What you carry at this position in your DNA and what research says about it.
Drug Metabolism Speed: 5/10 evidence, 28 publications.
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Sample genotype (not yours): T/T
Typical Drug Metabolism Speed
Standard clearance rates for medications metabolized by the NAT2 enzyme are expected. This genotype is associated with a typical risk of drug-induced liver damage and toxicity.
What this genotype means: Normal enzyme activity; Typical drug clearance rates; Standard risk of medication side effects.
Sample genotype (not yours): C/C
Slow Drug Metabolism Speed
Significantly slower clearance of certain medications and environmental toxins is expected. This genotype is strongly linked to a higher risk of drug toxicity, liver damage, and chemical-related cancers.
What this genotype means: Significantly reduced enzyme function; Slow clearance of medications; Increased susceptibility to environmental toxins.
Sample genotype (not yours): T/C
Slightly Slower Drug Metabolism Speed
Medications processed by the NAT2 enzyme may clear more slowly than average. This can elevate the risk of side effects or toxicity when taking specific drugs like isoniazid or phenytoin.
What this genotype means: Reduced enzyme activity; Slower clearance of certain medications; Elevated risk of drug-induced liver strain.
Gene function and biological role
Gene Function: The NAT2 gene encodes N-acetyltransferase 2, a critical liver enzyme responsible for metabolizing a wide range of foreign compounds, including environmental toxins and prescription medications [1]. This enzyme plays a central role in phase II detoxification by transferring acetyl groups to arylamine and hydrazine drugs [2]. Variations in this gene divide the population into rapid, intermediate, and slow acetylators, which directly dictates how quickly certain substances are cleared from the body [1] [2]. Slow clearance can lead to drug accumulation and toxicity, while rapid clearance may reduce the therapeutic efficacy of standard drug doses [2].
Variant Impact: The rs1801280 variant, also known as c.341T to C or p.Ile114Thr, causes an amino acid substitution from isoleucine to threonine in the NAT2 protein [3]. This specific structural change significantly reduces the stability and metabolic activity of the N-acetyltransferase 2 enzyme [4]. Because the threonine-encoding C allele is associated with a slow metabolizer phenotype, it is widely used in genetic panels to predict individual drug clearance rates [5]. Understanding this variation helps explain why some people experience severe side effects from standard doses of common medications [3] [5].
Key Insight: Slow drug metabolism can increase the risk of liver damage from common tuberculosis medications, but it may also alter how the body processes environmental toxins.
Location: NAT2. Chromosome 8 · 8p22 · 18.4 Mb
Origin Story: The evolutionary history of NAT2 variants suggests that the slow acetylation phenotype became highly prevalent in certain human populations as they transitioned from hunter-gatherer lifestyles to agricultural farming, which altered dietary exposures and chemical interactions in Central Asia and Europe.
Estimated prevalence by population
Global 39.1%; European 30.6%; African 48.4%; East Asian 92.8%; South Asian 43.6%; Americas 41.9%; Ashkenazi 30.5%; Finnish 28.2%; Middle Eastern 29.3%; Amish 40.9%.
Estimated TT genotype frequency.
Global 45.5%; European 49.4%; African 42.4%; East Asian 7.1%; South Asian 44.8%; Americas 45.6%; Ashkenazi 49.4%; Finnish 49.8%; Middle Eastern 49.7%; Amish 46.1%.
Estimated TC genotype frequency.
Global 15.4%; European 20.0%; African 9.3%; East Asian 0.1%; South Asian 11.5%; Americas 12.4%; Ashkenazi 20.0%; Finnish 22.0%; Middle Eastern 21.1%; Amish 13.0%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Pharmacogenomics
Drug Metabolism Enzyme Activity
Drug Metabolism Speed. Evidence: 4/10. Source: PMID 10667461. Typical Speed.
Antimicrobial & Antiviral Response
Isoniazid Toxicity. Evidence: 5/10. Source: PMID 18421452. Typical Risk.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Toxicity. Evidence: 5/10. Source: PMID 27488001. Typical Risk.
Cancer & Oncology
Urologic Cancers
Bladder Cancer. Evidence: 3/10. Source: PMID 16112301. Typical Risk.
Showing effects for C/C genotype
Drug Metabolism Speed. Evidence: 4/10. Source: PMID 10667461. Slow Speed.
Isoniazid Toxicity. Evidence: 5/10. Source: PMID 18421452. Increased Risk.
Phenytoin Toxicity. Evidence: 5/10. Source: PMID 27488001. Increased Risk.
Bladder Cancer. Evidence: 3/10. Source: PMID 16112301. Increased Risk.
Showing effects for T/C genotype
Drug Metabolism Speed. Evidence: 4/10. Source: PMID 10667461. Slightly Slower.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Possession of two copies of the reference T allele results in normal, fully functional N-acetyltransferase 2 enzyme activity [1]. This rapid or intermediate acetylation status allows the body to efficiently process and clear medications like the tuberculosis drug isoniazid and the antiseizure drug phenytoin [2]. Consequently, there is a significantly lower risk of experiencing drug-induced liver injury or systemic toxicity compared to those with the slow-metabolizing variant [2] [3]. Furthermore, typical enzyme activity helps efficiently detoxify environmental carcinogens, maintaining a baseline risk for bladder and other cancers associated with chemical exposures [4].
Normal enzyme activity; Typical drug clearance rates; Standard risk of medication side effects.
Sample genotype: CC (Homozygous)
Presence of two copies of the slow-metabolizing C allele leads to a pronounced reduction in N-acetyltransferase 2 enzyme function, classifying this profile as a slow acetylator [1]. This slow clearance rate dramatically increases the risk of severe liver injury during tuberculosis treatment with isoniazid, as toxic drug metabolites can accumulate in the liver [2]. Similarly, standard doses of the antiseizure medication phenytoin are much more likely to cause drug toxicity [3]. Beyond prescription drugs, slow acetylation impairs the detoxification of environmental carcinogens, such as those found in tobacco smoke and industrial dyes, which is linked to an elevated risk of developing bladder cancer [4].
Significantly reduced enzyme function; Slow clearance of medications; Increased susceptibility to environmental toxins.
Sample genotype: TC (Heterozygous)
Inheritance of one copy of the slow-metabolizing C allele reduces overall N-acetyltransferase 2 enzyme activity, often resulting in an intermediate metabolizer phenotype [1]. While many environmental toxins are still processed adequately, clearance of certain prescription drugs is noticeably delayed [2]. Clinical studies show that individuals with this genotype have an increased risk of liver damage when undergoing standard tuberculosis therapy with isoniazid [3]. There is also a higher likelihood of experiencing drug toxicity from the antiseizure medication phenytoin [4]. Being aware of this intermediate status can help guide medication choices and monitoring strategies under medical supervision [3] [4].
Reduced enzyme activity; Slower clearance of certain medications; Elevated risk of drug-induced liver strain.
Variants with shared genetic architecture
rs1495741 · NAT2 Gene · Chr 8 · Drug and Toxin Metabolism
rs1041983 · NAT2 Gene · Chr 8 · Drug Metabolism Speed
rs1495743 · NAT2 Gene · Chr 8 · Cholesterol Levels
Molecular genetics and epidemiology of the NAT1 and NAT2 acetylation polymorphisms.
Diverse point mutations in the human gene for polymorphic N-acetyltransferase.
Structure/function evaluations of single nucleotide polymorphisms in human N-acetyltransferase 2.
Content updated August 2026.
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