ArticleNature communications2024
Inhibition of urease-mediated ammonia production by 2-octynohydroxamic acid in hepatic encephalopathy.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Glutamine metabolism in health and disease.Signal transduction and targeted therapy · 2026Review
- Urease inhibitors: current advances, therapeutic potentials, and clinical challenges.Future medicinal chemistry · 2026Review
- Transparent and dynamic network-based risk assessment for development of hepatic encephalopathy.Communications medicine · 2025Article
- Harnessing microbial-derived metabolites in the urinary tract to prevent infection induced catheter encrustation.Nature communications · 2025Article
- L-asparaginase from the mangrove endophyteToxicology research · 2025Article
- Rapid assembly of biofilms from DNA released by SOS-inducing drugs in enteric bacteria.Scientific reports · 2025Article
- Design and synthesis of terephthalic dihydrazide analogues as dual inhibitors of glycation and urease.RSC advances · 2025Article
- A Small-Molecule Inhibitor of Gut Bacterial Urease Protects the Host from Liver Injury.ACS chemical biology · 2025Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic encephalopathy is a neuropsychiatric complication of liver disease which is partly associated with elevated ammonemia. Urea hydrolysis by urease-producing bacteria in the colon is often mentioned as one of the main routes of ammonia production in the body, yet research on treatments targeting bacterial ureases in hepatic encephalopathy is limited. Herein we report a hydroxamate-based urease inhibitor, 2-octynohydroxamic acid, exhibiting improved in vitro potency compared to hydroxamic acids that were previously investigated for hepatic encephalopathy. 2-octynohydroxamic acid shows low cytotoxic and mutagenic potential within a micromolar concentration range as well as reduces ammonemia in rodent models of liver disease. Furthermore, 2-octynohydroxamic acid treatment decreases cerebellar glutamine, a product of ammonia metabolism, in male bile duct ligated rats. A prototype colonic formulation enables reduced systemic exposure to 2-octynohydroxamic acid in male dogs. Overall, this work suggests that urease inhibitors delivered to the colon by means of colonic formulations represent a prospective approach for the treatment of hepatic encephalopathy.
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