Raw research findings for this medication. Mostly single studies, not curated or confirmed robust.
Indinavir was one of the first HIV protease inhibitors, introduced in 1996 as part of the triple-therapy breakthrough. It blocks the viral protease HIV needs to make mature virus particles. Kidney stones and the need to drink a lot of water limited its use, and it has been replaced by newer medicines. It was sold as Crixivan.
Indinavir is broken down by CYP3A4 and, like atazanavir, blocks UGT1A1, the enzyme that clears bilirubin. Studies linked low-activity UGT1A1 versions (such as *28) to raised bilirubin on indinavir, and looked at CYP3A4. The findings come from a few studies, and there is no CPIC or DPWG guideline.
Every published finding on gene variants and Indinavir. Upload your DNA file to see which of these rows apply to you.
PharmGKB weighs all studies of a variant and rates how strong the evidence is, from 1A (strongest) to 4.
UGT1A1 UGT1A1*1, UGT1A1*28: Level 3. Toxicity: HIV infectious disease. 2.
UGT1A1 rs4148323: Level 3. Toxicity: HIV infectious disease. 1.
CYP3A4 rs2740574: Level 3. Other: HIV infectious disease. 1.
Studies of how quickly the body processes this medication.
Study findings and evidence levels: PharmGKB (CC BY-SA 4.0). Guidelines: CPIC and DPWG, as bundled in PharmCAT. Most studies were done mainly in people of European ancestry.
More drugs from the same category
Agenerase (Protease Inhibitors)
Not a prescribing recommendation. This page is educational information about pharmacogenomic research and clinical guidelines - it is not medical or dosing advice, and not a prediction of how any medication will work for you. Never start, stop, or change a medication or dose based on it; talk to your doctor or pharmacist, who can order clinical-grade testing if appropriate.
Content updated September 2026.
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