ArticleArchives of toxicology2022
Identification and characterization of potent, selective, and efficacious inhibitors of human arylamine N-acetyltransferase 1.
Article in Archives of toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Insights into the computer-aided drug design and discovery based on anthraquinone scaffold for cancer treatment: A systematic review.PloS one · 2024Pooled it
- Mini-review: Human N-acetyltransferase genetic polymorphisms in susceptibility to aromatic amine and alkylaniline genotoxicity.The Journal of pharmacology and experimental therapeutics · 2025Review
- Towards precision medicine strategies using plasma proteomic profiling for suspected gallbladder cancer: A pilot study.JHEP reports : innovation in hepatology · 2025Article
- Small Molecule Inhibitors of Arylamine N-Acetyltransferase 1 Attenuate Cellular Respiration.ACS pharmacology & translational science · 2024Article
- Alizarin, an Agonist of AHR Receptor, Enhances CYP1A1 Enzyme Activity and Induces Transcriptional Changes in Hepatoma Cells.Molecules (Basel, Switzerland) · 2023Article
- Nuclear DNA and Mitochondrial Damage of the Cooked Meat Carcinogen 2-Amino-1-methyl-6-phenylimidazo[4,5-Chemical research in toxicology · 2023Article
- Upregulation of cytidine deaminase in NAT1 knockout breast cancer cells.Journal of cancer research and clinical oncology · 2023Article
- Effect of N-acetyltransferase 2 genetic polymorphism on 4,4'-methylenebis(2-chloroaniline)-induced genotoxicity and oxidative stress.Archives of toxicology · 2023Article
- Differences in β-naphthylamine metabolism and toxicity in Chinese hamster ovary cell lines transfected with human CYP1A2 and NAT2*4, NAT2*5B or NAT2*7B N-acetyltransferase 2 haplotypes.Archives of toxicology · 2022Article
- Hexavalent chromium increases the metabolism and genotoxicity of aromatic amine carcinogens 4-aminobiphenyl and β-naphthylamine in immortalized human lung epithelial cells.Toxicology and applied pharmacology · 2022Article
- Deletion of arylamine N-acetyltransferase 1 in MDA-MB-231 human breast cancer cells reduces primary and secondary tumor growth in vivo with no significant effects on metastasis.Molecular carcinogenesis · 2022Article
- Expression of arylamine N-acetyltransferase 2 activity in immortalized human bronchial epithelial cells.Toxicology and applied pharmacology · 2022Article
- Acetyl coenzyme A kinetic studies onFrontiers in pharmacology · 2022Article
- 560G>A (rs4986782) (R187Q) Single Nucleotide Polymorphism in Arylamine N-Acetyltransferase 1 Increases Affinity for the Aromatic Amine Carcinogens 4-Aminobiphenyl and N-Hydroxy-4-Aminobiphenyl: Implications for Cancer Risk Assessment.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Arylamine N-acetyltransferase 1 (NAT1) plays a pivotal role in the metabolism of carcinogens and is a drug target for cancer prevention and/or treatment. A protein-ligand virtual screening of 2 million chemicals was ranked for predicted binding affinity towards the inhibition of human NAT1. Sixty of the five hundred top-ranked compounds were tested experimentally for inhibition of recombinant human NAT1 and N-acetyltransferase 2 (NAT2). The most promising compound 9,10-dihydro-9,10-dioxo-1,2-anthracenediyl diethyl ester (compound 10) was found to be a potent and selective NAT1 inhibitor with an in vitro IC
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.