What you carry at this position in your DNA and what research says about it.
Medication Response: 9/10 evidence, 24 publications.
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Sample genotype (not yours): G/G
Normal Drug Metabolism
Standard processing of many common medications. Standard doses of drugs like codeine, tamoxifen, and beta-blockers are processed as expected.
What this genotype means: Normal processing of codeine and tramadol; Typical response to tamoxifen therapy; Standard clearance of beta-blockers.
Sample genotype (not yours): A/A
Slow Drug Metabolism
Two copies of the decreased-function variant are present. This can lead to poor activation of pain relievers or slower clearance of other medications.
What this genotype means: Significantly reduced pain relief from codeine; Higher risk of side effects from beta-blockers; Reduced therapeutic response to tamoxifen.
Sample genotype (not yours): G/A
Slightly Reduced Drug Metabolism
One copy of the decreased-function variant is present. Some medications may be processed slightly slower than typical, but usually without major clinical impacts.
What this genotype means: Slightly slower clearance of some antidepressants; Mildly reduced activation of codeine; Generally typical response to most therapies.
Gene function and biological role
Gene Function: Cytochrome P450 2D6 (CYP2D6) is a vital liver enzyme responsible for processing approximately 20% to 25% of all clinically prescribed medications [1]. It plays a crucial role in either breaking down active drugs to clear them from the body or converting inactive prodrugs into their active forms [1]. Genetic variations in this gene can dramatically alter how quickly or slowly an individual processes these substances [1]. This can lead to unexpected side effects from standard doses or a complete lack of therapeutic benefit [1].
Variant Impact: A missense mutation at rs1065852 changes the amino acid proline to serine at position 34 (p.Pro34Ser) [2]. This specific change destabilizes the resulting enzyme, leading to significantly reduced catalytic activity and lower thermal stability [2]. It is the defining marker for the CYP2D6*10 star allele, which is highly prevalent in East Asian populations [2]. Individuals carrying this variant are classified as intermediate or poor metabolizers for a wide range of common drugs [3].
Key Insight: This variant is the defining marker for the CYP2D6*10 allele, which is found in over half of the East Asian population but is far less common in people of European or African descent.
Location: CYP2D6. Chromosome 22 · 22q13.2 · 42.1 Mb
Estimated prevalence by population
Global 66.2%; European 60.4%; African 76.7%; East Asian 21.0%; South Asian 69.5%; Americas 71.8%; Ashkenazi 56.9%; Finnish 78.7%; Middle Eastern 77.6%; Amish 48.9%.
Estimated GG genotype frequency.
Global 29.5%; European 34.6%; African 21.8%; East Asian 49.7%; South Asian 27.8%; Americas 25.9%; Ashkenazi 37.1%; Finnish 20.0%; Middle Eastern 21.0%; Amish 42.1%.
Estimated GA genotype frequency.
Global 4.3%; European 5.0%; African 1.5%; East Asian 29.3%; South Asian 2.8%; Americas 2.3%; Ashkenazi 6.0%; Finnish 1.3%; Middle Eastern 1.4%; Amish 9.0%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Chemotherapy Response
Tamoxifen Response. Evidence: 8/10. Source: PMID 29978573. Typical Response.
Pain Medication Response
Pain Relief Response. Evidence: 8/10. Source: PMID 12051754. Typical Response.
Antidepressant & Psychiatric Drug Response
Antidepressant Response. Evidence: 9/10. Source: PMID 24302953. Typical Response.
Antipsychotic Side Effects. Evidence: 5/10. Source: PMID 16490169. Typical Risk.
Cardiovascular Drug Response
Beta-Blocker Response. Evidence: 8/10. Source: PMID 37952358. Typical Response.
Showing effects for A/A genotype
Tamoxifen Response. Evidence: 8/10. Source: PMID 29978573. Reduced Response.
Pain Relief Response. Evidence: 8/10. Source: PMID 12051754. Poor Response.
Antidepressant Response. Evidence: 9/10. Source: PMID 24302953. Altered Response.
Antipsychotic Side Effects. Evidence: 5/10. Source: PMID 16490169. Increased Risk.
Beta-Blocker Response. Evidence: 8/10. Source: PMID 37952358. Higher Sensitivity.
Showing effects for G/A genotype
Pain Relief Response. Evidence: 8/10. Source: PMID 12051754. Slightly Reduced.
Beta-Blocker Response. Evidence: 8/10. Source: PMID 37952358. Slightly Sensitive.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Two copies of the functional G allele ensure that the CYP2D6 enzyme has normal catalytic activity and stability [1]. Standard clinical doses of medications processed by this pathway are highly likely to work as intended [1]. For example, prodrugs like codeine and tramadol are efficiently converted into their active pain-relieving forms [1]. Similarly, the breast cancer therapy tamoxifen is processed normally, ensuring typical treatment outcomes [2]. There is no elevated risk of side effects or therapeutic failure due to this specific genetic marker [1].
Normal processing of codeine and tramadol; Typical response to tamoxifen therapy; Standard clearance of beta-blockers.
Sample genotype: AA (Homozygous)
Two copies of the A variant significantly reduce the stability and activity of the CYP2D6 enzyme [1]. This slow-metabolizer status means prodrugs like codeine and tramadol cannot be efficiently converted into their active forms, often resulting in inadequate pain relief [1]. Conversely, active medications like metoprolol or certain antidepressants are cleared much slower, increasing the risk of side effects at standard doses [2]. For breast cancer patients, this genotype is associated with a reduced response to tamoxifen, making alternative therapies like toremifene a consideration under medical guidance [3]. This variant is highly prevalent in East Asian populations, where it shapes regional prescribing guidelines [1].
Significantly reduced pain relief from codeine; Higher risk of side effects from beta-blockers; Reduced therapeutic response to tamoxifen.
Sample genotype: GA (Heterozygous)
Inheriting one copy of the A variant results in a moderately reduced level of CYP2D6 enzyme activity [1]. This intermediate metabolic state means some medications are processed slightly slower, though the body often compensates [1]. Prodrugs like codeine may provide slightly less pain relief, while active drugs like certain antidepressants might clear more slowly [2]. In most cases, standard doses are still tolerated well, but monitoring is helpful [1]. This genotype is very common, especially in populations of East Asian ancestry [1].
Slightly slower clearance of some antidepressants; Mildly reduced activation of codeine; Generally typical response to most therapies.
Variants with shared genetic architecture
rs28371725 · CYP2D6 Gene · Chr 22 · Medication Metabolism
rs3892097 · CYP2D6 Gene · Chr 22 · Medication Response
rs28371706 · CYP2D6 Gene · Chr 22 · Drug Metabolism
The need for education in pharmacogenomics: a regulatory perspective.
CYP2D6.10 present in human liver microsomes shows low catalytic activity and thermal stability.
CYP2D6 P34S Polymorphism and Outcomes of Escitalopram Treatment in Koreans with Major Depression.
Content updated August 2026.
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