What you carry at this position in your DNA and what research says about it.
Medication Sensitivity: 9/10 evidence, 69 publications.
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Sample genotype (not yours): A/A
Typical Drug Metabolism Speed
Standard processing of common medications is expected. The slow-acting CYP2C9*3 variant is absent.
What this genotype means: Standard clearance of warfarin and NSAIDs; Typical risk of medication side effects.
Sample genotype (not yours): A/C
Slower Drug Metabolism Speed
One copy of the slow-acting CYP2C9*3 variant is present. This reduces the ability to clear several common medications.
What this genotype means: Slower clearance of warfarin and NSAIDs; Increased risk of bleeding complications.
Sample genotype (not yours): C/C
Severely Slow Drug Metabolism Speed
Two copies of the slow-acting CYP2C9*3 variant are present. This drastically reduces the ability to clear many common medications.
What this genotype means: Severely slow clearance of warfarin and NSAIDs; High risk of drug toxicity and bleeding.
Gene function and biological role
Gene Function: CYP2C9 encodes a key liver enzyme in the cytochrome P450 family [1]. This enzyme is responsible for breaking down and clearing a wide variety of commonly prescribed medications [1]. These include blood thinners, nonsteroidal anti-inflammatory drugs, and certain diabetes therapies [1]. Variations in this gene can dramatically alter how quickly or slowly these drugs are cleared from the body [1].
Variant Impact: The rs1057910 variant, also known as CYP2C9*3, is a missense mutation that changes the amino acid isoleucine to leucine at position 359 [2]. This single structural change severely impairs the enzyme's ability to bind and break down its target drugs [2]. As a result, carriers of the variant allele experience significantly slower drug clearance [2]. This can lead to a dangerous buildup of medications in the bloodstream, increasing the risk of toxic side effects [2].
Key Insight: A single letter change in this gene can reduce the ability to clear certain common medications by up to 80 percent.
Location: CYP2C9. Chromosome 10 · 10q23.33 · 95.0 Mb
Estimated prevalence by population
Global 90.4%; European 87.2%; African 97.5%; East Asian 94.0%; South Asian 78.5%; Americas 90.4%; Ashkenazi 84.1%; Finnish 89.2%; Middle Eastern 87.5%; Amish 94.2%.
Estimated AA genotype frequency.
Global 9.3%; European 12.4%; African 2.5%; East Asian 6.0%; South Asian 20.2%; Americas 9.3%; Ashkenazi 15.2%; Finnish 10.5%; Middle Eastern 12.1%; Amish 5.7%.
Estimated AC genotype frequency.
Global 0.3%; European 0.4%; African < 0.1%; East Asian 0.1%; South Asian 1.3%; Americas 0.2%; Ashkenazi 0.7%; Finnish 0.3%; Middle Eastern 0.4%; Amish 0.1%.
Estimated CC genotype frequency.
Showing effects for A/A genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Warfarin Sensitivity. Evidence: 9/10. Source: PMID 19300499. Typical.
Adverse Drug Reactions
NSAID Bleeding Risk. Evidence: 6/10. Source: PMID 14707031. Typical Risk.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Sensitivity. Evidence: 8/10. Source: PMID 15805193. Typical.
Valproic Acid Metabolism. Evidence: 8/10. Source: PMID 38287884. Typical.
Diabetes Medication Response
Glipizide Response. Evidence: 8/10. Source: PMID 10208645. Typical.
Cardiovascular Drug Response
Losartan Metabolism. Evidence: 8/10. Source: PMID 11823761. Typical.
Showing effects for A/C genotype
Warfarin Sensitivity. Evidence: 9/10. Source: PMID 19300499. ~40% Slower Clearance.
NSAID Bleeding Risk. Evidence: 6/10. Source: PMID 14707031. Increased Risk.
Phenytoin Sensitivity. Evidence: 8/10. Source: PMID 15805193. Slower Metabolism.
Valproic Acid Metabolism. Evidence: 8/10. Source: PMID 38287884. Slower Metabolism.
Glipizide Response. Evidence: 8/10. Source: PMID 10208645. Slower Metabolism.
Losartan Metabolism. Evidence: 8/10. Source: PMID 11823761. Slower Metabolism.
Showing effects for C/C genotype
Warfarin Sensitivity. Evidence: 9/10. Source: PMID 19300499. ~80% Slower Clearance.
NSAID Bleeding Risk. Evidence: 6/10. Source: PMID 14707031. Highly Increased Risk.
Phenytoin Sensitivity. Evidence: 8/10. Source: PMID 15805193. Severely Slow.
Valproic Acid Metabolism. Evidence: 8/10. Source: PMID 38287884. Severely Slow.
Glipizide Response. Evidence: 8/10. Source: PMID 10208645. Severely Slow.
Losartan Metabolism. Evidence: 8/10. Source: PMID 11823761. Severely Slow.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Standard liver function is expected because you have two copies of the common A allele [1]. This genetic setup allows your body to break down medications like warfarin, ibuprofen, and certain blood pressure drugs at a normal, expected pace [1]. Because clearance rates are typical, standard baseline risks for side effects from these drugs apply [2]. Standard dosing guidelines generally work well without genetic adjustments [2]. However, other genetic and lifestyle factors can still influence how you respond to medications [1].
Standard clearance of warfarin and NSAIDs; Typical risk of medication side effects.
Sample genotype: AC (Heterozygous)
Enzyme activity is reduced by approximately 40 percent due to the presence of one C allele [1]. This slower clearance can cause medications like the blood thinner warfarin to build up in the system [2]. Consequently, these drugs produce a stronger effect and carry a higher bleeding risk [2]. There is also an elevated risk of gastrointestinal bleeding when taking common NSAID pain relievers like ibuprofen or celecoxib [3]. If these medications are ever needed, healthcare providers may adjust the dosage or choose alternative therapies [2].
Slower clearance of warfarin and NSAIDs; Increased risk of bleeding complications.
Sample genotype: CC (Homozygous)
Enzymatic breakdown of many common drugs is nearly absent due to having two copies of the C allele [1]. The body processes medications like warfarin, phenytoin, and glipizide up to 80 percent slower than normal [2]. This severe impairment can lead to a rapid, dangerous accumulation of these drugs in the bloodstream [2]. Severe bleeding risks are highly elevated when taking warfarin or standard NSAID pain relievers [3]. Additionally, taking the anti-epilepsy drug phenytoin carries a significantly higher risk of severe adverse skin reactions [4]. Sharing these genetic findings with a doctor before starting any of these medications is highly recommended [1].
Severely slow clearance of warfarin and NSAIDs; High risk of drug toxicity and bleeding.
Variants with shared genetic architecture
rs1799853 · CYP2C9 Gene · Chr 10 · Medication Sensitivity
rs28371685 · CYP2C9 Gene · Chr 10 · Medication Metabolism
rs28371686 · CYP2C9 Gene · Chr 10 · Medication Response
The role of the CYP2C9-Leu359 allelic variant in the tolbutamide polymorphism.
Genetic association between sensitivity to warfarin and expression of CYP2C9*3.
Genetic variants associated with phenytoin-related severe cutaneous adverse reactions.
Content updated August 2026.
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