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Calcium channel blockers inhibit SARS-CoV-2 infection in epithelial lung cells

August 20, 2020

View ORCID ProfileMarco R. Straus, Miya Bidon, Tiffany Tang, Gary R. Whittaker, Susan Daniel

doi: https://doi.org/10.1101/2020.07.21.214577

PDF: https://www.biorxiv.org/content/10.1101/2020.07.21.214577v2.full.pdf

Abstract

COVID-19 has infected more than 22 million people worldwide causing over 750.000 deaths. The disease is caused by the severe acute respiratory syndrome coronavirus (CoV) 2 (SARS-CoV-2), which shares a high sequence similarity to SARS-CoV. Currently there are no vaccinations available to provide protection and the only antiviral therapy in active use in patients is remdesivir, which currently provides only limited benefit. Hence, there is an urgent need for antiviral therapies against SARS-CoV2. SARS-CoV requires Ca2+ ions for host cell entry and based on the similarity between SARS-CoV and SARS-CoV-2 it is highly likely that the same requirements exist for the two viruses. Here, we tested whether FDA-approved calcium channel blocker (CCB) drugs are efficacious to inhibit the spread of SARS-CoV-2 in cell culture. Our data shows that amlodipine, felodipine, and nifedipine limit the growth of SARS-CoV-2 in epithelial kidney (Vero E6) and epithelial lung (Calu-3) cells. We observed some differences in the inhibition efficacy of the drugs in the two different cell lines, but with felodipine and nifedipine having the greatest effect. Overall, our data suggest that CCBs have a high potential to treat SARS-CoV-2 infections and their current FDA approval would allow for a fast repurposing of these drugs.

Competing Interest Statement

The authors have declared no competing interest.

https://www.biorxiv.org/content/10.1101/2020.07.21.214577v2

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