Raw research findings for this medication. Mostly single studies, not curated or confirmed robust.
Tipifarnib is an experimental farnesyltransferase inhibitor: it blocks the enzyme that attaches a fatty anchor to proteins such as HRAS, which they need to send growth signals. It has been studied for head and neck cancers with HRAS mutations and for some blood cancers, and is not approved for routine use.
Tipifarnib is broken down by CYP3A4 and UGT1A1 and carried by ABCB1. The gene studies listed looked at ABCB1, CYP3A4, CYP3A5 and UGT1A1 for its levels. Whether it works is thought to depend on HRAS mutations in the tumour, which are acquired, not inherited. There is no CPIC or DPWG guideline.
Every published finding on gene variants and Tipifarnib. 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.
ABCB1 rs1128503: Level 3. Metabolism/PK: Neoplasms. 1.
Studies of how quickly the body processes this medication.
ABCB1 rs1045642: Allele G is not associated with decreased metabolism of tipifarnib.
ABCB1 rs2032582: Allele T is not associated with increased metabolism of tipifarnib.
CYP3A4 rs2740574: Allele C is not associated with decreased metabolism of tipifarnib.
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
Zokinvy (Farnesyltransferase 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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