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Pharmacogenomics of arylamine N-acetyltransferases--from drug metabolism to drug discovery.

Arylamine N-acetyltransferase (NAT) was first identified as the enzyme responsible in humans for the inactivation of the antitubercular drug isoniazid, and in the 1960s, it was identified that the variation in inactivation of isoniazid was genetically controlled. Hence, NAT has been a well-recognized model system for pharmacogenomics for 40 years. There is now a large body of information on the NATs in humans such that SNP profiles corresponding to ‘slow’ acetylators have been identified. This SNP profile varies amongst different ethnic groups, and the number of different ethnic groups for which information is available is increasing. This information is particularly important in view of the prevalence of tuberculosis in developing countries, where the response to isoniazid in the initial phase of treatment depends on the acetylation type, although it appears to be less important in the continuation phase of the disease. It is the NAT2 isoenzyme that controls the rate of acetylation of isoniazid in humans, and there is a good correlation between SNP pattern in NAT2 and the slow acetylator phenotype. However, particularly in heterozygotes with one slow allele, there is a wide distribution of in vivo acetylation rates. There appear to have been no reports of substrate induction of NAT2 in humans, although there have been reports of glucocorticoid control of expression in animal models which could help to account for the differences in acetylation rate within apparently identical genotypes, as determined by the SNPs that are currently known. In humans, there are two functional NAT genes and a pseudogene. In the case of human NAT2, there is a non-coding exon ~ 8 kb upstream. Whilst progress has been made in