<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zubiete-Franco I</submitter><funding>Simons Foundation</funding><funding>Irving A Hansen Memorial Foundation</funding><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIH</funding><funding>Don Monti Memorial Research Foundation</funding><pagination>150763</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11490372</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>734</volume><pubmed_abstract>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&lt;sub>2&lt;/sub>O&lt;sub>2&lt;/sub>. Notably, these changes in phospho-tyrosine levels were able to affect cell </pubmed_abstract><journal>Biochemical and biophysical research communications</journal><pubmed_title>Famotidine increases cellular phospho-tyrosine levels.</pubmed_title><pmcid>PMC11490372</pmcid><funding_grant_id>R01 CA053840</funding_grant_id><funding_grant_id>R37 CA053840</funding_grant_id><funding_grant_id>P30 CA045508</funding_grant_id><funding_grant_id>R01 DK124907</funding_grant_id><pubmed_authors>Tonks NK</pubmed_authors><pubmed_authors>Zubiete-Franco I</pubmed_authors></additional><is_claimable>false</is_claimable><name>Famotidine increases cellular phospho-tyrosine levels.</name><description>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&lt;sub>2&lt;/sub>O&lt;sub>2&lt;/sub>. Notably, these changes in phospho-tyrosine levels were able to affect cell </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2026-06-05T16:35:17.107Z</modification><creation>2026-05-18T03:13:09.923Z</creation></dates><accession>S-EPMC11490372</accession><cross_references><pubmed>39362028</pubmed><doi>10.1016/j.bbrc.2024.150763</doi></cross_references></HashMap>