What you carry at this position in your DNA and what research says about it.
Medication Response: 8/10 evidence, 9 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): C/C
Typical Medication Metabolism
Two copies of the common C allele result in normal CES1 enzyme activity. Your body metabolizes medications like clopidogrel, methylphenidate, and enalapril at a typical rate.
What this genotype means: Standard drug clearance rates; Typical response to clopidogrel and methylphenidate; Normal activation of enalapril.
Sample genotype (not yours): C/T
Altered Medication Response
Carrying one copy of the T allele reduces your CES1 enzyme activity. This can slow down the metabolism of several common medications, potentially increasing side effects or altering how well they work.
What this genotype means: Slower breakdown of methylphenidate; Enhanced antiplatelet response to clopidogrel; Increased risk of capecitabine toxicity.
Sample genotype (not yours): T/T
Significantly Slower Medication Metabolism
Carrying two copies of the T allele severely reduces your CES1 enzyme activity. This significantly alters how your body processes multiple medications, increasing the risk of side effects or changing drug efficacy.
What this genotype means: Highly reduced clearance of methylphenidate; Strongly enhanced antiplatelet response to clopidogrel; Impaired activation of enalapril.
Gene function and biological role
Gene Function: The CES1 gene encodes carboxylesterase 1, a major enzyme primarily found in the liver that is responsible for metabolizing a wide variety of ester- and amide-containing drugs [1]. It plays a critical role in either deactivating active drugs or activating prodrugs so they can exert their therapeutic effects [1]. For example, CES1 is the sole enzyme responsible for the breakdown and deactivation of methylphenidate, a common ADHD medication [2]. Conversely, it also deactivates clopidogrel, an antiplatelet medication, meaning that reduced CES1 activity actually leads to higher levels of clopidogrel's active form [3]. Genetic variations in this gene can therefore lead to significant differences in drug safety and efficacy [4].
Variant Impact: The rs71647871 variant, also known as G143E or Gly144Glu, is a missense mutation in the CES1 gene that results in an amino acid change from glycine to glutamate [5]. This specific alteration occurs near the enzyme's active site and severely impairs its catalytic function, making it a well-known loss-of-function variant [5]. Because of this loss of function, individuals carrying the variant allele metabolize certain medications much more slowly than typical [6]. This slower metabolism can lead to drug accumulation and increased side effects for some medications, while enhancing the therapeutic response of others [7]. The variant is relatively rare, with a global frequency of around 1 percent [4].
Key Insight: A single genetic change in CES1 can have opposite clinical effects depending on the drug, making some medications work better while making others more toxic.
Location: CES1. Chromosome 16 · 16q12.2 · 55.8 Mb
Estimated prevalence by population
Global 98.0%; European 97.1%; African 99.5%; East Asian > 99.9%; South Asian 98.6%; Americas 97.9%; Ashkenazi 95.4%; Finnish 97.9%; Middle Eastern 96.6%; Amish 99.3%.
Estimated CC genotype frequency.
Global 2.0%; European 2.9%; African 0.5%; East Asian < 0.1%; South Asian 1.4%; Americas 2.1%; Ashkenazi 4.6%; Finnish 2.1%; Middle Eastern 3.3%; Amish 0.7%.
Estimated CT genotype frequency.
Global < 0.1%; European < 0.1%; African < 0.1%; East Asian < 0.1%; South Asian < 0.1%; Americas < 0.1%; Ashkenazi 0.1%; Finnish < 0.1%; Middle Eastern < 0.1%; Amish < 0.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Clopidogrel Response. Evidence: 8/10. Source: PMID 25704243. Typical Response.
Antidepressant & Psychiatric Drug Response
Methylphenidate Response. Evidence: 5/10. Source: PMID 19733552. Typical Metabolism.
Cardiovascular Drug Response
Enalapril Response. Evidence: 5/10. Source: PMID 25919042. Typical Activation.
Chemotherapy Response
Capecitabine Toxicity. Evidence: 5/10. Source: PMID 38004528. Typical Risk.
Anesthesia Response
Remimazolam Response. Evidence: 5/10. Source: PMID 39884809. Typical Metabolism.
Showing effects for C/T genotype
Clopidogrel Response. Evidence: 8/10. Source: PMID 25704243. Enhanced Response.
Methylphenidate Response. Evidence: 5/10. Source: PMID 19733552. Slower Metabolism.
Enalapril Response. Evidence: 5/10. Source: PMID 25919042. Slower Activation.
Capecitabine Toxicity. Evidence: 5/10. Source: PMID 38004528. Increased Risk.
Remimazolam Response. Evidence: 5/10. Source: PMID 39884809. Slower Metabolism.
Showing effects for T/T genotype
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Having the C/C genotype means you have normal, fully functional carboxylesterase 1 enzyme levels in your liver. This is the most common genotype globally, occurring in approximately 98 percent of the population. When taking medications metabolized by CES1, such as the ADHD treatment methylphenidate, your body breaks them down at a standard rate [1]. For prodrugs like the blood pressure medication enalapril, your liver activates them efficiently to help manage your cardiovascular health [2]. Similarly, clopidogrel is processed normally, maintaining standard antiplatelet effects without unexpected drug accumulation [3]. Your risk of experiencing severe side effects from chemotherapy agents like capecitabine remains at the typical baseline [4].
Standard drug clearance rates; Typical response to clopidogrel and methylphenidate; Normal activation of enalapril.
Sample genotype: CT (Heterozygous)
Carrying one copy of the T allele results in a partially dysfunctional CES1 enzyme, which slows down your drug metabolism. For the ADHD medication methylphenidate, this slower clearance can lead to higher drug levels in your blood, meaning you may be more sensitive to it, with a greater risk of side effects [1]. When taking the antiplatelet drug clopidogrel, however, reduced CES1 activity is actually beneficial, as it prevents the drug's inactivation and leads to a stronger anti-clotting effect [2]. Conversely, prodrugs like enalapril may be activated more slowly, potentially reducing their immediate blood pressure-lowering efficacy [3]. Additionally, you may have an increased risk of severe toxicities, such as Hand-Foot Syndrome, when undergoing chemotherapy with capecitabine [4].
Slower breakdown of methylphenidate; Enhanced antiplatelet response to clopidogrel; Increased risk of capecitabine toxicity.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele means you have a profound loss of CES1 enzyme activity, leading to highly altered drug processing. Your body will deactivate methylphenidate extremely slowly, which can cause the drug to accumulate and significantly increase the risk of stimulant-related side effects [1]. For clopidogrel therapy, this severe enzyme deficiency leads to much higher levels of the active drug, resulting in a highly pronounced antiplatelet response and lower clotting risk [2]. However, prodrugs like enalapril that require CES1 for activation will be processed very slowly, which could impair their therapeutic effectiveness [3]. You also face a substantially higher risk of severe drug toxicity and Hand-Foot Syndrome if treated with the chemotherapy drug capecitabine [4].
Highly reduced clearance of methylphenidate; Strongly enhanced antiplatelet response to clopidogrel; Impaired activation of enalapril.
Variants with shared genetic architecture
rs2244613 · CES1 Gene · Chr 16 · Anticoagulant Response
rs28399504 · CYP2C19 Gene · Chr 10 · Drug Metabolism
rs41291556 · CYP2C19 Gene · Chr 10 · Clopidogrel Response
Carboxylesterase 1 gene polymorphism and methylphenidate response in ADHD.
Carboxylesterase 1 as a determinant of clopidogrel metabolism and activation.
Pharmacogenomics knowledge for personalized medicine.
The impact of CES1 genotypes on the pharmacokinetics of methylphenidate in healthy Danish subjects.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com