ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Trypstatin as a Novel TMPRSS2 Inhibitor with Broad-Spectrum Efficacy against Corona and Influenza Viruses.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed.
- Novel endogenous protein-based strategies to inhibit clinically relevant bacterial AB-type toxins including pertussis toxin.Archives of toxicology · 2026Review
- Lock out: targeting TMPRSS2 to block influenza and coronaviruses.Journal of virology · 2026Review
- Broad-acting antivirals: the pursuit of pan-viral therapeutics in the era of pandemics.Journal of virology · 2026Review
- Searching for Novel Antiviral Agents as COVID19 Treatments: Guanidino Diaryl Thioureas.ChemMedChem · 2026Article
- Article
- A Computational Perspective to Intermolecular Interactions and the Role of the Solvent on Regulating Protein Properties.Chemical reviews · 2025Review
- Trypstatin as a Novel TMPRSS2 Inhibitor with Broad-Spectrum Efficacy against Corona and Influenza Viruses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
25 authors.
Funding
Abstract
Respiratory viruses, such as SARS-CoV-2 and influenza, exploit host proteases like TMPRSS2 for entry, making TMPRSS2 a prime antiviral target. Here, the identification and characterization of Trypstatin, a 61-amino acid Kunitz-type protease inhibitor derived from human hemofiltrate are reported. Trypstatin inhibits TMPRSS2 and related proteases with high potency, exhibiting half-maximal inhibitory concentration values in the nanomolar range, comparable to the small molecule inhibitor camostat mesylate. In vitro assays demonstrate that Trypstatin effectively blocks spike-driven entry of SARS-CoV-2, SARS-CoV-1, MERS-CoV, and hCoV-NL63, as well as hemagglutinin-mediated entry of influenza A and B viruses. In primary human airway epithelial cultures, Trypstatin significantly reduces SARS-CoV-2 replication and retained activity in the presence of airway mucus. In vivo, intranasal administration of Trypstatin to SARS-CoV-2-infected Syrian hamsters reduces viral titers and alleviates clinical symptoms. These findings highlight Trypstatin's potential as a broad-spectrum antiviral agent against TMPRSS2-dependent respiratory viruses.
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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.