Gene Name	Entrez ID	Drug Name	Chembl ID	Interaction Types	Sources	publications
NAT2	10	ALCOHOL	CHEMBL545		NCI	12071337
NAT2	10	INTERFERON ALFA-2A	CHEMBL2108508		NCI	7650291
NAT2	10	THALIDOMIDE	CHEMBL468		PharmGKB
NAT2	10	DOCETAXEL	CHEMBL92		PharmGKB
NAT2	10	GARLIC	CHEMBL2108463		NCI	10234471, 9862023
NAT2	10	ISONIAZID	CHEMBL64		PharmGKB
NAT2	10	CYCLOPHOSPHAMIDE	CHEMBL88		NCI	8774842
NAT2	10	PACLITAXEL	CHEMBL428647		NCI	11955677
NAT2	10	ISOSORBIDE DINITRATE	CHEMBL6622		PharmGKB
NAT2	10	PYRAZINAMIDE	CHEMBL614		PharmGKB
NAT2	10	SULFAMETHAZINE	CHEMBL446		PharmGKB
NAT2	10	ASPIRIN	CHEMBL25		NCI	9839158
NAT2	10	BUTYLATED HYDROXYTOLUENE	CHEMBL146		NCI	11807928

Gene Name	Variant	Alleles	Chemical	Phenotype Category	Significance	Notes	Sentence	Publications	Annotation ID
NAT2	NAT2*4	*4	isoniazid	metabolism/PK	not stated	Fast acetylators (two fast alleles NAT2*4, *12, *13) were grouped together, compared to intermediate (one fast and one slow allele) and slow acetylators (two slow alleles NAT2*5, *6, *7, *14) in an analysis of clearance of isoniazid in infants over time from 3 months old to 24 months (normalized for 70kg body weight). Fast acetylators displayed an increase in clearance over this time period, also seen in intermediate acetylators but in slow acetylators clearance remained constant over time.	NAT2 *4 is associated with increased clearance of isoniazid in children with HIV.	21558457	981476144
NAT2	NAT2*13A	*13A	isoniazid	metabolism/PK	not stated	Fast acetylators (two fast alleles NAT2*4, *12, *13) were grouped together, compared to intermediate (one fast and one slow allele) and slow acetylators (two slow alleles NAT2*5, *6, *7, *14) in an analysis of clearance of isoniazid in infants over time from 3 months old to 24 months (normalized for 70kg body weight). Fast acetylators displayed an increase in clearance over this time period, also seen in intermediate acetylators but in slow acetylators clearance remained constant over time.	NAT2 *13A is associated with increased clearance of isoniazid in children with HIV.	21558457	981476156
NAT2	NAT2*5A	*5A	isoniazid	metabolism/PK	not stated	Fast acetylators (two fast alleles NAT2*4, *12, *13) were grouped together, compared to intermediate (one fast and one slow allele) and slow acetylators (two slow alleles NAT2*5, *6, *7, *14) in an analysis of clearance of isoniazid in infants over time from 3 months old to 24 months (normalized for 70kg body weight). Fast acetylators displayed an increase in clearance over this time period, also seen in intermediate acetylators but in slow acetylators clearance remained constant over time.	NAT2 *5A is associated with decreased clearance of isoniazid in children with HIV.	21558457	981476160
NAT2	NAT2*6A	*6A	isoniazid	metabolism/PK	not stated	Fast acetylators (two fast alleles NAT2*4, *12, *13) were grouped together, compared to intermediate (one fast and one slow allele) and slow acetylators (two slow alleles NAT2*5, *6, *7, *14) in an analysis of clearance of isoniazid in infants over time from 3 months old to 24 months (normalized for 70kg body weight). Fast acetylators displayed an increase in clearance over this time period, also seen in intermediate acetylators but in slow acetylators clearance remained constant over time.	NAT2 *6A is associated with decreased clearance of isoniazid in children with HIV.	21558457	981476164
NAT2	NAT2*7A	*7A	isoniazid	metabolism/PK	not stated	Fast acetylators (two fast alleles NAT2*4, *12, *13) were grouped together, compared to intermediate (one fast and one slow allele) and slow acetylators (two slow alleles NAT2*5, *6, *7, *14) in an analysis of clearance of isoniazid in infants over time from 3 months old to 24 months (normalized for 70kg body weight). Fast acetylators displayed an increase in clearance over this time period, also seen in intermediate acetylators but in slow acetylators clearance remained constant over time.	NAT2 *7A is associated with decreased clearance of isoniazid in children with HIV.	21558457	981476168
NAT2	NAT2*14A	*14A	isoniazid	metabolism/PK	not stated	Fast acetylators (two fast alleles NAT2*4, *12, *13) were grouped together, compared to intermediate (one fast and one slow allele) and slow acetylators (two slow alleles NAT2*5, *6, *7, *14) in an analysis of clearance of isoniazid in infants over time from 3 months old to 24 months (normalized for 70kg body weight). Fast acetylators displayed an increase in clearance over this time period, also seen in intermediate acetylators but in slow acetylators clearance remained constant over time.	NAT2 *14A is associated with decreased clearance of isoniazid in children with HIV.	21558457	981476172
NAT2	NAT2*13A, NAT2*4, NAT2*5B, NAT2*6A, NAT2*6J, NAT2*7B, NAT2*7G	*5B/*7B + *5B/*5B + *5B/*6A + *5B/*6J + *5B/*7G + *6A/*7B	isoniazid	metabolism/PK	yes	Isoniazid exposure (AUC0-24), clearance and half life were all significantly different between rapid and slow acetylators. Other PK parameters were not. Haplotypes were predicted using PHASE.	NAT2 *5B/*7B + *5B/*5B + *5B/*6A + *5B/*6J + *5B/*7G + *6A/*7B (assigned as slow acetylator phenotype) is associated with decreased metabolism of isoniazid in children with Tuberculosis as compared to NAT2 *4/*4 + *13A/*13A (assigned as rapid acetylator phenotype) .	24533708	1184233189
NAT2	NAT2*12A, NAT2*13A, NAT2*4, NAT2*5B, NAT2*5C, NAT2*6A, NAT2*6J, NAT2*6O, NAT2*7B, NAT2*7G	*5B/*7B + *5B/*5B + *5B/*6A + *5B/*6J + *5B/*7G + *6A/*7B	isoniazid	metabolism/PK	yes	Isoniazid half life was significantly different between intermediate and slow acetylators: all other PK parameters were not. Haplotypes were predicted using PHASE.	NAT2 *5B/*7B + *5B/*5B + *5B/*6A + *5B/*6J + *5B/*7G + *6A/*7B (assigned as slow acetylator phenotype) is associated with decreased clearance of isoniazid in children with Tuberculosis as compared to NAT2 *4/*5B + *4/*6A + *4/*5C + *4/*6O + *4/*7G + *5B/*12A + *6A/*13A (assigned as intermediate acetylator phenotype) .	24533708	1184233225
NAT2	NAT2*4, NAT2*6	*4	sulfamethoxazole	metabolism/PK	yes	as measured by plasma sulfamethoxazole AUC 0-24. Please note; this was combined analysis of rapid acetylators vs slow acetylators. Slow acetylators; genotype *5/*6, *6/*6, *6/*7, *7/*7). Rapid acetylators; genotype *4/*4. There was no significant difference with intermediate acetylators. Genotyped 3 SNPs; *5 (T341C, rs1801280), *6 (G590A, rs1799930), *7 (G857A, rs1799931).	NAT2 *4 is associated with increased metabolism of sulfamethoxazole in people with Kidney Transplantation as compared to NAT2 *6.	22106207	981477852
NAT2	NAT2*4, NAT2*7	*4	sulfamethoxazole	metabolism/PK	yes	as measured by plasma sulfamethoxazole AUC 0-24. Please note; this was combined analysis of rapid acetylators vs slow acetylators. Slow acetylators; genotype *5/*6, *6/*6, *6/*7, *7/*7). Rapid acetylators; genotype *4/*4. There was no significant difference with intermediate acetylators. Genotyped 3 SNPs; *5 (T341C, rs1801280), *6 (G590A, rs1799930), *7 (G857A, rs1799931).	NAT2 *4 is associated with increased metabolism of sulfamethoxazole in people with Kidney Transplantation as compared to NAT2 *7.	22106207	981477856
NAT2	NAT2*4, NAT2*5	*5	sulfapyridine	metabolism/PK	yes	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele and one *4 allele). Variant alleles = NAT2*5, *6, *7. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points. AUC N-acetylsulfapyradine/ AUC sulfapyradine was significantly different between all three phenotype groups.	NAT2 *5 is associated with decreased metabolism of sulfapyridine in healthy individuals as compared to NAT2 *4.	19560446	981501641
NAT2	NAT2*4, NAT2*5	*5	sulfasalazine	metabolism/PK	no	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele and one *4 allele). Variant alleles = NAT2*5, *6, *7. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points - none were significantly different between the three groups.	NAT2 *5 is not associated with metabolism of sulfasalazine in healthy individuals as compared to NAT2 *4.	19560446	981501654
NAT2	NAT2*4, NAT2*6A, NAT2*7B	*6A/*7B	isoniazid	metabolism/PK	yes	Analysis combined slow acetylators (genotype *6A/*6A, *6A/*7B, *7B/*7B) and compared to rapid (genoytype *4/*4) or intermediate acetylators (*4/*5B, *4/*6A, *4/*7B).	NAT2 *6A/*7B is associated with decreased metabolism of isoniazid in people with Tuberculosis as compared to NAT2 *4/*4.	18544910	981344553
NAT2	NAT2*4, NAT2*7	*7	sulfasalazine	metabolism/PK	no	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele and one *4 allele). Variant alleles = NAT2*5, *6, *7. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points - none were significantly different between the three groups.	NAT2 *7 is not associated with metabolism of sulfasalazine in healthy individuals as compared to NAT2 *4.	19560446	981501662
NAT2	NAT2*4, NAT2*7B	*7B/*7B	isoniazid	metabolism/PK	yes	Analysis combined slow acetylators (genotype *6A/*6A, *6A/*7B, *7B/*7B) and compared to rapid (genoytype *4/*4) or intermediate acetylators (*4/*5B, *4/*6A, *4/*7B).	NAT2 *7B/*7B is associated with decreased metabolism of isoniazid in people with Tuberculosis as compared to NAT2 *4/*4.	18544910	981344565
NAT2	NAT2*5B, NAT2*6A	*5B/*6A	sulfapyridine	metabolism/PK	yes	slow acetylators (two variants *5B, *5C, *6A, *7B) were grouped and compared to rapid acetylators (genotypes *4/*4, *4/*5B,*4/*6A, *4/*7B, *5B/*12A). Significant differences in several PK parameters were observed.	NAT2 *5B/*6A is associated with decreased metabolism of sulfapyridine in healthy individuals.	20040334	981501607
NAT2	NAT2*4	*4	isoniazid	metabolism/PK	not stated	88% of overall variability in isoniazid clearance was accounted for by the number of NAT2*4 alleles.	NAT2 *4 is associated with increased clearance of isoniazid in healthy individuals.	15855489	981848260
NAT2	NAT2*7	*7/*7	isoniazid	metabolism/PK	not stated		NAT2 *7/*7 is associated with decreased metabolism of isoniazid in people with Lupus Erythematosus, Systemic as compared to NAT2 *4/*4.	16531626	981851600
NAT2	NAT2*5, NAT2*7	*5/*7	isoniazid	metabolism/PK	not stated		NAT2 *5/*7 is associated with decreased metabolism of isoniazid in people with Lupus Erythematosus, Systemic as compared to NAT2 *4/*4.	16531626	981851604
NAT2	NAT2*6A	*6A/*6A	sulfapyridine	metabolism/PK	yes	slow acetylators (two variants *5B, *5C, *6A, *7B) were grouped and compared to rapid acetylators (genotypes *4/*4, *4/*5B,*4/*6A, *4/*7B, *5B/*12A). Significant differences in several PK parameters were observed.	NAT2 *6A/*6A is associated with decreased metabolism of sulfapyridine in healthy individuals.	20040334	981501615
NAT2	NAT2*4	*4/*4	sulfasalazine	metabolism/PK	no	(rapid acetylators) compared to intermediate (one variant allele) or slow acetylators (two variant alleles). Variant alleles = NAT2*5B, *6A, *7B. No significant difference was seen in AUC0-48, CLtotal/F or Cmax values between rapid, intermediate and slow acetylators with the rs2231142 genotype GG or the GT genotype (intergenotypic analysis) - suggesting NAT2 polymorphisms are not involved in sulfasalazine PK.	NAT2 *4/*4 is not associated with clearance of sulfasalazine in healthy individuals.	18167504	981501404
NAT2	NAT2*4, NAT2*6A	*6A/*6A	isoniazid	metabolism/PK	yes	Analysis combined slow acetylators (genotype *6A/*6A, *6A/*7B, *7B/*7B) and compared to rapid (genoytype *4/*4) or intermediate acetylators (*4/*5B, *4/*6A, *4/*7B).	NAT2 *6A/*6A is associated with decreased metabolism of isoniazid in people with Tuberculosis as compared to NAT2 *4/*4.	18544910	981344548
NAT2	NAT2*4, NAT2*6A	*6A	sulfapyridine	metabolism/PK	yes	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele). Variant alleles = NAT2*5B, *6A, *7B. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points. AUC N-acetylsulfapyradine/ AUC sulfapyradine was significantly decreased in slow vs rapid or intermediate acetylators, cumulative urinary excretion of sulfapyradine was significantly higher in slow vs rapid or intermediate acetylators, and cumulative urinary excretion of N-acetylsulfapyradine was significantly lower in slow vs rapid or intermediate acetylators.	NAT2 *6A is associated with decreased metabolism of sulfapyridine in healthy individuals as compared to NAT2 *4.	18167504	981501514
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. Before treatment the patients were phenotyped for polymorphic acetylation by means of the sulphamethazine test. High hydralazine levels (>0.5 pg/ml) were measured in slow acetylators with an SMZ ratio above 35%, whereas all rapid acetylators and some slow acetylators exhibited lower hydralazine levels.	NAT2 slow acetylator is associated with increased concentrations of hydralazine in people with Hypertension as compared to NAT2 intermediate and rapid acetylators.	1136859	1451141940
NAT2	NAT2*5B	*5B/*5B	1,7-dimethylxanthine	metabolism/PK	not stated	AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *5B/*5B is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982023773
NAT2	NAT2*6A	*6A/*6A	1,7-dimethylxanthine	metabolism/PK	not stated	AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *6A/*6A is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982023791
NAT2	NAT2*5A, NAT2*6C	*5A/*6C	1,7-dimethylxanthine	metabolism/PK	not stated	or genotype *5B/*6A. AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *5A/*6C is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982024292
NAT2	NAT2*11A, NAT2*5C	*11A/*5C	1,7-dimethylxanthine	metabolism/PK	not stated	AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was increased in men with these genotype compared to 'slow acetylators'.	NAT2 *11A/*5C is associated with increased metabolism of 1,7-dimethylxanthine in men.	17011540	982024316
NAT2	NAT2*5A, NAT2*5B	*5A/*5B	1,7-dimethylxanthine	metabolism/PK	not stated	AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *5A/*5B is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982023766
NAT2	NAT2*4	*4	caffeine	metabolism/PK	yes	Caffeine urinary metabolites in carriers of *4 were combined together as 'fast acetylators' and compared with those from slow acetylators (two 'slow' alleles *5, *6 or *7).	NAT2 *4 is associated with increased metabolism of caffeine in healthy individuals.	22105431	982023752
NAT2	NAT2*12	*12	1,7-dimethylxanthine	metabolism/PK	not stated	Men with genotypes *12A/*5A, *12C/*5D. AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was increased in men with these genotypes compared to 'slow acetylators'.	NAT2 *12 is associated with increased metabolism of 1,7-dimethylxanthine in men.	17011540	982024323
NAT2	NAT2*5A, NAT2*5C	*5A/*5C	1,7-dimethylxanthine	metabolism/PK	not stated	AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *5A/*5C is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982023779
NAT2	NAT2*5B, NAT2*7B	*5B/*7B	1,7-dimethylxanthine	metabolism/PK	not stated	AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *5B/*7B is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982023785
NAT2	NAT2*6A, NAT2*7B	*6A/*7B	1,7-dimethylxanthine	metabolism/PK	not stated	AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *6A/*7B is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982023797
NAT2	NAT2*5B, NAT2*6A	*5B/*6A	1,7-dimethylxanthine	metabolism/PK	not stated	or genotype *5A/*6C. AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was reduced in men with this genotype.	NAT2 *5B/*6A is associated with decreased metabolism of 1,7-dimethylxanthine in men.	17011540	982024286
NAT2	NAT2*13, NAT2*6A	*13	1,7-dimethylxanthine	metabolism/PK	not stated	Men with genotypes *13/*6A, *13/*6B, or *13/*7A. AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was increased in men with these genotypes compared to 'slow acetylators'.	NAT2 *13 is associated with increased metabolism of 1,7-dimethylxanthine in men.	17011540	982024298
NAT2	NAT2*14, NAT2*19, NAT2*4, NAT2*5, NAT2*6, NAT2*7	*4/*4	isoniazid	"dosage","metabolism/PK"	yes	Patients were given an isoniazid dose based on NAT2 acetylator status or a standard dose. Slow acetylators (carriers of two variant alleles *19, *14, *5, *6, or *7) who had their dose adjusted had a reduced incidence of liver injury as compared to those who received a standard dose, and fast acetylators (*4/*4, either given standard dose or 1.5x standard dose) who had their dose adjusted had a reduced incidence of early treatment failure (at 8 weeks) as compared to those who received a standard dose.	NAT2 *4/*4 is associated with increased dose of isoniazid in people with Tuberculosis as compared to NAT2 *19 + *14 + *5 + *6 + *7.	23150149	981851641
NAT2	NAT2*4	*4	1,7-dimethylxanthine	metabolism/PK	not stated	Men with genotypes *4/*5B, *4/*6A, or *4/*7A. AFMU/(AFMU+1U+1X) metabolic ratio was measured in urine after caffeine dosage...metabolism of paraxanthine (17X, 1,7-dimethylxanthine) by NAT2 to form AFMU was increased in men with these genotypes compared to 'slow acetylators'.	NAT2 *4 is associated with increased metabolism of 1,7-dimethylxanthine in men.	17011540	982024307
NAT2	NAT2*6	*6/*6	isoniazid	metabolism/PK	not stated		NAT2 *6/*6 is associated with decreased metabolism of isoniazid in people with Lupus Erythematosus, Systemic as compared to NAT2 *4/*4.	16531626	981851619
NAT2	NAT2*5, NAT2*6	*5/*6	isoniazid	metabolism/PK	not stated		NAT2 *5/*6 is associated with decreased metabolism of isoniazid in people with Lupus Erythematosus, Systemic as compared to NAT2 *4/*4.	16531626	981851608
NAT2	rs1799930	AA	isoniazid	metabolism/PK	yes	This variant is associated with increased AUC of isoniazid at week 8.	Genotype AA is associated with increased exposure to isoniazid in people with HIV Infections and Tuberculosis as compared to genotypes AG + GG.	30779340	1450807565
NAT2	NAT2*4, NAT2*5	*4	sulfamethoxazole	metabolism/PK	yes	as measured by plasma sulfamethoxazole AUC 0-24. Please note; this was combined analysis of rapid acetylators vs slow acetylators. Slow acetylators; genotype *5/*6, *6/*6, *6/*7, *7/*7). Rapid acetylators; genotype *4/*4. There was no significant difference with intermediate acetylators. Genotyped 3 SNPs; *5 (T341C, rs1801280), *6 (G590A, rs1799930), *7 (G857A, rs1799931).	NAT2 *4 is associated with increased metabolism of sulfamethoxazole in people with Kidney Transplantation as compared to NAT2 *5.	22106207	981477848
NAT2	NAT2*5B	*5B/*5B	sulfapyridine	metabolism/PK	yes	slow acetylators (two variants *5B, *5C, *6A, *7B) were grouped and compared to rapid acetylators (genotypes *4/*4, *4/*5B,*4/*6A, *4/*7B, *5B/*12A). Significant differences in several PK parameters were observed.	NAT2 *5B/*5B is associated with decreased metabolism of sulfapyridine in healthy individuals.	20040334	981501598
NAT2	NAT2*5B, NAT2*5C	*5B/*5C	sulfapyridine	metabolism/PK	yes	slow acetylators (two variants *5B, *5C, *6A, *7B) were grouped and compared to rapid acetylators (genotypes *4/*4, *4/*5B,*4/*6A, *4/*7B, *5B/*12A). Significant differences in several PK parameters were observed.	NAT2 *5B/*5C is associated with decreased metabolism of sulfapyridine in healthy individuals.	20040334	981501603
NAT2	NAT2*5B, NAT2*7B	*5B/*7B	sulfapyridine	metabolism/PK	yes	slow acetylators (two variants *5B, *5C, *6A, *7B) were grouped and compared to rapid acetylators (genotypes *4/*4, *4/*5B,*4/*6A, *4/*7B, *5B/*12A). Significant differences in several PK parameters were observed.	NAT2 *5B/*7B is associated with decreased metabolism of sulfapyridine in healthy individuals.	20040334	981501611
NAT2	NAT2*7B	*7B/*7B	sulfapyridine	metabolism/PK	yes	slow acetylators (two variants *5B, *5C, *6A, *7B) were grouped and compared to rapid acetylators (genotypes *4/*4, *4/*5B,*4/*6A, *4/*7B, *5B/*12A). Significant differences in several PK parameters were observed.	NAT2 *7B/*7B is associated with decreased metabolism of sulfapyridine in healthy individuals.	20040334	981501619
NAT2	rs1799930	AA	isoniazid	"toxicity","metabolism/PK"	yes	Clearance was also significantly decreased in patients with the GA compared to those with GG, and levels were significantly decreased in patients with AA compared to GA.	Genotype AA is associated with decreased clearance of isoniazid in people with Tuberculosis as compared to genotype GG.	19891553	981240165
NAT2	rs4646244	AT	isoniazid	"toxicity","metabolism/PK"	yes	TT vs AA or TA vs AA was not statistically significant - possibly due to low numbers of AA patients. Peak serum levels of isoniazid were also significantly higher in TA vs TT, and the ratio of acetyl isoniazid: isoniazid significantly lower in TA vs TT, and AA vs TT.	Genotype AT is associated with decreased clearance of isoniazid in people with Tuberculosis as compared to genotype TT.	19891553	981240151
NAT2	NAT2*4, NAT2*7B	*7B	sulfapyridine	metabolism/PK	yes	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele). Variant alleles = NAT2*5B, *6A, *7B. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points. AUC N-acetylsulfapyradine/ AUC sulfapyradine was significantly decreased in slow vs rapid or intermediate acetylators, cumulative urinary excretion of sulfapyradine was significantly higher in slow vs rapid or intermediate acetylators, and cumulative urinary excretion of N-acetylsulfapyradine was significantly lower in slow vs rapid or intermediate acetylators.	NAT2 *7B is associated with decreased metabolism of sulfapyridine in healthy individuals as compared to NAT2 *4.	18167504	981501499
NAT2	NAT2*4, NAT2*5B	*5B	sulfapyridine	metabolism/PK	yes	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele). Variant alleles = NAT2*5B, *6A, *7B. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points. AUC N-acetylsulfapyradine/ AUC sulfapyradine was significantly decreased in slow vs rapid or intermediate acetylators, cumulative urinary excretion of sulfapyradine was significantly higher in slow vs rapid or intermediate acetylators, and cumulative urinary excretion of N-acetylsulfapyradine was significantly lower in slow vs rapid or intermediate acetylators.	NAT2 *5B is associated with decreased metabolism of sulfapyridine in healthy individuals as compared to NAT2 *4.	18167504	981501518
NAT2	NAT2*12A	*12A	isoniazid	metabolism/PK	not stated	Fast acetylators (two fast alleles NAT2*4, *12, *13) were grouped together, compared to intermediate (one fast and one slow allele) and slow acetylators (two slow alleles NAT2*5, *6, *7, *14) in an analysis of clearance of isoniazid in infants over time from 3 months old to 24 months (normalized for 70kg body weight). Fast acetylators displayed an increase in clearance over this time period, also seen in intermediate acetylators but in slow acetylators clearance remained constant over time.	NAT2 *12A is associated with increased clearance of isoniazid in children with HIV.	21558457	981476152
NAT2	NAT2*4	*4	isoniazid	metabolism/PK	yes	individuals heterozygous or homozygous for the *4 allele have increased metabolism of isoniazid and can be classed as 'rapid acetylators' compared to individuals with two variant alleles rs1799929 (481T), rs1799930 (590A), rs1208 (803G) or rs1799931 (857A) (slow acetylators).	NAT2 *4 is associated with increased metabolism of isoniazid in healthy individuals.	21479500	981939860
NAT2	NAT2*4, NAT2*7	*7	sulfapyridine	metabolism/PK	yes	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele and one *4 allele). Variant alleles = NAT2*5, *6, *7. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points. AUC N-acetylsulfapyradine/ AUC sulfapyradine was significantly different between all three phenotype groups.	NAT2 *7 is associated with decreased metabolism of sulfapyridine in healthy individuals as compared to NAT2 *4.	19560446	981501650
NAT2	NAT2*4, NAT2*6	*6	sulfapyridine	metabolism/PK	yes	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele and one *4 allele). Variant alleles = NAT2*5, *6, *7. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points. AUC N-acetylsulfapyradine/ AUC sulfapyradine was significantly different between all three phenotype groups.	NAT2 *6 is associated with decreased metabolism of sulfapyridine in healthy individuals as compared to NAT2 *4.	19560446	981501646
NAT2	NAT2*4, NAT2*6	*6	sulfasalazine	metabolism/PK	no	slow acetylators (two variant alleles) compared to (rapid acetylators *4/*4 - no variant alleles) and intermediate acetylators (one variant allele and one *4 allele). Variant alleles = NAT2*5, *6, *7. A single oral dose of sulfasalazine was given and pharmacokinetic parameters were measured at different times points - none were significantly different between the three groups.	NAT2 *6 is not associated with metabolism of sulfasalazine in healthy individuals as compared to NAT2 *4.	19560446	981501658
NAT2	NAT2*4	*4	isoniazid	metabolism/PK	not stated	rapid and intermediate acetylators (carriers of *4) had increased metabolism of isoniazid compared to slow acetylators.Genotype determined by RFLP using RFLP using KpnI, TaqI, BamH to distinguish between NAT2*4 and *5B, *6A, *7B, respectively. Homozygous *4 = rapid, heterozygous *4 = intermediate, homozygous variant alleles = slow acetylators.	NAT2 *4 is associated with increased metabolism of isoniazid in people with Tuberculosis.	21753138	981939971
NAT2	NAT2*5	*5/*5	isoniazid	metabolism/PK	not stated		NAT2 *5/*5 is associated with decreased metabolism of isoniazid in people with Lupus Erythematosus, Systemic as compared to NAT2 *4/*4.	16531626	981851612
NAT2	NAT2*4	*4/*4	isoniazid	metabolism/PK	yes	compared to *4/*5, *4/*6, *4/*7 (grouped 'intermediate' genotypes).	NAT2 *4/*4 is associated with increased metabolism of isoniazid in people with Tuberculosis.	16182272	981851586
NAT2	NAT2*4	*4/*4	isoniazid	metabolism/PK	yes	compared to *6/*6, *6/*7, *7/*7 (grouped 'slow' genotypes).	NAT2 *4/*4 is associated with increased metabolism of isoniazid in people with Tuberculosis.	16182272	981851591
NAT2	NAT2*4, NAT2*5, NAT2*6, NAT2*7	*4/*5 + *4/*6 + *4/*7	hydralazine	metabolism/PK	yes	RA group had faster weight-adjusted hydralazine apparent oral clearance (70.0 ± 13.6 vs 20.1 ± 6.9 L/h, P < .05), lower dose-normalized area under the concentration-time curve (AUC; 1.5 ± 0.8 vs 5.9 ± 3.7 ng·h/mL, P < .05), lower dose-normalized peak concentrations (0.77 ± 0.51 vs 4.04 ± 3.18 ng/mL, P < .05), and larger weight-adjusted apparent oral volume of distribution (302 ± 112 vs 116 ± 45 L/kg, P < .05) compared to slow acetylators. Single-nucleotide polymorphisms (SNPs) in the NAT2 coding region and their corresponding haplotypes were determined using 4-SNP assays, that is, rs181280,c.341T > C; rs1799930, c.590G > A; rs1799931,c.857G > A; rs1801279, c.191G > A, with TaqMan Assays. Subjects were classified as slow acetylators if they had 2 reduced-activity NAT2 alleles (*5, *6, *7, or*14), or rapid acetylators if they carried 1 reduced-activity allele and 1 fully functional allele (*4) or 2 fully functional alleles.	NAT2 *4/*5 + *4/*6 + *4/*7 (assigned as rapid acetylator phenotype) are associated with increased metabolism of hydralazine in women with Hypertension as compared to NAT2 *5/*5 + *5/*6 + *5/*7 + *6/*6 (assigned as slow acetylator phenotype) .	31257615	1451135223
NAT2	NAT2*4, NAT2*5	*5/*5	isoniazid	metabolism/PK	yes	Slow acetylators (a combination of two slow alleles NAT2*5, *6 or *7) had higher isoniazid plasma concentrations and bioavailability compared to rapid (*4/*4) and intermediate acetylators (*4 allele combined with *5, *6 or *7). Patients with *7/*7 genotype had the highest levels.	NAT2 *5/*5 (assigned as slow acetylator phenotype) is associated with decreased metabolism of isoniazid in people with Tuberculosis as compared to NAT2 *4/*4 (assigned as rapid acetylator phenotype) .	24383060	1183702439
NAT2	NAT2*4, NAT2*7	*7/*7	isoniazid	metabolism/PK	yes	Slow acetylators (a combination of two slow alleles NAT2*5, *6 or *7) had higher isoniazid plasma concentrations and bioavailability compared to rapid (*4/*4) and intermediate acetylators (*4 allele combined with *5, *6 or *7). Patients with *7/*7 genotype had the highest levels.	NAT2 *7/*7 (assigned as slow acetylator phenotype) is associated with decreased metabolism of isoniazid in people with Tuberculosis as compared to NAT2 *4/*4 (assigned as rapid acetylator phenotype) .	24383060	1183702422
NAT2	NAT2*4, NAT2*6	*6/*6	isoniazid	metabolism/PK	yes	Slow acetylators (a combination of two slow alleles NAT2*5, *6 or *7) had higher isoniazid plasma concentrations and bioavailability compared to rapid (*4/*4) and intermediate acetylators (*4 allele combined with *5, *6 or *7). Patients with *7/*7 genotype had the highest levels.	NAT2 *6/*6 (assigned as slow acetylator phenotype) is associated with decreased metabolism of isoniazid in people with Tuberculosis as compared to NAT2 *4/*4 (assigned as rapid acetylator phenotype) .	24383060	1183702431
NAT2	NAT2*14, NAT2*5, NAT2*6, NAT2*7	*5 + *6 + *7 + *14	dipyrone	metabolism/PK	yes	N-demethylation of the active metabolite MAA is diminished in carriers of the CYP2C19*2 allele and in NAT2-slow acetylators. "The inferred slow NAT2 phenotype is strongly associated with a decrease in the acetylation ratio and in the recovery of AAA. This effect is associated to all NAT2 slow alleles analyzed, but a differential effect is observed: Individuals who were homozygous for the NAT2*6 allele displayed a significantly lower AAA recovery and lower acetylation ratio as compared to individuals homozygous for the NAT2*5 allele"	NAT2 *5 + *6 + *7 + *14 (assigned as slow acetylator phenotype) are associated with decreased metabolism of dipyrone in healthy individuals.	25241292	1451139042
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	yes	Note, NAT2 not specified just categorized in slow and rapid acetylator. Acetylation phenotype, as determined by sulfamethazine acetylation rate, was an important determinant of the plasma level of hydralazine. The ratio of plasma concentration to daily dose of hydralazine averaged 1.7 times higher in slow acetylators than in fast acetylators.	NAT2 slow acetylator is associated with increased concentrations of hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	5026380	1451140220
NAT2	NAT2 rapid acetylator		hydralazine	"dosage","efficacy"	yes	Note, NAT2 not specified just categorized in slow and rapid acetylator. Acetylation phenotype, as determined by sulfamethazine acetylation rate, was an important determinant of the plasma level of hydralazine. Fast acetylators also required significantly higher doses of hydralazine for adequate blood pressure control than did slow acetylators. In contrast, the mean plasma concentration of hydralazine which produced a satisfactory blood pressure reduction was the same in both groups.	NAT2 rapid acetylator is associated with increased dose of hydralazine in people with Hypertension as compared to NAT2 slow acetylator.	5026380	1451140186
NAT2	NAT2*14, NAT2*5, NAT2*6, NAT2*7	*5/*14 + *5/*5 + *5/*6 + *5/*7 + *6/*14 + *6/*6 + *7/*6	hydralazine	efficacy	yes	Only slow acetylators showed a significant decreased in systolic blood pressure (clinic, ambulatory 24h, ambulatory daytime, ambulatory night-time) and diastolic blood pressure (clinic, ambulatory night-time) - p-value applies to all.	NAT2 *5/*14 + *5/*5 + *5/*6 + *5/*7 + *6/*14 + *6/*6 + *7/*6 (assigned as slow acetylator phenotype) is associated with response to hydralazine in people with resistant hypertension.	24444407	1184174521
NAT2	NAT2*12, NAT2*13, NAT2*4	*12/*12 + *13/*13 + *4/*12 + *4/*13 + *4/*4	hydralazine	efficacy	no	Only slow acetylators showed a significant decreased in systolic blood pressure (clinic, ambulatory 24h, ambulatory daytime, ambulatory night-time) and diastolic blood pressure (clinic, ambulatory night-time). P-value applies to all blood pressure measurements.	NAT2 *12/*12 + *13/*13 + *4/*12 + *4/*13 + *4/*4 (assigned as rapid acetylator phenotype) is not associated with response to hydralazine in people with resistant hypertension.	24444407	1184174554
NAT2	NAT2*12, NAT2*13, NAT2*14, NAT2*4, NAT2*5, NAT2*6, NAT2*7	*4/*14 + *4/*5 + *4/*6 + *4/*7 + *5/*12 + *5/*13 + *6/*12 + *6/*13	hydralazine	efficacy	no	Only slow acetylators showed a significant decreased in systolic blood pressure (clinic, ambulatory 24h, ambulatory daytime, ambulatory night-time) and diastolic blood pressure (clinic, ambulatory night-time). P-value applies to all blood pressure measurements.	NAT2 *4/*14 + *4/*5 + *4/*6 + *4/*7 + *5/*12 + *5/*13 + *6/*12 + *6/*13 (assigned as intermediate acetylator phenotype) is not associated with response to hydralazine in people with resistant hypertension.	24444407	1184174568
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	yes	Note, NAT2 not specified just categorized in slow and rapid acetylator. The phenotyping was done by administering oral standard hydralazine dose of 150 mg/day in three divided doses. The 24 hour urinary MTP/hydralazine ratio was used to categorize patients into slow and fast acetylators. Of the patients studied 69.9% were slow acetylators while 30.4% were fast acetylators. The mean 24 hour urinary MTP/hydralazine ratio for slow acetylators was 1.01 +/- 0.95. This was significantly different from the fast acetylators where the mean 24 hour urinary MTP/hydralazine ratio was 10.6 +/- 4.4 (P < 0.001).	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	1396201	1451138220
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. Subjects received 500 mg by oral route of sulfamethazine and urine was collected 0 – 6 h after medication. Acetylated and unchanged sulfamethazine were determined and the ratio of acetylated/ unchanged sulfamethazine was determined. Subjects were classified as fast or slow acetylators taking a cut-off ratio of 70%. PK studied with orally administrated a single dose of hydralazine with a slow-release tablet of 182 mg regardless of their acetylation phenotype. For fast acety- lators, maximum concentrations of hydrala- zine in plasma appeared with an average of 2.8 ± 2.5 h after drug administration, with a mean value of 208.4 ± 56.9 ng/ml, whereas for slow acetylators we observed that the mean value of the maximum concentration was 470.4 ± 162.8 ng/ml, and the tmax 4.4 h. pharmacokinetic parameters for fast and slow acetylators show that the Cmax, the tmax and the area under the curve values of hydralazine in slow acetylators are almost twice compared to the fast acetylators.	NAT2 slow acetylator is associated with increased concentrations of hydralazine in healthy individuals as compared to NAT2 rapid acetylator.	21781652	1451138770
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	yes	Note, NAT2 not specified just categorized in slow and rapid acetylator. Patients were phenotyped by the sulfamethazine method. Patients undergoing maintenance therapy with hydralazine doses of 25, 50, 75, 100, or 150mg given twice daily. Other drugs received were as follows: atenolol (31patients);bendroflumethiazide (28);oxprenolol (3); hydrochlorothiazide with amiloride HC1 (9); allopurinol (2); propranolol (9);furosemide (2); cyclopenthiazide with potasium chloride (5); methyldopa (3); digoxin (3); clonidine (1);bethanidine (1);lorazepam (1).Some drugs were only received by rapid acetylators,or slow acetylators. The 3-OHMTR:HP ratio is lower in the slow acetylator at both 100-mg (p<0.01) and 200-mg (p< 0.01) daily dose level than in rapid acetylators. The greatest phenotype difference in the ratio 3-OHMTP:HP is after a 200-mg daily dose; although there is a difference (p<0.01) in the average ratio after 100 mg; the frequency distribution reveals overlap between the acetylator phenotype at 100-mg dose and shows no discrimination after 50-mg doses.	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	7471604	1451139280
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	no	Note, NAT2 not specified just categorized in slow and rapid acetylator. The patients were acetylator phenotyped with sulfamethazine. Hydralazine and two of its acetylated metabolites, methyltriazolophthalazine (MTP) and 3-hydroxymethyltriazolophthalazine (HOMTP) are measured. Excretion of hydralazine and HOMTP but not MTP was found to be related to the acetylator phenotype. Metabolic ratio HOMTP: hydralazine showed a bimodal distribution and the average ratio for slow acetylators (1.6) was lower than the ratio in rapid acetylators (14.9) p<0.001. It was of interest that the excretion of MTP, the primary acetylated metabolite, was similar in both phenotypes.	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	7408395	1451139502
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	yes	Note, NAT2 not specified just categorized in slow and rapid acetylator. Acetylators were determined by phenotyping with a single dose of sulfamethazine. Subjects were divided into rapid (A1 > 50) and slow (A1 < 50) acetylator groups. Hydralazine and HPH kinetics was determined after single and repeated oral doses of hydralazine in eight hypertensive patients. Hydralazine bioavailability in the fast acetylator group (9.5% single dose, 6.6% repeated doses) and in the slow acetylator group (31.3% single dose, 39.3% repeated doses). Peak plasma levels were lower than those reported with nonspecific assays: 0.32 microM for the single dose and 0.14 microM for repeated doses in the fast acetylator group and 1.03 microM for the single dose and 0.96 microM repeated doses in the slow acetylator group. After single and repeated doses, AUC was significantly greater in slow than in rapid acetylator groups. Elimination half-lifes were phenotype independent, ranging from 4 to 6 hr.	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	7438695	1451139946
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	yes	Note, NAT2 not specified just categorized in slow and rapid acetylator. Patients were phenotyped as rapid or slow acetylators. Urine from slow acetylators contained significantly more hydrazine than urine from rapid acetylators at both 100- and 200-mg dose levels (p < 0.02 and 0.001, respectively).	NAT2 slow acetylator is associated with increased concentrations of hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	445966	1451140180
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. Patients' acetylator status was determined by the sulphamethazine method. Subjects were undergoing maintenance therapy with hydralazine, twice daily 100 mg. Patients had been receiving in conjunction with hydralazine a number of other drugs: (numbers of patients indicated):chlorethiazole 1+; bendrofluazide 8; atenolol 7; clonidine 1+; glyceryltrinitrate 1*; propranolol 6; methyldopa 6; oxprenolo l2; digoxin 2+; frusemide 2; naproxen 1+; diazepam 1*; navidrex 2*, moduretic 4; SlowK 7; bethanidine 2 and hydrochlorothiazide 1* (+These drugs were only administered to rapid acetylators; *these drugs were only administered to slow acetylators). The level of the acetylated metabolites NAcHPZ and TP (terminal product of the primary acetylation pathway) are higher in the rapid compared with the slow acetylator phenotype. Conversely the level of PZ is significantly higher in slow compared with rapid acetylators.	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	7259927	1451140360
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	yes	Note, NAT2 not specified just categorized in slow and rapid acetylator. Acetylation ability was determined by the sulfamethazine method. For certain comparisons patients were divided into rapid or slow acetylators on the basis of an acetylation index greater or less than 50%, respectively. The clearance of hydralazine from blood was 42.7 +/- 8.9 ml/min-1/kg-1 in the 9 patients studied. This value was not related to acetylation index. In those patients with indexes above 50% (rapid acetylators) the apparent hepatic clearance was higher than in patients with indexes below 50% (slow acetylators), 19.5 +/- 1.0 versus 14.6 +/- 1.7 ml/min-1/kg-l, respectively. The AUC and Cp values for both the single and multiple oral doses were significantly lower (P less than 0.001) in rapid than in slow acetylators.	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in men with Hypertension as compared to NAT2 rapid acetylator.	7284051	1451140400
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. Subjects received 500 mg by oral route of sulfamethazine and urine was collected 0 – 6 h after medication. Acetylated and unchanged sulfamethazine were determined and the ratio of acetylated/ unchanged sulfamethazine was determined. Subjects were classified as fast or slow acetylators taking a cut-off ratio of 70%. Hydralazine was administered in as a slow-release tablet containing 182 mg for fast and 83 mg for slow acetylators. mean concentrations of plas- ma hydralazine were 239.1 ng/ml and 259.2 ng/ml for fast and slow patients, respectively. The respective medians being 222.1 ng/ ml and 265.5 ng/ml. These differences were not significantly different, p = 0.3868. Subjects also received other medications to treat neoplasms.	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in people with Neoplasms as compared to NAT2 rapid acetylator.	21781652	1451138866
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. Patients received a single oral 500-mg dose (two 250-mg tablets) of sulfamethazine and urine was collected within the ensuing 6 h for acetylator status phenotyping. Afterward, patients began treatment (day –7) with a daily dose of a slow-release formulation of hydralazine tablets containing either 182 mg for rapid-acetylators or 83 mg for slow- acetylators. Plasmatic levels of hydralazine were analyzed in 10 patients in whom plasma samples were available at different time-points during treatment. Distribution of these patients according to acetylator phenotype was four and six for slow and rapid, respectively. Mean plasma levels of hydralazine ranged from 204.8–275.1 ng/mL for rapid-acetylators, whereas these mean values were 252.1–344.2 ng/mL in slow- acetylators. Overall means were 246 and 299 ng/mL, respectively, which were not statistically significant different (p = 0.2445). The subjects received also other drugs to treat neoplasms.	NAT2 slow acetylator is associated with decreased metabolism of hydralazine in people with Neoplasms as compared to NAT2 rapid acetylator.	17183730	1451138920
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	no	Note, NAT2 not specified just categorized in slow and rapid acetylator. Patients received a single oral dose of 500 mg of sulphamethazine, and urine was collected within the ensuing 6 h for phenotyping of acetylator status as reported. Patients began treatment (day –7) with a daily dose of a slow-release formulation of hydralazine tablets containing either 182 mg for rapid, or 83 mg for slow, acetylators.Mean plasma level of hydralazine was 108.0 ng/ml (SD, 85.9) for slow acetylators (7 patients), whereas mean value was 288.4 (SD, 278.5) for rapid acetylators (3 patients), this difference statistically significant (P = 0.0151.) Subjects also received magnesium valproate tablets and both were administered until the last day of the final chemotherapy cycle. Chemotherapy comprised cisplatin, carboplatin, paclitaxel, vinorelbine, gemcitabine, pemetrexed, topotecan, doxorubicin, cyclophosphamide, or anastrozole.	NAT2 slow acetylator is not associated with decreased metabolism of hydralazine in people with Neoplasms as compared to NAT2 rapid acetylator.	17761710	1451138603
NAT2	NAT2*4, NAT2*5, NAT2*6, NAT2*7	*5/*5 + *5/*6 + *5/*7	hydralazine	metabolism/PK	not stated	Rapid acetylators were given a higher dose. The average means  SE of AUC0-inf and Cmax in fast (given dose 182 mg) and slow acetylators (given dose 83 mg) were 1583 +/- 243 and 1696 +/- 197 ng h/mL, 93 4  6 8 and 112 5  17 2 ng/mL, respectively. None of the determined and calculated parameters was significantly different (a = 0 05) between the two groups. Three SNPs (rs1801280, rs1799930 and rs1799931) were chosen as tag SNPs for NAT2 alleles with reduced activity (NAT2*5, *6 and *7). *4 seemed to be assigned in the absence of *5, *6, *7.	NAT2 *5/*5 + *5/*6 + *5/*7 (assigned as slow acetylator phenotype) are associated with decreased metabolism of hydralazine in healthy individuals as compared to NAT2 *4/*4 (assigned as rapid acetylator phenotype) .	24702251	1451136500
NAT2	NAT2 rapid acetylator		hydralazine	"dosage","efficacy"	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. The acetylator status was determined by phenotyping using sulfamethazine or dapsone, not further specified. After 2 to 4 weeks on diuretic, patients were maintained on diuretic and randomized to a hydralazine treatment regimen. A total of 36 patients were prescribed supplemental beta-blockers in addition. Only 9 patients were classified as "intermediate" acetylators, and they were therefore included as "slow" acetylators. Additionally, 6 patients' acetylator classification was unknown due to protocol violations. Sitting diastolic blood pressure (BP) was selected as the response variable. The daily dose that elicited 50% of the maximum response was 0.87 mg/kg for slow acetylators and 1.68 mg/kg for fast acetylators. The acetylator class was an important factor in describing the data but the difference between the two classes might not be as statistically significant as the value 0.025 indicated when multiple testing is taken into account.	NAT2 rapid acetylator is associated with increased dose of hydralazine in people with Hypertension as compared to NAT2 slow acetylator.	2231320	1451141481
NAT2	NAT2 slow acetylator		hydralazine	metabolism/PK	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. Acetylator phenotype was determined following oral sulfamethazine. Acetylator index was defined as the ratio, multiplied by 100, of acetylated-to-total sulfamethazine in plasma. Among the nine subjects, the acetylator index ranged from 18 to 82. The distribution of the acetylator index was not bimodal but rather included one or two patients in each decile from the second through the ninth.The plasma concentration of hydralazine after a standard oral dose varied by as much as 15-fold among individuals and was lower in rapid than slow acetylator phenotype patients. (1 dose and 5 dose regimes were studied; subjects also received diuretics). Study established an inverse correlation between acetylator index and both the peak plasma concentration of hydralazine and the AUC. IT is probable that the inverse relationship of acetylator index to BP response is due to the former's effect on bioavailability and therefore the plasma concentration of hydralazine.	NAT2 slow acetylator is associated with increased concentrations of hydralazine in men with Hypertension as compared to NAT2 rapid acetylator.	7298112	1451141600
NAT2	NAT2 rapid acetylator		hydralazine	"dosage","efficacy"	yes	To reduce the systolic BP by 20 mmHg, 1.0 mg/kg of hydralazine was needed in slow acetylators; rapid acetylators needed a significantly higher dose of 1.4 mg/kg. Note, NAT2 not specified just categorized in slow and rapid acetylator. Before treatment the patients were phenotyped for polymorphic acetylation by means of the sulphamethazine test: 12 proved to be slow and 11 rapid acetylators. Also the patients were co-treated to hydralazine (37.5-150 mg daily) with oxprenolol (60mg daily). A significant correlation was found between daily doses of hydralazine and the plasma hydralazine levels, separately in slow (r =0.480) and in rapid (r =0.580) acetylators. The antihypertensive response to hydralazine correlated well to plasma hydralazine levels. The average reduction of supine diastolic pressure in slow acetylators (23 mmHg) was significantly more (p<0.05) than in rapid acetylators (15 mmHg). This indicates that slow acetylators were slightly more responsive to a given dose of hydralazine. In order to reduce supine systolic BP by 20 mmHg or more, 1.O mg/kg HZ was needed in slow acetylators and 1.4 mg/kg in rapid. This difference is statistically significant (p <0.05). The dose-response slope of diastolic pressure is fairly flat.	NAT2 rapid acetylator is associated with increased dose of hydralazine in people with Hypertension as compared to NAT2 slow acetylator.	1136859	1451141845
NAT2	NAT2 slow acetylator		hydralazine	efficacy	not stated	Note, NAT2 not specified just categorized in slow and rapid acetylator. Phenotyping method not stated. Patients were treated with cyclopenthiazide, oxprenolol and hydralazine. Patients who were slow acetylators had significantly better blood pressure control. Only five out of nine fast acetylator patients achieved satisfactory blood pressure control, compared with 19 out of 20 slow acetylator patients (P < 0 . 02).	NAT2 slow acetylator is associated with increased response to hydralazine in people with Hypertension as compared to NAT2 rapid acetylator.	318493	1451141965
NAT2	NAT2 haplotype		sulfasalazine	other	yes	Among NAT2 slow acetylators, 26.7% ceased sulphasalazine treatment due to adverse effects during the first 12 months of therapy. This is in contrast to rapid acetylators (7.7%) and intermediate acetylators (26.7%). After adjusting for baseline DAS28, smoking status and gender, each decrement in acetylator status (rapid --> intermediate --> slow) was associated with an increased risk in cessation of therapy. Most common adverse events were nausea/vomiting and fatigue/lethargy; please refer to paper for full list. NAT2 acetylator status determined using the rs1801280 and rs1041983 SNPs.	NAT2 slow acetylator is associated with increased discontinuation of sulfasalazine in people with Arthritis, Rheumatoid.	24394199	1184747634
NAT2	NAT2 haplotype		sulfasalazine	efficacy	no	NAT2 acetylator status (slow, intermediate, rapid) was not associated with likelihood of achieving remission after 12 months of treatment. Remission defined as an SDAI of <3.3. NAT2 acetylator status determined using the rs1801280 and rs1041983 SNPs.	NAT2 slow acetylator is not associated with response to sulfasalazine in people with Arthritis, Rheumatoid.	24394199	1184747654
NAT2	NAT2 haplotype		efavirenz	metabolism/PK	not stated	Genotype for metabolizer status determined from rs1801279, rs1801280, rs1799930, and rs1799931. Patients were taking both efavirenz and antituberculosis therapy rifampin.	NAT2 poor metabolizer genotype is associated with increased clearance of efavirenz in people with HIV and Tuberculosis as compared to NAT2 normal metabolizer genotype.	25722197	1447947578
NAT2	NAT2 slow acetylator		isoniazid	metabolism/PK	yes	Serum concentrations of isoniazid were significantly lower in NAT2 rapid acetylators (2.55 mg/L) as compared to slow acetylators (6.78 mg/L). Slow acetylators were defined as those with any two slow alleles. Intermediate and rapid acetylators were defined as those with one or two wild-type NAT*4 alleles, respectively. The authors also provided suggested doses for individuals based on NAT2 acetylator status and weight. Those with genotype-based dosing were more frequently in the therapeutic range as compared to those given standard dosing.	NAT2 slow acetylator is associated with decreased concentrations of isoniazid in people with Tuberculosis as compared to NAT2 rapid acetylator.	26491254	1448261868
NAT2	rs1495741	AG + GG	iguratimod	efficacy	yes	There are two places in the text where the variant is also referred to as rs1495742 but this appears to be a typo.	Genotypes AG + GG is associated with decreased clinical benefit to iguratimod in people with Arthritis, Rheumatoid as compared to genotype AA.	29517409	1449270432