What you carry at this position in your DNA and what research says about it.
Anticoagulant Response: 7/10 evidence, 11 publications.
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Sample genotype (not yours): G/G
Lower Dabigatran Bleeding Risk but Higher Chemotherapy Toxicity
Processing of certain blood thinners and chemotherapy drugs is significantly altered. Dabigatran is activated more slowly, reducing the risk of bleeding complications. However, capecitabine treatment carries a higher risk of severe side effects like hand-foot syndrome.
What this genotype means: Lower risk of bleeding on dabigatran; Higher risk of capecitabine side effects; Reduced active dabigatran levels.
Sample genotype (not yours): G/T
Altered Response to Anticoagulants and Chemotherapy
Blood levels of several common medications may deviate from typical ranges. Bleeding risk is reduced when taking dabigatran, but increased when taking other common anticoagulants. Chemotherapy with capecitabine also carries an elevated risk of toxic side effects.
What this genotype means: Lower risk of bleeding on dabigatran; Higher risk of bleeding on other DOACs; Higher risk of capecitabine side effects.
Sample genotype (not yours): T/T
Higher Bleeding Risk with Common Anticoagulants
Standard doses of several blood thinners may lead to higher active drug levels. This elevation increases the risk of bleeding complications during treatment. Conversely, the risk of severe toxicity from the chemotherapy drug capecitabine is typical.
What this genotype means: Higher risk of bleeding on dabigatran; Higher risk of bleeding on other DOACs; Typical risk of capecitabine side effects.
Gene function and biological role
Gene Function: Carboxylesterase 1 is a major liver enzyme responsible for hydrolyzing a wide variety of prodrugs and endogenous esters. It plays a critical role in activating the anticoagulant prodrug dabigatran etexilate into its active, clot-preventing form [1]. Additionally, this enzyme is involved in the initial metabolic breakdown of the chemotherapy drug capecitabine [2]. Variations in this gene can significantly alter enzyme activity, leading to differences in drug clearance, efficacy, and side effects [1] [2].
Variant Impact: This single nucleotide polymorphism is located in an intron of the CES1 gene and influences the expression levels of the carboxylesterase 1 enzyme. The presence of the G allele is associated with reduced enzyme expression in the liver, which slows down the activation of certain prodrugs [3]. Consequently, individuals carrying the G allele tend to have lower active levels of drugs like dabigatran in their bloodstream [3]. Conversely, this same reduction in enzyme activity can alter the processing of other medications, such as capecitabine, affecting toxicity profiles [2].
Key Insight: The same genetic variant that protects you from bleeding on one blood thinner can increase your risk of severe skin toxicity on a chemotherapy drug.
Location: CES1. Chromosome 16 · 16q12.2 · 55.8 Mb
Estimated prevalence by population
Global 6.0%; European 3.4%; African 6.0%; East Asian 35.6%; South Asian 16.7%; Americas 5.7%; Ashkenazi 5.3%; Finnish 3.9%; Middle Eastern 5.7%; Amish 11.1%.
Estimated GG genotype frequency.
Global 34.1%; European 30.0%; African 37.0%; East Asian 48.1%; South Asian 48.3%; Americas 36.3%; Ashkenazi 35.5%; Finnish 31.8%; Middle Eastern 36.3%; Amish 44.4%.
Estimated GT genotype frequency.
Global 59.9%; European 66.6%; African 57.0%; East Asian 16.2%; South Asian 34.9%; Americas 58.0%; Ashkenazi 59.2%; Finnish 64.2%; Middle Eastern 58.0%; Amish 44.4%.
Estimated TT genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Dabigatran Bleeding Risk. Evidence: 7/10. Source: PMID 23467860. Lower Bleeding Risk.
DOAC Bleeding Risk. Evidence: 6/10. Source: PMID 36309848. Typical Bleeding Risk.
Chemotherapy Response
Capecitabine Toxicity. Evidence: 6/10. Source: PMID 28139840. Higher Toxicity Risk.
Showing effects for G/T genotype
DOAC Bleeding Risk. Evidence: 6/10. Source: PMID 36309848. Higher Bleeding Risk.
Showing effects for T/T genotype
Dabigatran Bleeding Risk. Evidence: 7/10. Source: PMID 23467860. Higher Bleeding Risk.
Capecitabine Toxicity. Evidence: 6/10. Source: PMID 28139840. Typical Toxicity Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Hepatic activation of the anticoagulant prodrug dabigatran is reduced in the presence of two copies of the G allele [1]. This slower conversion leads to lower active drug concentrations in the bloodstream, which significantly decreases the likelihood of experiencing bleeding complications during treatment [1] [2]. However, this altered metabolic rate does not appear to compromise the drug's ability to prevent strokes [1]. In contrast, when undergoing chemotherapy with capecitabine, this genotype is linked to an increased risk of early-onset drug toxicity [3]. Patients are more likely to experience severe hand-foot syndrome, characterized by painful redness and swelling on the palms and soles, as well as severe diarrhea [3] [4].
Lower risk of bleeding on dabigatran; Higher risk of capecitabine side effects; Reduced active dabigatran levels.
Sample genotype: GT (Heterozygous)
Carrying one copy of the G allele results in intermediate carboxylesterase 1 activity, creating a complex drug-response profile. When treated with the anticoagulant dabigatran, active drug levels are lower, which helps protect against bleeding events [1] [2]. However, this protective effect does not extend to other direct oral anticoagulants like apixaban, edoxaban, or rivaroxaban, where bleeding risks may actually be elevated [3]. Furthermore, processing of the cancer drug capecitabine is altered, raising the likelihood of experiencing severe side effects [4]. These toxicities frequently manifest as severe diarrhea or hand-foot syndrome, which can require treatment interruptions [4] [5].
Lower risk of bleeding on dabigatran; Higher risk of bleeding on other DOACs; Higher risk of capecitabine side effects.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele is associated with typical, fully active levels of the carboxylesterase 1 enzyme. When taking the prodrug dabigatran, rapid and efficient conversion leads to higher active drug concentrations in the body [1]. While this ensures robust prevention of blood clots, it also significantly increases the risk of minor and major bleeding events compared to G allele carriers [1] [2]. Similar elevations in bleeding risk have been observed with other direct oral anticoagulants, including apixaban, edoxaban, and rivaroxaban [3]. On the other hand, the risk of experiencing severe early-onset toxicities from capecitabine chemotherapy, such as hand-foot syndrome, remains at the typical baseline level [4].
Higher risk of bleeding on dabigatran; Higher risk of bleeding on other DOACs; Typical risk of capecitabine side effects.
Variants with shared genetic architecture
rs71647871 · CES1 Gene · Chr 16 · Medication Response
rs56038477 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
rs2072671 · CDA Gene · Chr 1 · Chemotherapy Sensitivity
Pharmacogenetics of dabigatran etexilate interindividual variability.
Capecitabine-induced hand-foot syndrome: A pharmacogenetic study beyond DPYD.
Genetic determinants of dabigatran plasma levels and their relation to bleeding.
Content updated August 2026.
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