What you carry at this position in your DNA and what research says about it.
Statin Response: 8/10 evidence, 12 publications.
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Sample genotype (not yours): C/C
Typical Statin Response and Baseline Muscle Pain Risk
Standard OATP1B1 transporter function ensures typical clearance of statin medications from the bloodstream. The risk of experiencing statin-associated muscle pain remains at the average baseline level.
What this genotype means: Typical statin clearance; Average risk of statin-induced muscle pain.
Sample genotype (not yours): A/A
Highly Efficient Statin Clearance and Minimal Muscle Pain Risk
Two copies of the increased-function variant maximize the transport of statins into liver cells. This highly efficient clearance significantly lowers systemic drug exposure, minimizing the risk of muscle side effects.
What this genotype means: Maximally efficient statin clearance; Lowest risk of statin-induced muscle pain; Slightly higher urate levels.
Sample genotype (not yours): C/A
Enhanced Statin Clearance and Lower Muscle Pain Risk
Possessing one copy of the increased-function variant enhances the clearance of statins into the liver. This efficient transport lowers drug levels in the blood, reducing the likelihood of muscle-related side effects.
What this genotype means: More efficient statin clearance; Reduced risk of statin-induced muscle pain; Slightly slower grazoprevir metabolism.
Gene function and biological role
Gene Function: The SLCO1B1 gene encodes the organic anion-transporting polypeptide 1B1 (OATP1B1), a crucial transporter protein located on the surface of liver cells [1]. This transporter acts as a gatekeeper, actively moving compounds from the blood into the liver for processing and clearance [1]. Among its primary targets are endogenous substances like bilirubin and widely prescribed medications, particularly cholesterol-lowering statins [1]. Variations in this gene can significantly alter how efficiently the transporter functions, directly impacting drug levels in the bloodstream [2]. Consequently, SLCO1B1 is one of the most clinically important genes in pharmacogenomics, guiding personalized medication choices and dosing [2].
Variant Impact: The rs11045819 variant represents a single nucleotide change in the SLCO1B1 gene that alters the amino acid at position 155 from proline to threonine (p.Pro155Thr). This specific molecular change is the defining marker of the SLCO1B1*14 haplotype, which is classified as an increased-function variant. Unlike loss-of-function variants that slow down drug clearance, this change enhances the transporter's ability to move certain substances into liver cells [1]. Research indicates that this increased activity lowers the systemic concentration of statins in the bloodstream, potentially reducing the risk of muscle-related side effects [1]. Additionally, this enhanced uptake can lead to a more pronounced cholesterol-lowering response to specific statin therapies [2].
Key Insight: This variant actually increases transporter function, helping clear statins from the blood faster and lowering the risk of muscle pain.
Location: SLCO1B1. Chromosome 12 · 12p12.1 · 21.2 Mb
Estimated prevalence by population
Global 77.6%; European 70.7%; African 84.9%; East Asian 99.7%; South Asian 91.9%; Americas 80.9%; Ashkenazi 62.1%; Finnish 80.3%; Middle Eastern 78.2%; Amish 34.4%.
Estimated CC genotype frequency.
Global 20.7%; European 26.7%; African 14.5%; East Asian 0.3%; South Asian 8.0%; Americas 18.1%; Ashkenazi 33.4%; Finnish 18.6%; Middle Eastern 20.4%; Amish 48.5%.
Estimated CA genotype frequency.
Global 1.7%; European 2.5%; African 0.6%; East Asian < 0.1%; South Asian 0.2%; Americas 1.0%; Ashkenazi 4.5%; Finnish 1.1%; Middle Eastern 1.3%; Amish 17.1%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Lipid-Lowering Drug Response
Statin Response. Evidence: 8/10. Source: PMID 23100282. Typical Response.
Antimicrobial & Antiviral Response
Grazoprevir Metabolism. Evidence: 8/10. Source: PMID 31250727. Typical Metabolism.
Cardiovascular & Metabolic
Gout & Uric Acid
Uric Acid Levels. Evidence: 7/10. Source: PMID 33356394. Typical Levels.
Nutrition & Metabolism
Blood Chemistry & Metabolites
Amino Acid Levels. Evidence: 8/10. Source: PMID 41044249. Typical Levels.
Showing effects for A/A genotype
Statin Response. Evidence: 8/10. Source: PMID 23100282. Enhanced Response.
Grazoprevir Metabolism. Evidence: 8/10. Source: PMID 31250727. Slower Metabolism.
Uric Acid Levels. Evidence: 7/10. Source: PMID 33356394. Higher Levels.
Amino Acid Levels. Evidence: 8/10. Source: PMID 41044249. Higher Levels.
Showing effects for C/A genotype
Uric Acid Levels. Evidence: 7/10. Source: PMID 33356394. Slightly Higher.
Amino Acid Levels. Evidence: 8/10. Source: PMID 41044249. Slightly Higher.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Inheriting two copies of the common C allele results in standard OATP1B1 transporter activity, which represents the typical baseline for drug clearance in the general population [1]. When taking statins like simvastatin or atorvastatin, blood concentrations of the active drug remain within the expected therapeutic range [1]. This typical exposure level translates to an average, baseline risk of developing statin-associated muscle symptoms or myopathy [1]. Clinical studies show that standard cholesterol-lowering efficacy is achieved with typical dosing regimens [2]. While this genotype does not offer the protective benefits of the increased-function variant, it also does not carry the elevated risks associated with loss-of-function variants [2]. Standard clinical guidelines apply when selecting and dosing statin therapies. This baseline state represents the most common genetic profile globally.
Typical statin clearance; Average risk of statin-induced muscle pain.
Sample genotype: AA (Homozygous)
Inheriting two copies of the A allele results in highly efficient OATP1B1 transporter activity, maximizing the clearance of statins from the bloodstream into the liver [1]. This rapid clearance significantly decreases systemic exposure to medications like simvastatin, which dramatically lowers the risk of developing statin-associated muscle symptoms [1]. Because statins are concentrated more effectively in the liver where they perform their therapeutic action, this genotype is associated with an enhanced lipid-lowering response, particularly for fluvastatin [2]. Clinical evidence supports the role of this increased-function phenotype in promoting excellent statin tolerance and efficacy. On the other hand, this highly active transporter state is also associated with slightly higher circulating levels of urate, which is a key biomarker for gout risk [3]. Additionally, the metabolism of certain non-statin drugs like grazoprevir may be slower due to altered transport dynamics [4]. These findings demonstrate that while the variant is highly beneficial for cardiovascular therapies, it can introduce minor metabolic trade-offs.
Maximally efficient statin clearance; Lowest risk of statin-induced muscle pain; Slightly higher urate levels; Slower grazoprevir metabolism.
Sample genotype: CA (Heterozygous)
Possessing a single A allele leads to a moderate increase in OATP1B1 transporter function, facilitating more efficient uptake of medications into liver cells [1]. This enhanced transport reduces the systemic exposure and circulating levels of statins in the bloodstream, which is directly linked to a lower risk of statin-induced muscle pain and myopathy [1]. Because the liver receives the drug more effectively, some individuals may also experience an improved cholesterol-lowering response, particularly with therapies like fluvastatin [2]. Clinical guidelines recognize this increased-function state as a favorable factor for statin tolerance. However, this same increased transport capacity can slightly alter the clearance of other compounds, such as the hepatitis C medication grazoprevir, which may show slower metabolism in carriers [3]. This dual effect highlights how a single genetic change can have divergent impacts depending on the specific drug prescribed. Understanding these pharmacogenomic nuances helps clinicians tailor therapies to maximize efficacy while avoiding adverse reactions.
More efficient statin clearance; Reduced risk of statin-induced muscle pain; Slightly slower grazoprevir metabolism.
Variants with shared genetic architecture
rs4149056 · SLCO1B1 Gene · Chr 12 · Statin Side Effect Risk
rs4149081 · SLCO1B1 Gene · Chr 12 · Statin Response
rs11045879 · SLCO1B1 Gene · Chr 12 · Chemotherapy Toxicity Risk
Content updated August 2026.
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