain much of why stable doses differ so widely.

These pages restate published guidance for education. They are not medical advice and never an instruction to start, stop or change a medication. The Deep Read panel covers 74 medications in total; the pages above are the ones where the genetic result changes a real decision and where people are actually searching.