What you carry at this position in your DNA and what research says about it.
Medication Metabolism: 8/10 evidence, 49 publications.
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Sample genotype (not yours): G/G
Normal Medication Metabolism
Standard metabolism of many common medications is typical here. This includes normal activation of the antiplatelet drug clopidogrel, ensuring typical protection against blood clots.
What this genotype means: Normal activation of clopidogrel; Standard clearance of acid reflux drugs; Typical risk of medication side effects.
Sample genotype (not yours): A/A
Poor Medication Metabolism
Very slow processing of several common medications is expected here. This significantly reduces the effectiveness of the antiplatelet drug clopidogrel and increases the risk of side effects with other drugs.
What this genotype means: Severely reduced activation of clopidogrel; Very slow clearance of acid reflux drugs; Highest risk of chemotherapy side effects.
Sample genotype (not yours): G/A
Intermediate Medication Metabolism
Slower processing of several common medications occurs with this genotype. This can reduce the effectiveness of the antiplatelet drug clopidogrel and increase the risk of side effects with other drugs.
What this genotype means: Reduced activation of clopidogrel; Slower clearance of acid reflux drugs; Increased risk of chemotherapy side effects.
Gene function and biological role
Gene Function: The CYP2C19 gene encodes a crucial liver enzyme belonging to the cytochrome P450 family [1]. This enzyme is responsible for metabolizing a wide array of commonly prescribed medications, including antiplatelet agents, antidepressants, and proton pump inhibitors [2]. Variations in this gene can dramatically alter how quickly or slowly these drugs are processed in the body [3]. Some genetic changes lead to a complete loss of enzyme function, while others can increase its activity [4].
Variant Impact: The rs4244285 variant is a single nucleotide change in the CYP2C19 gene that defines the well-known CYP2C19*2 star allele [5]. This specific change creates an abnormal splice site during gene transcription, resulting in a non-functional enzyme [1]. Because the enzyme cannot perform its normal role, individuals carrying this variant experience significantly reduced metabolism of several medications [2]. This loss-of-function effect is particularly critical for prodrugs like clopidogrel, which require active CYP2C19 metabolism to become effective [6].
Key Insight: This variant is a synonymous change that does not alter the amino acid sequence directly, yet it completely disables the enzyme by disrupting how the gene's genetic code is spliced together.
Location: CYP2C19. Chromosome 10 · 10q23.33 · 94.8 Mb
Estimated prevalence by population
Global 69.4%; European 72.6%; African 67.7%; East Asian 47.3%; South Asian 44.6%; Americas 75.7%; Ashkenazi 75.3%; Finnish 66.2%; Middle Eastern 83.6%; Amish 66.8%.
Estimated GG genotype frequency.
Global 27.5%; European 25.2%; African 29.1%; East Asian 42.9%; South Asian 44.4%; Americas 22.6%; Ashkenazi 22.9%; Finnish 30.3%; Middle Eastern 15.7%; Amish 29.8%.
Estimated GA genotype frequency.
Global 3.0%; European 2.2%; African 3.1%; East Asian 9.7%; South Asian 11.0%; Americas 1.7%; Ashkenazi 1.7%; Finnish 3.5%; Middle Eastern 0.7%; Amish 3.3%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Clopidogrel Response. Evidence: 8/10. Source: PMID 19106083. Normal Response.
Chemotherapy Response
Chemotherapy Toxicity. Evidence: 8/10. Source: PMID 29507678. Typical Risk.
Antiepileptic & Mood-Stabilizer Response
Antiepileptic Drug Metabolism. Evidence: 8/10. Source: PMID 36718958. Normal Metabolism.
Anesthesia Response
Diazepam Response. Evidence: 8/10. Source: PMID 32134726. Typical Side Effects.
Organ Systems
Digestive & Gut Disorders
Acid Reflux Drug Response. Evidence: 3/10. Source: PMID 9867757. Typical Cure Rate.
Showing effects for A/A genotype
Clopidogrel Response. Evidence: 8/10. Source: PMID 19106083. Poor Response.
Chemotherapy Toxicity. Evidence: 8/10. Source: PMID 29507678. Increased Toxicity.
Antiepileptic Drug Metabolism. Evidence: 8/10. Source: PMID 36718958. Slower Metabolism.
Diazepam Response. Evidence: 8/10. Source: PMID 32134726. More Side Effects.
Acid Reflux Drug Response. Evidence: 3/10. Source: PMID 9867757. Highest Cure Rate.
Showing effects for G/A genotype
Clopidogrel Response. Evidence: 8/10. Source: PMID 19106083. Reduced Response.
Acid Reflux Drug Response. Evidence: 3/10. Source: PMID 9867757. Higher Cure Rate.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Livers with two copies of the normal-functioning gene produce fully active CYP2C19 enzymes [1]. When prescribed the antiplatelet drug clopidogrel, the body efficiently converts it into its active form to help prevent blood clots [2]. This normal metabolic rate is also associated with typical clearance of proton pump inhibitors used for acid reflux [3]. While there are no elevated drug levels to increase treatment success in some cases, the heightened risk of side effects seen in slower metabolizers is avoided [4]. Response to other medications like certain antidepressants and anti-seizure drugs is expected to be standard [5]. Standard clearance rates help maintain predictable drug concentrations in the bloodstream. This predictability allows healthcare providers to use standard dosing guidelines with confidence. Overall, this represents the baseline metabolic profile for a wide variety of clinical therapies.
Normal activation of clopidogrel; Standard clearance of acid reflux drugs; Typical risk of medication side effects.
Sample genotype: AA (Homozygous)
Two copies of the loss-of-function variant mean there is little to no active CYP2C19 enzyme function [1]. When taking clopidogrel, the body cannot effectively convert the drug into its active form, leaving the system with a significantly reduced antiplatelet response [2]. This lack of activation is associated with a substantially higher risk of cardiovascular events, including stent thrombosis and heart attacks [3]. On the other hand, very slow clearance of proton pump inhibitors leads to sustained drug levels, resulting in exceptionally high cure rates for H. pylori infections and ulcers [4]. However, this slow metabolism also increases susceptibility to drug toxicity and side effects from medications like diazepam and chemotherapy agents [5]. Alternative antiplatelet therapies are frequently recommended for individuals with this profile. Standard doses of many other medications may lead to unexpected accumulation and adverse reactions. Knowing this status is highly valuable for personalizing future medical treatments.
Severely reduced activation of clopidogrel; Very slow clearance of acid reflux drugs; Highest risk of chemotherapy side effects.
Sample genotype: GA (Heterozygous)
One copy of the loss-of-function variant reduces overall CYP2C19 enzyme activity [1]. When taking clopidogrel, the body may not convert enough of the drug into its active form, leading to a diminished antiplatelet effect [2]. This can result in a higher risk of adverse cardiovascular events such as stent clotting or heart attacks during treatment [3]. Conversely, slower metabolism of proton pump inhibitors can lead to higher drug levels, which may actually improve cure rates for acid reflux and ulcers [4]. However, an increased risk of side effects or toxicity with medications like diazepam or certain chemotherapies is also possible [5]. This intermediate metabolic state often requires careful monitoring of drug levels. Doctors may consider alternative therapies or adjusted doses depending on the specific medication. It represents a common genetic variation that influences daily medical care.
Reduced activation of clopidogrel; Slower clearance of acid reflux drugs; Increased risk of chemotherapy side effects.
Variants with shared genetic architecture
rs28399504 · CYP2C19 Gene · Chr 10 · Drug Metabolism
rs41291556 · CYP2C19 Gene · Chr 10 · Clopidogrel Response
rs12777823 · CYP2C19 Gene · Chr 10 · Medication Response
The major genetic defect responsible for the polymorphism of S-mephenytoin metabolism in humans.
CYP2C19*17 is associated with decreased breast cancer risk.
Genetic determinants of response to clopidogrel and cardiovascular events.
Content updated August 2026.
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