Alternate COVID-19 Treatment does not Inhibit Mitochondria
Kendall Wallace, PhD, Professor of Biomedical Sciences, and Jim Bjork, Researcher 3 in the Wallace lab, published their article "Molnupiravir; molecular and functional descriptors of mitochondrial safety" in the publication Toxicology and Applied Pharmacology. Molnupiravir, a new oral antiviral drug recently approved by the FDA, is administered to adult patients infected with COVID-19 who present severe risks of hospitalization or death, and who have no other treatment options.
Molnupiravir was approved by the U.S. FDA in December 2021 for the emergency treatment of patients infected by the Coronavirus but unresponsive to alternate therapies and at risk of rapid progress. Being a nucleoside analog, it shares a concern for other members of this drug class for interfering with the amount and translation of mitochondrial DNA to critical mitochondrial substituents. The result is a dramatic loss of cell bioenergetics and the associated symptoms of muscle fatigue and neurological dysfunction to mention a few. In this investigation, Wallace and Bjork examined whether the Molnupiravir may cause similar clinical complications during drug therapy. Their findings revealed that Molnupiravir, at doses that exceed therapeutic drug concentrations, does not interfere with the mitochondrial genome or its expression and does not inhibit mitochondrial bioenergetics, suggesting that the clinical safety of Molnupiravir is not confounded by mitochondrial off-target effects.