ArticleThe Journal of biological chemistry2021
Famotidine inhibits toll-like receptor 3-mediated inflammatory signaling in SARS-CoV-2 infection.
Article in The Journal of biological chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- Spike 1 protein of SARS-CoV-2 induces endothelial inflammation and vascular dysfunction through interferon ISG15-dependent mechanisms.Cardiovascular research · 2026Article
- Famotidine increases cellular phospho-tyrosine levels.Biochemical and biophysical research communications · 2024Article
- Identification of druggable host dependency factors shared by multiple SARS-CoV-2 variants of concern.Journal of molecular cell biology · 2024Article
- How the immune response to the structural proteins of SARS-CoV-2 affects the retinal vascular endothelial cells: an immune thrombotic and/or endotheliopathy process with in silico modeling.Immunologic research · 2024Article
- Article
- Effectiveness of famotidine on the risk of poor prognosis in patients with COVID-19: A nationwide cohort study in Korea.Heliyon · 2023Article
- Network-based drug repurposing for the treatment of COVID-19 patients in different clinical stages.Heliyon · 2023Article
- Cellular Sensors and Viral Countermeasures: A Molecular Arms Race between Host and SARS-CoV-2.Viruses · 2023Review
- In silico investigation of the therapeutic and prophylactic potential of medicinal substances bearing guanidine moieties against COVID-19.Chemicke zvesti · 2023Article
- Pathophysiology of Post-COVID syndromes: a new perspective.Virology journal · 2022Review
- Review
- Methodology-Centered Review of Molecular Modeling, Simulation, and Prediction of SARS-CoV-2.Chemical reviews · 2022Review
- HJournal of anesthesia · 2022Article
- The Priming Potential of Interferon Lambda-1 for Antiviral Defense in the Oral Mucosa.Inflammation · 2022Article
- Combinational benefit of antihistamines and remdesivir for reducing SARS-CoV-2 replication and alleviating inflammation-induced lung injury in mice.Zoological research · 2022Article
- Famotidine activates the vagus nerve inflammatory reflex to attenuate cytokine storm.Molecular medicine (Cambridge, Mass.) · 2022Article
- The Role of Nuclear Factor Kappa B (NF-κB) in Development and Treatment of COVID-19: Review.International journal of molecular sciences · 2022Review
- The Pathophysiology of Long COVID throughout the Renin-Angiotensin System.Molecules (Basel, Switzerland) · 2022Review
- Famotidine activates the vagus nerve inflammatory reflex to attenuate cytokine storm.Research square · 2022Article
- The association between famotidine and in-hospital mortality of patients with COVID-19.Journal of medical virology · 2022Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apart from prevention using vaccinations, the management options for COVID-19 remain limited. In retrospective cohort studies, use of famotidine, a specific oral H2 receptor antagonist (antihistamine), has been associated with reduced risk of intubation and death in patients hospitalized with COVID-19. In a case series, nonhospitalized patients with COVID-19 experienced rapid symptom resolution after taking famotidine, but the molecular basis of these observations remains elusive. Here we show using biochemical, cellular, and functional assays that famotidine has no effect on viral replication or viral protease activity. However, famotidine can affect histamine-induced signaling processes in infected Caco2 cells. Specifically, famotidine treatment inhibits histamine-induced expression of Toll-like receptor 3 (TLR3) in SARS-CoV-2 infected cells and can reduce TLR3-dependent signaling processes that culminate in activation of IRF3 and the NF-κB pathway, subsequently controlling antiviral and inflammatory responses. SARS-CoV-2-infected cells treated with famotidine demonstrate reduced expression levels of the inflammatory mediators CCL-2 and IL6, drivers of the cytokine release syndrome that precipitates poor outcome for patients with COVID-19. Given that pharmacokinetic studies indicate that famotidine can reach concentrations in blood that suffice to antagonize histamine H2 receptors expressed in mast cells, neutrophils, and eosinophils, these observations explain how famotidine may contribute to the reduced histamine-induced inflammation and cytokine release, thereby improving the outcome for patients with COVID-19.
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Registered trials
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