Aditya Rawat: Clopidogrel, CYP2C19 and the Role of Pharmacogenetics
Aditya Rawat, Trainee Pharmacy Assistant at City Hospital and Research Centre, Haryana, India, shared a post on LinkedIn about recent article, Yo Han Jung et al, published in JAMA, adding:
“A drug only works if your body actually turns it on.
This week in Pharmacology we started on prodrugs.
These are medicines that are inactive as swallowed and need the liver to convert them.
Clopidogrel, a widely used antiplatelet after stroke and heart attack, is a classic example. Its activation depends heavily on one enzyme, CYP2C19.
I read a 2025 JAMA Network Open trial that followed 2,910 stroke patients in South Korea, all genotyped for CYP2C19.
61 percent carried a loss of function allele.
Over six months, carriers had more cardiovascular events than non carriers (2.7 percent vs 1.6 percent).
After adjustment, non carriers had roughly 42 percent lower risk, with no difference in bleeding.
What stood out to me:
- The common variants link straight back to molecular biology. 2 disrupts splicing and 3 introduces a premature stop codon.
- The absolute difference is small and the trial wasn’t randomised, so this supports, rather than proves, genotype guided prescribing.
- A platelet function test didn’t predict outcomes, but the genotype did.
It’s a neat case where pharmacokinetics, genetics and clinical outcomes all meet in one tablet.”
Title: Cytochrome P450 2C19 Genotypes and Clopidogrel in Patients With Ischemic Stroke
Authors: Yo Han Jung, Tae-Jin Song, Jinkwon Kim, Hee-Kwon Park, Sang Won Han, Young Dae Kim, Jong-Ho Park, Jae-Kwan Cha, Hyun Young Park, Sung-Il Sohn, Sungwook Yu, Jun Hong Lee, Dong Hoon Shin, Eung-Gyu Kim, Hye Sun Lee, Kyung-Yul Lee
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