What you carry at this position in your DNA and what research says about it.
Medication Response: 8/10 evidence, 28 publications.
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Sample genotype (not yours): C/C
Normal Medication Metabolism
You have two functional copies of the CYP2D6 gene, resulting in normal enzyme activity. This means you likely process standard doses of many common medications as expected.
What this genotype means: Normal clearance of CYP2D6-metabolized drugs; Efficient activation of prodrugs like codeine; Typical risk of medication side effects.
Sample genotype (not yours): C/T
Typical Medication Metabolism
You carry one functional copy and one nonfunctional copy of the CYP2D6 gene. Your body generally maintains normal drug metabolism, though clearance of some medications may be slightly slower.
What this genotype means: Generally normal drug clearance; Slightly reduced metabolism of some beta-blockers; Potential for milder Alzheimer's pathology.
Sample genotype (not yours): T/T
Slow Medication Metabolism
You carry two nonfunctional copies of the CYP2D6 gene, making you a poor metabolizer. This significantly increases your risk of side effects from many common drugs and prevents some medications from working.
What this genotype means: High risk of side effects from beta-blockers and antidepressants; Inability to activate codeine, tramadol, and tamoxifen; Elevated levels of potato-derived solanidine.
Gene function and biological role
Gene Function: The CYP2D6 gene encodes cytochrome P450 2D6, a key liver enzyme responsible for metabolizing approximately 25% of all clinically used medications [1]. This enzyme processes a wide variety of therapeutic drugs, including antidepressants, beta-blockers, antipsychotics, and opioids [1]. It is also involved in activating prodrugs, such as converting codeine into its active form, morphine [1]. Because of its critical role in drug clearance, genetic variations in this gene can dramatically alter how a person responds to standard medication doses [1]. The gene is highly polymorphic, leading to phenotypes ranging from poor to ultra-rapid metabolizers [1].
Variant Impact: The rs3892097 variant, commonly known as the CYP2D6*4 allele, is a single nucleotide polymorphism that disrupts a splice acceptor site in the CYP2D6 gene [2]. This splicing defect prevents the proper formation of messenger RNA, resulting in a completely nonfunctional enzyme [2]. It is the most common nonfunctional variant of CYP2D6, particularly in populations of European ancestry [3]. Individuals carrying two copies of this variant lack functional CYP2D6 activity entirely, making them poor metabolizers [2]. This deficiency leads to slow clearance of many drugs or an inability to activate certain prodrugs [2].
Key Insight: This variant is the single most common cause of poor drug metabolism in people of European descent, directly impacting how the body processes a quarter of all prescribed medications.
Location: CYP2D6. Chromosome 22 · 22q13.2 · 42.1 Mb
Estimated prevalence by population
Global 74.2%; European 64.2%; African 85.3%; East Asian 98.7%; South Asian 79.7%; Americas 75.6%; Ashkenazi 66.5%; Finnish 81.6%; Middle Eastern 80.6%; Amish 58.0%.
Estimated CC genotype frequency.
Global 23.5%; European 31.8%; African 14.1%; East Asian 1.3%; South Asian 19.2%; Americas 22.7%; Ashkenazi 30.1%; Finnish 17.5%; Middle Eastern 18.3%; Amish 36.3%.
Estimated CT genotype frequency.
Global 2.3%; European 3.9%; African 0.6%; East Asian < 0.1%; South Asian 1.2%; Americas 1.7%; Ashkenazi 3.4%; Finnish 0.9%; Middle Eastern 1.0%; Amish 5.7%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Drug Metabolism Enzyme Activity
Medication Response. Evidence: 8/10. Source: PMID 18070221. Normal Response.
Cardiovascular Drug Response
Beta-Blocker Response. Evidence: 8/10. Source: PMID 18784654. Typical Response.
Neurology & Mental Health
Neurodegenerative Diseases
Alzheimer's Pathology. Evidence: 7/10. Source: PMID 7574463. Typical Pathology.
Nutrition & Metabolism
Blood Chemistry & Metabolites
Solanidine Levels. Evidence: 6/10. Source: PMID 37277652. Typical Levels.
Showing effects for C/T genotype
Medication Response. Evidence: 8/10. Source: PMID 18070221. Typical Response.
Alzheimer's Pathology. Evidence: 7/10. Source: PMID 7574463. Milder Pathology.
Solanidine Levels. Evidence: 6/10. Source: PMID 37277652. Slightly Elevated.
Showing effects for T/T genotype
Medication Response. Evidence: 8/10. Source: PMID 18070221. Poor Metabolism.
Beta-Blocker Response. Evidence: 8/10. Source: PMID 18784654. High Bradycardia Risk.
Solanidine Levels. Evidence: 6/10. Source: PMID 37277652. Elevated Levels.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Two copies of the functional C allele classify you as an extensive (normal) metabolizer of drugs processed by the CYP2D6 pathway [1]. This includes a wide range of common therapeutics, such as beta-blockers, antidepressants, and pain relievers [1]. You are likely to experience typical efficacy and standard side-effect risks when taking these medications at standard prescribed doses [1]. Additionally, you can efficiently convert prodrugs like codeine into their active, pain-relieving forms [1]. Your body also maintains normal clearance of dietary compounds like solanidine, a natural glycoalkaloid found in potatoes [2]. While your medication response is typical, you do not carry the variant associated with milder synaptic pathology in Alzheimer's disease [3].
Normal clearance of CYP2D6-metabolized drugs; Efficient activation of prodrugs like codeine; Typical risk of medication side effects.
Sample genotype: CT (Heterozygous)
One copy of the nonfunctional T allele (CYP2D6*4) typically results in normal or slightly reduced enzyme activity [1]. In clinical settings, most individuals with this genotype are still classified as extensive metabolizers and process medications normally [1]. However, you may experience slightly slower clearance of certain drugs, such as the beta-blocker bisoprolol or the antidepressant fluoxetine, compared to those with two functional copies [2] [3]. Your body is still able to activate prodrugs like codeine effectively under normal circumstances [1]. Interestingly, carrying this variant has been associated with a potential benefit of milder synaptic pathology in Alzheimer's disease [4]. However, some studies suggest that carriers exposed to high levels of agricultural pesticides may have an increased susceptibility to Parkinson's disease [1].
Generally normal drug clearance; Slightly reduced metabolism of some beta-blockers; Potential for milder Alzheimer's pathology.
Sample genotype: TT (Homozygous)
Two nonfunctional T alleles mean you lack functional CYP2D6 enzyme activity entirely, classifying you as a poor metabolizer [1]. This deficiency dramatically slows the clearance of many common medications, leading to drug buildup and a high risk of side effects [1]. For example, taking beta-blockers like metoprolol can lead to an abnormally slow heart rate, known as bradycardia [2]. Similarly, standard doses of tricyclic antidepressants can cause severe adverse effects due to slow clearance [1]. Conversely, you cannot efficiently activate prodrugs like codeine or tramadol, meaning these pain relievers may provide little to no relief [1]. You also have reduced activation of tamoxifen, potentially lowering its effectiveness in breast cancer therapy [1]. On the non-medication side, you have elevated levels of solanidine from dietary potatoes due to slow clearance [3].
High risk of side effects from beta-blockers and antidepressants; Inability to activate codeine, tramadol, and tamoxifen; Elevated levels of potato-derived solanidine.
Variants with shared genetic architecture
rs1065852 · CYP2D6 Gene · Chr 22 · Medication Response
rs28371725 · CYP2D6 Gene · Chr 22 · Medication Metabolism
rs28371706 · CYP2D6 Gene · Chr 22 · Drug Metabolism
Influence of the CYP2D6*4 polymorphism on dose, switching and discontinuation of antidepressants.
Identification of the primary gene defect at the cytochrome P450 CYP2D locus.
The CYP2D6B allele is associated with a milder synaptic pathology in Alzheimer's disease.
Content updated August 2026.
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