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Gene Variant Linked to Risk of Stroke and Heart Attack for Those on Plavix

NIGMS Media Availability

August 25, 2009
Alisa Machalek, NIGMS


A new study reports that a gene variant carried by about a third of the population plays a major role in this group’s response to an anti-clotting medicine, clopidogrel (Plavix). People with the variant produce a defective version of the CYP2C19 enzyme and are less able to activate the drug.

One of the world’s best-selling medicines, Plavix prevents blood clots in people with heart disease by keeping platelets from sticking together. But about 30 percent of people respond poorly to the drug and are at increased risk for dangerous events like strokes and heart attacks.

By performing a sophisticated method called a genome-wide association study in two distinct populations, Pennsylvania Amish and residents of urban Baltimore, the researchers found that a common variant of the CYP2C19 gene is a key determinant of how people respond to Plavix. The CYP2C19 enzyme chemically modifies the drug inside the body, converting it to the active form.


"Association of Cytochrome P450 2C19 Genotype with the Antiplatelet Effect and Clinical Efficacy of Clopidogrel Therapy" by Alan R. Shuldiner, Jeffrey R. O’Connell, Kevin P. Bliden, et. al. The paper will appear in the August 26, 2009, issue of the Journal of the American Medical Association.


Rochelle M. Long, Ph.D., director of the National Institutes of Health Pharmacogenetics Research Network, is available to comment on this work and its importance to the field of pharmacogenetics.


To schedule an interview, contact Alisa Machalek in the NIGMS Office of Communications and Public Liaison at 301-496-7301 or



More information on the Pharmacogenetics Research Network is available at /Research/FeaturedPrograms/PGRN/.

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This page last reviewed on November 14, 2014