Famotidine increases cellular phospho-tyrosine levels.
Covid-19
Famotidine
Histamine 2 receptor
Interferon alpha
Reactive oxygen species
Tyrosine phosphorylation
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
28 Sep 2024
28 Sep 2024
Historique:
received:
23
09
2024
accepted:
27
09
2024
medline:
3
10
2024
pubmed:
3
10
2024
entrez:
3
10
2024
Statut:
aheadofprint
Résumé
While vaccines were being developed, the SARS-CoV-2 pandemic triggered a race to find known drugs that could be quickly repurposed to treat patients. One such candidate was famotidine, which retrospective cohort studies had shown increased survival in hospitalized patients. Computational studies had suggested that famotidine may target early viral proteases; however, ultimately, famotidine was shown not to function as a viral inhibitor. In contrast, we have observed a change in the cellular levels of phospho-tyrosine in A549 lung epithelial cells following treatment with famotidine. This quick change in phosphorylation was due mainly to a dose-dependent increase in cellular production of H
Identifiants
pubmed: 39362028
pii: S0006-291X(24)01299-3
doi: 10.1016/j.bbrc.2024.150763
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
150763Informations de copyright
Copyright © 2024 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Nicholas K. Tonks reports financial support was provided by National Institute of Health grants CA53840 and DK124907, the CSHL Cancer Centre Support Grant CA45508, the Robertson Research Fund of CSHL, the Don Monti Memorial Research Foundation, theHansen Foundation, and theSimons Foundation. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.