<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Eadon MT</submitter><funding>NIEHS NIH HHS</funding><funding>National Institutes of Health (NIH)</funding><funding>National Institute of Corrections</funding><funding>NHGRI NIH HHS</funding><funding>NIC</funding><funding>American Lebanese Syrian Associated Charities</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>National Human Genome Research Institute</funding><funding>ALSAC</funding><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>1430-1436</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12641075</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>118(6)</volume><pubmed_abstract>Hydralazine is a vasodilator typically used in the treatment of resistant hypertension and heart failure. N-acetyltransferase 2 (NAT2) catalyzes the metabolism of hydralazine into inactive metabolites. NAT2 poor metabolizers (historically referred to as "slow acetylators") are predicted to have increased plasma hydralazine concentrations compared with NAT2 rapid and intermediate metabolizers (historically referred to as "rapid acetylators" and "intermediate acetylators," respectively), which may lead to both increased clinical efficacy and adverse effects, including drug-induced systemic lupus erythematosus. This guideline summarizes the evidence from the literature relevant to NAT2/hydralazine and provides recommendations for hydralazine prescribing based on NAT2 genotype-predicted acetyl</pubmed_abstract><journal>Clinical pharmacology and therapeutics</journal><pubmed_title>Clinical Pharmacogenetics Implementation Consortium Guideline for NAT2 Genotype and Hydralazine Therapy.</pubmed_title><pmcid>PMC12641075</pmcid><funding_grant_id>U24HG013077</funding_grant_id><funding_grant_id>P30-ES030283</funding_grant_id><funding_grant_id>R3‐5GM145383</funding_grant_id><funding_grant_id>P30 ES030283</funding_grant_id><funding_grant_id>U24HG010615</funding_grant_id><funding_grant_id>P30‐ES030283</funding_grant_id><funding_grant_id>R01 HG011800</funding_grant_id><funding_grant_id>U24 HG010615</funding_grant_id><funding_grant_id>T32 ES011564</funding_grant_id><funding_grant_id>R01HG013416</funding_grant_id><funding_grant_id>P20‐GM113226</funding_grant_id><funding_grant_id>P20-GM113226</funding_grant_id><funding_grant_id>P20 GM113226</funding_grant_id><funding_grant_id>U24 HG013077</funding_grant_id><funding_grant_id>T32-ES011564</funding_grant_id><funding_grant_id>T32‐ES011564</funding_grant_id><funding_grant_id>R35 GM145383</funding_grant_id><funding_grant_id>R01 HG013416</funding_grant_id><funding_grant_id>K08‐CA250418</funding_grant_id><funding_grant_id>P42‐ES023716</funding_grant_id><funding_grant_id>P42-ES023716</funding_grant_id><funding_grant_id>K08 CA250418</funding_grant_id><funding_grant_id>K08-CA250418</funding_grant_id><funding_grant_id>R01HG011800</funding_grant_id><funding_grant_id>R3-5GM145383</funding_grant_id><funding_grant_id>P42 ES023716</funding_grant_id><pubmed_authors>Eadon MT</pubmed_authors><pubmed_authors>Chapman AB</pubmed_authors><pubmed_authors>Whirl-Carrillo M</pubmed_authors><pubmed_authors>Klein TE</pubmed_authors><pubmed_authors>Hein DW</pubmed_authors><pubmed_authors>Elchynski AL</pubmed_authors><pubmed_authors>Limdi NA</pubmed_authors><pubmed_authors>Donnelly RS</pubmed_authors><pubmed_authors>Andersen MA</pubmed_authors><pubmed_authors>Duarte JD</pubmed_authors><pubmed_authors>Gaedigk A</pubmed_authors><pubmed_authors>Sosinski L</pubmed_authors><pubmed_authors>Caudle KE</pubmed_authors><pubmed_authors>Lteif C</pubmed_authors><pubmed_authors>Desta Z</pubmed_authors><pubmed_authors>Karol SE</pubmed_authors><pubmed_authors>Zubiaur P</pubmed_authors><pubmed_authors>Cooper-DeHoff RM</pubmed_authors><pubmed_authors>Agundez JAG</pubmed_authors></additional><is_claimable>false</is_claimable><name>Clinical Pharmacogenetics Implementation Consortium Guideline for NAT2 Genotype and Hydralazine Therapy.</name><description>Hydralazine is a vasodilator typically used in the treatment of resistant hypertension and heart failure. N-acetyltransferase 2 (NAT2) catalyzes the metabolism of hydralazine into inactive metabolites. NAT2 poor metabolizers (historically referred to as "slow acetylators") are predicted to have increased plasma hydralazine concentrations compared with NAT2 rapid and intermediate metabolizers (historically referred to as "rapid acetylators" and "intermediate acetylators," respectively), which may lead to both increased clinical efficacy and adverse effects, including drug-induced systemic lupus erythematosus. This guideline summarizes the evidence from the literature relevant to NAT2/hydralazine and provides recommendations for hydralazine prescribing based on NAT2 genotype-predicted acetyl</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-05T16:55:06.612Z</modification><creation>2026-06-05T03:06:44.847Z</creation></dates><accession>S-EPMC12641075</accession><cross_references><pubmed>40974042</pubmed><doi>10.1002/cpt.70071</doi></cross_references></HashMap>