ArticleInternational journal of molecular sciences2025
C-Terminal Analogues of Camostat Retain TMPRSS2 Protease Inhibition: New Synthetic Directions for Antiviral Repurposing of Guanidinium-Based Drugs in Respiratory Infections.
Article in International journal of molecular sciences, 2025. 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.
- Omics Approaches in Hantavirus Research: Current Advances, Challenges, and Future Perspectives.Biotech (Basel (Switzerland)) · 2026Review
- Broad-acting antivirals: the pursuit of pan-viral therapeutics in the era of pandemics.Journal of virology · 2026Review
- Review
- Recent Advances in Lanthanide Complexes in Biological Systems: Coordination Principles and Interactions with Biomolecules.International journal of molecular sciences · 2026Review
- Natural and Synthetic Peptides as Alternatives to Antibiotics in Intestinal Infections-A Review.Antibiotics (Basel, Switzerland) · 2026Review
- West Nile Virus: Epidemiology, Surveillance, and Prophylaxis with a Comparative Insight from Italy and Iran.Vaccines · 2026Review
- Host factors in parainfluenza virus replication: from entry to innate immunity evasion.Frontiers in immunology · 2026Review
- Precision Therapeutics Through Bioactive Compounds: Metabolic Reprogramming, Omics Integration, and Drug Repurposing Strategies.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The recent global coronavirus pandemic highlighted the ever-present threat of respiratory virus outbreaks and the consequent need for ongoing research into antiviral therapy. To this end, structural analogues of the guanidinium-based drug camostat mesylate have been synthesised to probe their potential inhibition of Transmembrane Serine Protease 2 (TMPRSS2), a human protease that is essential for infection by many respiratory viruses, including Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Our in vitro fluorescence-based protease assays and supporting computational docking studies suggest that C-terminal camostat analogues retain TMPRSS2 inhibition potencies (IC
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Registered trials
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