What you carry at this position in your DNA and what research says about it.
Drug Metabolism: 8/10 evidence, 22 publications.
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Sample genotype (not yours): G/G
Normal Drug Metabolism
Enzymes function at a typical rate, processing standard medications as expected. This avoids the therapeutic failures or toxicities associated with slow metabolism.
What this genotype means: Typical activation of clopidogrel; Standard clearance of acid reflux medications; Normal processing of certain antidepressants.
Sample genotype (not yours): A/A
Very Slow Drug Metabolism
Two non-functional copies of the gene result in a complete lack of active enzyme. This significantly impacts how several common medications work in the body.
What this genotype means: Severely impaired activation of clopidogrel; Significantly prolonged clearance of acid reflux drugs; High risk of side effects from certain antidepressants.
Sample genotype (not yours): G/A
Slower Drug Metabolism
Carrying one non-functional copy of the gene reduces overall enzyme activity. This can lead to slower activation of some drugs and slower clearance of others.
What this genotype means: Reduced activation of clopidogrel; Slower clearance of proton pump inhibitors; Slightly increased risk of antidepressant 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 processing and clearing approximately ten percent of clinically prescribed medications [2]. It plays a dual role in pharmacology by either breaking down active drugs to clear them from the body or activating inactive prodrugs so they can exert their therapeutic effects [1]. Variations in this gene directly influence how rapidly or slowly an individual processes these medications [2]. Consequently, genetic testing of this gene is widely used to personalize drug selection and dosing [2].
Variant Impact: This variant, known as CYP2C19*3, is a single nucleotide transition from G to A that introduces a premature stop codon at position 212 of the protein sequence [1]. This stop-gained mutation, designated as p.Trp212Ter, results in a severely truncated and completely non-functional enzyme [1]. Because the enzyme cannot perform its catalytic duties, individuals carrying this variant experience altered processing of various medications [3]. The variant is particularly relevant in East Asian populations, where its frequency is significantly higher than in other ancestral groups [3].
Key Insight: This single letter change completely shuts down the CYP2C19 enzyme, turning a normal drug-processing pathway into a dead end.
Location: CYP2C19. Chromosome 10 · 10q23.33 · 94.8 Mb
Estimated prevalence by population
Global 99.5%; European > 99.9%; African 99.9%; East Asian 88.2%; South Asian 99.0%; Americas 99.9%; Ashkenazi 100.0%; Finnish 100.0%; Middle Eastern 100.0%; Amish 100.0%.
Estimated GG genotype frequency.
Global 0.5%; European < 0.1%; African 0.1%; East Asian 11.5%; South Asian 1.0%; Americas 0.1%; Ashkenazi 0.0%; Finnish 0.0%; Middle Eastern 0.0%; Amish 0.0%.
Estimated GA genotype frequency.
Global < 0.1%; European < 0.1%; African < 0.1%; East Asian 0.4%; South Asian < 0.1%; Americas < 0.1%; Ashkenazi 0.0%; Finnish 0.0%; Middle Eastern 0.0%; Amish 0.0%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Clopidogrel Response. Evidence: 8/10. Source: PMID 23517020. Typical Efficacy.
Antidepressant & Psychiatric Drug Response
Antidepressant Levels. Evidence: 8/10. Source: PMID 21270786. Typical Levels.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Sensitivity. Evidence: 8/10. Source: PMID 28391407. Typical Risk.
Antimicrobial & Antiviral Response
Tuberculosis Drug Rash. Evidence: 8/10. Source: PMID 30458875. Typical Risk.
Organ Systems
Digestive & Gut Disorders
Acid Reflux Drug Response. Evidence: 3/10. Source: PMID 19136640. Typical Clearance.
Showing effects for A/A genotype
Clopidogrel Response. Evidence: 8/10. Source: PMID 23517020. Poor Efficacy.
Antidepressant Levels. Evidence: 8/10. Source: PMID 21270786. Very High Levels.
Phenytoin Sensitivity. Evidence: 8/10. Source: PMID 28391407. High Toxicity Risk.
Tuberculosis Drug Rash. Evidence: 8/10. Source: PMID 30458875. Lower Rash Risk.
Acid Reflux Drug Response. Evidence: 3/10. Source: PMID 19136640. Very Slow Clearance.
Showing effects for G/A genotype
Clopidogrel Response. Evidence: 8/10. Source: PMID 23517020. Reduced Efficacy.
Antidepressant Levels. Evidence: 8/10. Source: PMID 21270786. Higher Levels.
Phenytoin Sensitivity. Evidence: 8/10. Source: PMID 28391407. Higher Toxicity Risk.
Acid Reflux Drug Response. Evidence: 3/10. Source: PMID 19136640. Slower Clearance.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Two copies of the fully functional gene mean the liver produces normal levels of active CYP2C19 enzyme. Standard doses of common medications, including the antiplatelet drug clopidogrel, are processed and activated efficiently [1]. Proton pump inhibitors used for acid reflux, such as omeprazole, are cleared from the body at a typical rate [2]. Antidepressants like escitalopram and sertraline are also metabolized normally, maintaining expected therapeutic levels in the bloodstream [2]. There is no elevated genetic risk of toxicity or adverse reactions when taking these standard medications.
Typical activation of clopidogrel; Standard clearance of acid reflux medications; Normal processing of certain antidepressants.
Sample genotype: AA (Homozygous)
Two copies of the non-functional variant result in a poor metabolizer phenotype with virtually no active CYP2C19 enzyme. This status severely impairs the body's ability to activate the antiplatelet drug clopidogrel, which can significantly increase the risk of cardiovascular events or stent complications [1]. Medications that are normally deactivated by this enzyme, such as proton pump inhibitors and SSRI antidepressants, will build up to much higher levels in the bloodstream [2]. While higher levels of acid reflux medications can actually improve the eradication of stomach infections, elevated antidepressant levels greatly increase the risk of adverse side effects [2]. There is also a heightened risk of severe cutaneous adverse reactions when taking the antiseizure medication phenytoin [3].
Severely impaired activation of clopidogrel; Significantly prolonged clearance of acid reflux drugs; High risk of side effects from certain antidepressants.
Sample genotype: GA (Heterozygous)
One copy of the non-functional variant means the liver produces fewer active enzymes, resulting in an intermediate metabolizer status. This reduction in enzyme activity can lead to decreased activation of the blood thinner clopidogrel, potentially reducing its ability to prevent blood clots [1]. Conversely, medications that require breakdown to be cleared, such as acid reflux drugs and certain antidepressants, may linger in the body longer [2]. While this can sometimes improve the effectiveness of acid reflux treatments, it may also increase the risk of side effects from antidepressants [2]. Additionally, there is a slightly higher risk of adverse reactions to the antiseizure drug phenytoin [3].
Reduced activation of clopidogrel; Slower clearance of proton pump inhibitors; Slightly increased risk of antidepressant 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
CPIC: Clinical Pharmacogenetics Implementation Consortium of the Pharmacogenomics Research Network.
High frequencies of CYP2C19 mutations and poor metabolism of proguanil in Vanuatu.
Content updated August 2026.
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