Vandetanib Blocks the Cytokine Storm in SARS-CoV-2-Infected Mice
Ana C. Puhl, Giovanni Freitas Gomes, Samara Damasceno, Ethan J. Fritch, James A. Levi, Nicole J. Johnson, Frank Scholle, Lakshmanane Premkumar, Brett L. Hurst, Felipe Lee-Montiel, Flávio P. Veras, Sabrina Setembre Batah, Alexandre Todorovic Fabro, Nathaniel J. Moorman, Boyd L. Yount, Rebekah J. Dickmander, Ralph S. Baric, Kenneth H. Pearce, Fernando Q. Cunha, José C. Alves‐Filho, Thiago M. Cunha, Sean Ekins
Abstract
/mL for HCoV-229E. The in vivo efficacy of vandetanib was assessed in a mouse model of SARS-CoV-2 infection and statistically significantly reduced the levels of IL-6, IL-10, and TNF-α and mitigated inflammatory cell infiltrates in the lungs of infected animals but did not reduce viral load. Vandetanib also decreased CCL2, CCL3, and CCL4 compared to the infected animals. Vandetanib additionally rescued the decreased IFN-1β caused by SARS-CoV-2 infection in mice to levels similar to that in uninfected animals. Our results indicate that the FDA-approved anticancer drug vandetanib is worthy of further assessment as a potential therapeutic candidate to block the COVID-19 cytokine storm.