What you carry at this position in your DNA and what research says about it.
Medication Response: 6/10 evidence, 33 publications.
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Sample genotype (not yours): C/C
Typical Clearance with Specific Drug Sensitivities
Standard transporter expression provides typical clearance for most medications, but some chemotherapy and immunosuppressant regimens may carry elevated toxicity risks.
What this genotype means: Typical response to statin medications; Increased risk of toxicity with FOLFOX chemotherapy; Altered metabolism of certain immunosuppressants.
Sample genotype (not yours): C/T
Altered Clearance for Specific Medications
A single copy of the variant allele alters transporter expression, leading to drug-specific changes in clearance, side effects, and therapeutic response.
What this genotype means: Reduced response to atorvastatin and simvastatin; Increased risk of neutropenia during certain chemotherapies; Altered processing of transplant medications.
Sample genotype (not yours): T/T
Altered Clearance and Increased Sensitivity to Certain Drugs
Two copies of the variant allele significantly modify transporter levels, reducing the clearance of several drugs and increasing the risk of specific toxicities.
What this genotype means: Higher risk of neurotoxicity with oxaliplatin and fluorouracil; Reduced effectiveness of standard statin doses; Highly variable methotrexate elimination rates.
Gene function and biological role
Gene Function: The ABCC2 gene encodes multidrug resistance-associated protein 2 (MRP2), an ATP-dependent efflux transporter expressed primarily in the liver, kidneys, and intestines [1]. This membrane transporter plays a critical role in the elimination of endogenous compounds, such as bilirubin, and a wide variety of foreign substances [1]. By pumping drugs and their metabolites into the bile or urine, MRP2 directly influences the systemic exposure and clearance of many common medications [2]. Variations in this gene can alter the expression or function of the transporter, leading to significant differences in drug efficacy and the risk of adverse side effects [2].
Variant Impact: Located in the 5-prime untranslated region (5 UTR) near the promoter, rs717620 is a single nucleotide polymorphism that influences the transcription and translation of the ABCC2 gene [3]. The transition from a cytosine (C) to a thymine (T) allele alters the secondary structure of the mRNA, which can impact the binding efficiency of the translation machinery [4]. This molecular change leads to altered expression levels of the MRP2 transporter in tissues like the liver and kidneys [3]. Consequently, this variant is widely studied for its role in modifying the pharmacokinetics and toxicities of several therapeutic agents [4].
Key Insight: This variant alters the physical folding of the mRNA molecule, which directly changes how efficiently the cellular machinery can translate the genetic code into functional transporter proteins.
Location: ABCC2. Chromosome 10 · 10q24.2 · 99.8 Mb
Estimated prevalence by population
Global 71.9%; European 64.2%; African 88.0%; East Asian 63.0%; South Asian 78.0%; Americas 70.0%; Ashkenazi 62.3%; Finnish 65.7%; Middle Eastern 73.5%; Amish 59.7%.
Estimated CC genotype frequency.
Global 25.4%; European 31.8%; African 11.6%; East Asian 32.8%; South Asian 20.6%; Americas 27.3%; Ashkenazi 33.2%; Finnish 30.7%; Middle Eastern 24.4%; Amish 35.1%.
Estimated CT genotype frequency.
Global 2.7%; European 3.9%; African 0.4%; East Asian 4.3%; South Asian 1.4%; Americas 2.7%; Ashkenazi 4.4%; Finnish 3.6%; Middle Eastern 2.0%; Amish 5.2%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Chemotherapy Response
Chemotherapy Toxicity. Evidence: 5/10. Source: PMID 22868256. Increased FOLFOX Risk.
Immunosuppressant & Biologic Response
Methotrexate Clearance. Evidence: 6/10. Source: PMID 23069858. Typical Clearance.
Immunosuppressant Risk. Evidence: 5/10. Source: PMID 30345879. Higher Graft Risk.
Lipid-Lowering Drug Response
Statin Response. Evidence: 5/10. Source: PMID 22186618. Typical Response.
Neurology & Mental Health
Cognitive Performance
Executive Function. Evidence: 6/10. Source: PMID 36150907. Associated.
Showing effects for C/T genotype
Chemotherapy Toxicity. Evidence: 5/10. Source: PMID 22868256. Altered Risk Profile.
Methotrexate Clearance. Evidence: 6/10. Source: PMID 23069858. Variable Clearance.
Statin Response. Evidence: 5/10. Source: PMID 22186618. Poorer Response.
Showing effects for T/T genotype
Chemotherapy Toxicity. Evidence: 5/10. Source: PMID 22868256. Higher Neurotoxicity.
Immunosuppressant Risk. Evidence: 5/10. Source: PMID 30345879. Slower Metabolism.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Standard transporter levels are maintained, resulting in typical baseline clearance for many common medications [1]. Clinical studies of the FOLFOX chemotherapy regimen (fluorouracil, leucovorin, and oxaliplatin) show that this common genotype is associated with an increased risk of overall drug toxicity [2]. When undergoing renal transplantation, patients with this profile may experience slower metabolism of mycophenolic acid and tacrolimus, which has been linked to an increased likelihood of graft failure and kidney damage [3]. ClinVar evaluations confirm that this genotype is entirely benign regarding hereditary conditions like Dubin-Johnson syndrome.
Typical response to statin medications; Increased risk of toxicity with FOLFOX chemotherapy; Altered metabolism of certain immunosuppressants.
Sample genotype: CT (Heterozygous)
Transporter expression is moderately altered, creating a highly drug-specific clearance profile [1]. Patients taking statins such as atorvastatin or simvastatin may experience a poorer cholesterol-lowering response [1]. During chemotherapy with cisplatin or fluorouracil, there is an increased risk of developing severe neutropenia, a condition characterized by low white blood cell counts [2]. Studies on immunosuppressive therapies like tacrolimus and mycophenolic acid indicate a higher likelihood of kidney damage and graft failure [3]. Methotrexate clearance is highly variable, with studies showing conflicting patterns of accelerated versus delayed elimination [4]. This intermediate state does not cause hereditary liver disorders.
Reduced response to atorvastatin and simvastatin; Increased risk of neutropenia during certain chemotherapies; Altered processing of transplant medications.
Sample genotype: TT (Homozygous)
Transporter levels are significantly modified, which can delay the excretion of various therapeutic compounds [1]. When treated with oxaliplatin, fluorouracil, or leucovorin, there is a documented increase in the severity of neurotoxicity and neutropenia [2]. Cholesterol-lowering therapies using simvastatin or atorvastatin often show a poorer response, meaning standard doses may be less effective [3]. Slower metabolism of immunosuppressants like tacrolimus and mycophenolic acid is common, though the risk of graft failure is less pronounced than in C allele carriers [4]. Methotrexate processing is highly unpredictable, with some individuals experiencing delayed elimination and elevated toxicity [5]. This genetic profile is classified as completely benign for Dubin-Johnson syndrome.
Higher risk of neurotoxicity with oxaliplatin and fluorouracil; Reduced effectiveness of standard statin doses; Highly variable methotrexate elimination rates.
Variants with shared genetic architecture
rs3740066 · ABCC2 Gene · Chr 10 · Pregnancy Liver Health
rs8187710 · ABCC2 Gene · Chr 10 · Chemotherapy Heart Risk
rs2273697 · ABCC2 Gene · Chr 10 · Carbamazepine Side Effects
Effect of ABCC2 (MRP2) transport function on erythromycin metabolism.
The Impact of ABCC2 -24C>T Gene Polymorphism on Graft Survival in Kidney Transplant Recipients.
Pharmacogenetic analysis of adjuvant FOLFOX for Korean patients with colon cancer.
Content updated August 2026.
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