What you carry at this position in your DNA and what research says about it.
Drug Clearance Speed: 6/10 evidence, 28 publications.
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Sample genotype (not yours): C/C
Rapid Drug Clearance and Lower Toxicity Risk
Typical or rapid drug metabolism is associated with this genetic profile. It provides a lower risk of liver damage when taking certain tuberculosis medications.
What this genotype means: Rapid to intermediate drug clearance; Lower risk of anti-TB drug-induced liver injury.
Sample genotype (not yours): C/T
Intermediate Drug Clearance and Moderate Toxicity Risk
Intermediate drug metabolism occurs when carrying one copy of the T allele. This moderately increases the risk of side effects from certain medications.
What this genotype means: Intermediate drug clearance speed; Moderately increased risk of liver toxicity from tuberculosis drugs.
Sample genotype (not yours): T/T
Slow Drug Clearance and Elevated Toxicity Risk
Slow drug metabolism occurs when carrying two copies of the T allele. This significantly increases the risk of liver damage and side effects from specific medications.
What this genotype means: Slow drug clearance speed; Significantly higher risk of liver toxicity from tuberculosis drugs; Increased risk of phenytoin toxicity.
Gene function and biological role
Gene Function: The NAT2 gene encodes N-acetyltransferase 2, a key phase II liver enzyme responsible for metabolizing and detoxifying various drugs and foreign compounds [1]. It plays a critical role in the clearance of arylamine and hydrazine drugs, such as the tuberculosis medication isoniazid [2]. Genetic variations in this gene divide individuals into rapid, intermediate, and slow acetylators [2]. Slow acetylators have reduced enzyme activity, leading to slower drug clearance and a higher risk of side effects [3]. Conversely, rapid acetylators clear drugs quickly, which can sometimes reduce treatment efficacy [3].
Variant Impact: The rs1799929 variant is a synonymous nucleotide change (481C>T) in the coding region of the NAT2 gene [4]. Although it does not change the amino acid sequence directly, it is a key marker linked to the slow acetylator haplotype NAT2*5 [4]. Carrying the T allele is strongly associated with a reduced rate of drug acetylation [1]. This slower metabolism increases exposure to certain medications, elevating the risk of drug-induced liver injury [5].
Key Insight: This synonymous variant does not alter the protein sequence directly, yet it serves as a major genetic tag for slow drug metabolism.
Location: NAT2. Chromosome 8 · 8p22 · 18.4 Mb
Estimated prevalence by population
Global 42.2%; European 32.3%; African 54.8%; East Asian 92.9%; South Asian 48.1%; Americas 43.7%; Ashkenazi 31.9%; Finnish 31.0%; Middle Eastern 31.1%; Amish 43.8%.
Estimated CC genotype frequency.
Global 44.0%; European 49.1%; African 38.4%; East Asian 7.0%; South Asian 42.5%; Americas 44.8%; Ashkenazi 49.2%; Finnish 49.3%; Middle Eastern 49.3%; Amish 44.8%.
Estimated CT genotype frequency.
Global 13.7%; European 18.6%; African 6.7%; East Asian 0.1%; South Asian 9.4%; Americas 11.5%; Ashkenazi 18.9%; Finnish 19.6%; Middle Eastern 19.6%; Amish 11.4%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Antimicrobial & Antiviral Response
Isoniazid Toxicity. Evidence: 6/10. Source: PMID 18421452. Lower Risk.
Rifampin Toxicity. Evidence: 6/10. Source: PMID 18421452. Lower Risk.
Antiepileptic & Mood-Stabilizer Response
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Typical Risk.
Cancer & Oncology
Gynecological Cancers
Cervical Cancer. Evidence: 3/10. Source: PMID 19823052. Typical Risk.
Showing effects for C/T genotype
Isoniazid Toxicity. Evidence: 6/10. Source: PMID 18421452. Increased Risk.
Rifampin Toxicity. Evidence: 6/10. Source: PMID 18421452. Increased Risk.
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. Increased Risk.
Showing effects for T/T genotype
Isoniazid Toxicity. Evidence: 6/10. Source: PMID 18421452. High Risk.
Rifampin Toxicity. Evidence: 6/10. Source: PMID 18421452. High Risk.
Phenytoin Toxicity. Evidence: 6/10. Source: PMID 27488001. High Risk.
Cervical Cancer. Evidence: 3/10. Source: PMID 19823052. ~7.4x Higher Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Rapid or intermediate drug clearance is typical for this genetic profile, which lacks the slow-metabolizing T allele [1]. Studies show a significantly lower risk of drug-induced liver injury during standard tuberculosis treatments involving isoniazid, rifampin, and pyrazinamide [2]. Because the enzyme clears these medications efficiently, toxic byproducts are less likely to accumulate in liver tissue [3]. However, very rapid clearance can occasionally reduce the effectiveness of standard drug doses, though this is manageable with clinical oversight [4]. This genotype is also associated with a typical baseline risk for other conditions linked to slow acetylation, such as cervical cancer [5].
Rapid to intermediate drug clearance; Lower risk of anti-TB drug-induced liver injury.
Sample genotype: CT (Heterozygous)
Possessing one copy of the slow-metabolizing T allele results in intermediate drug clearance [1]. Clinical studies indicate a moderately increased risk of liver damage when treated with standard tuberculosis therapies like isoniazid and rifampin [2]. The intermediate metabolism speed can cause a mild accumulation of drug metabolites compared to rapid metabolizers [3]. Additionally, there is a documented risk of increased toxicity when taking the antiseizure medication phenytoin [4]. While generally well-tolerated, knowing this status helps clinicians optimize drug choices and monitor liver enzymes if therapy is required [5].
Intermediate drug clearance speed; Moderately increased risk of liver toxicity from tuberculosis drugs.
Sample genotype: TT (Homozygous)
Slow acetylator status is typical for this genetic profile due to the presence of two copies of the slow-metabolizing allele [1]. This slow clearance rate is strongly linked to a higher likelihood of drug-induced liver injury during tuberculosis therapy with isoniazid, rifampin, and pyrazinamide [2]. Slower breakdown allows toxic drug intermediates to build up and damage hepatic cells [3]. There is also an increased risk of toxicity from the antiseizure medication phenytoin [4]. Furthermore, some research suggests a potential link between the slow-metabolizing status and an increased susceptibility to cervical cancer [5]. Knowing this genotype is highly valuable for personalizing drug dosages and implementing proactive liver monitoring during treatment [6].
Slow drug clearance speed; Significantly higher risk of liver toxicity from tuberculosis drugs; Increased risk of phenytoin toxicity.
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
N-acetyltransferase 2 gene polymorphism in patients with cervical cancer.
Content updated August 2026.
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