Drug-first pharmacogenomics, with live MCP-backed inference.
Search a drug, review the genotype / phenotype table, and paste de-identified genotype text to see a likely traffic signal and the short clinical relevance summary.
Clopidogrel
CYP2C19 is the primary PGx driver for clopidogrel activation and response.
Evidence snapshot
- 2 curated genotype / phenotype rows, both guideline-anchored.
- CPIC 2022 CYP2C19-clopidogrel guideline and PharmGKB clinical annotation.
Genotype / phenotype table
Relevant genes first. Click a row to inspect relevance, or paste genotype text to auto-select a likely match.
| Gene | Genotype / phenotype context | Signal label | Traffic signal | Why it matters |
|---|---|---|---|---|
CYP2C19Likely traffic signal | Reference / no seeded altered-function signal reference | Likely traffic signal | green | partial or inferred baseline No seeded altered-function PGx signal is being assumed for this gene context. |
CYP2C19Traffic signal | Intermediate or poor metabolizer reduced or sensitive | Traffic signal | red | CPIC guideline-backed Reduced bioactivation can lower antiplatelet effect and increase residual ischemic risk. |
CYP2C19Traffic signal | Rapid or ultrarapid metabolizer increased function present | Traffic signal | yellow | CPIC guideline-backed Higher active metabolite exposure may increase bleeding sensitivity in some settings. |
Evidence snapshot
Clinical and patient summaries
Clinician note
The strongest signal is CYP2C19 loss of function. Increased-function contexts are relevant but more context-dependent than the red reduced-function scenario.
Patient explanation
Some CYP2C19 gene patterns can change how clopidogrel is activated. The table shows the direction of that PGx signal in educational form.