Salicylanilides Reduce SARS-CoV-2 Replication and Suppress Induction of Inflammatory Cytokines in a Rodent Model.

ACS Infect Dis

Departments of Chemistry and Immunology, The Skaggs Institute for Chemical Biology, Worm Institute of Research and Medicine (WIRM), The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, United States.

Published: August 2021

AI Article Synopsis

  • The SARS-CoV-2 virus has caused the COVID-19 pandemic, affecting individuals with a range of symptoms from asymptomatic to severe respiratory issues.
  • Researchers have screened a library of compounds called salicylanilides, finding one that effectively reduces viral loads and mitigates weight loss in mice infected with SARS-CoV-2.
  • This leads to the conclusion that salicylanilides show promise as potential therapeutics for COVID-19 due to their antiviral activity and favorable pharmacokinetic properties.

Article Abstract

SARS-CoV-2 virus has recently given rise to the current COVID-19 pandemic where infected individuals can range from being asymptomatic, yet highly contagious, to dying from acute respiratory distress syndrome. Although the world has mobilized to create antiviral vaccines and therapeutics to combat the scourge, their long-term efficacy remains in question especially with the emergence of new variants. In this work, we exploit a class of compounds that has previously shown success against various viruses. A salicylanilide library was first screened in a SARS-CoV-2 activity assay in Vero cells. The most efficacious derivative was further evaluated in a prophylactic mouse model of SARS-CoV-2 infection unveiling a salicylanilide that can reduce viral loads, modulate key cytokines, and mitigate severe weight loss involved in COVID-19 infections. The combination of anti-SARS-CoV-2 activity, cytokine inhibitory activity, and a previously established favorable pharmacokinetic profile for the lead salicylanilide renders salicylanilides in general as promising therapeutics for COVID-19.

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Source
http://dx.doi.org/10.1021/acsinfecdis.1c00253DOI Listing

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