Fluvoxamine: A Review of Its Mechanism of Action and Its Role in COVID-19

• Type of Material: Article
• Authors: Vikas Sukhatme, Emory University; Angela M Reiersen, Washington University; Sharat J Vayttaden, Independent Researcher, Montgomery Village; Vidula Sukhatme, Emory University
• Language: English
• Date: 2021-04-20
• Publisher: FRONTIERS MEDIA SA
• Publication Version: Final Published Version
• Copyright Statement: © 2021 Sukhatme, Reiersen, Vayttaden and Sukhatme.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.3389/fphar.2021.652688
• Title of Journal or Parent Work: FRONTIERS IN PHARMACOLOGY
• Volume: 12
• Start Page: 652688
• End Page: 652688
• Grant/Funding Information: Morningside Center for Innovative and Affordable Medicine at Emory University.
• Keywords: Life Sciences & Biomedicine; Pharmacology & Pharmacy; ENDOPLASMIC-RETICULUM STRESS; SIGMA-RECEPTORS; SEROTONIN REUPTAKE INHIBITORS; acute respiratory distress syndrome; MAST-CELLS; THERAPEUTIC TARGET; cytokine storm; inflammation; Science & Technology; RAT MODEL; interleukins; VIRUS; FUNCTIONAL INHIBITORS; PLATELET SEROTONIN; SARS-CoV-2; ACTIVATION
• Research Categories: Health Sciences, Epidemiology; Health Sciences, Medicine and Surgery; Health Sciences, Public Health

Abstract

Fluvoxamine is a well-tolerated, widely available, inexpensive selective serotonin reuptake inhibitor that has been shown in a small, double-blind, placebo-controlled, randomized study to prevent clinical deterioration of patients with mild coronavirus disease 2019 (COVID-19). Fluvoxamine is also an agonist for the sigma-1 receptor, through which it controls inflammation. We review here a body of literature that shows important mechanisms of action of fluvoxamine and other SSRIs that could play a role in COVID-19 treatment. These effects include: reduction in platelet aggregation, decreased mast cell degranulation, interference with endolysosomal viral trafficking, regulation of inositol-requiring enzyme 1α-driven inflammation and increased melatonin levels, which collectively have a direct antiviral effect, regulate coagulopathy or mitigate cytokine storm, which are known hallmarks of severe COVID-19.