Gilead's Remdesivir Could Stop SARS-CoV-2 from Replicating, Find Researchers

This finding comes close on the heels of research demonstrating how the drug worked against the Middle East Respiratory Syndrome (MERS) virus, a related coronavirus.

Remdesivir is an investigational nucleotide analog with broad-spectrum antiviral activity, but is not approved anywhere globally for any use. Remdesivir has demonstrated in vitro and in vivo activity in animal models against the viral pathogens MERS and SARS, which are also coronaviruses and are structurally similar to COVID-19. The limited preclinical data on remdesivir in MERS and SARS indicate that remdesivir may have potential activity against COVID-19. Remdesivir has also shown promising results in the treatment of COVID-19 of 14 coronavirus-infected patients in Japan. Overall, seven clinical trials have been initiated to determine whether remdesivir is a safe and effective treatment for COVID-19.

In the new research published in the Journal of Biological Chemistry, the scientists from the University of Alberta have demonstrated how remdesivir, developed in 2014 to fight the Ebola epidemic, works in detail, likening the polymerase to the engine of the virus, responsible for synthesizing the virus' genome. The lab's work shows how remdesivir tricks the virus by mimicking its building blocks.

According to the scientists, the latest evidence, along with previously published studies in animal and cell culture models, means that remdesivir can be classified as a "direct-acting antiviral" against SARS-CoV-2, a term first used to describe newer classes of antivirals that interfere with specific steps of the hepatitis C virus (HCV) life cycle. The scientists believe that the discovery of that direct action reinforces the promise of clinical trials for remdesivir in COVID-19 patients, which are already underway around the world.

“We were optimistic that we would see the same results against the SARS-CoV-2 virus,” said Matthias Götte, chair of medical microbiology and immunology at the University of Alberta. “If you target the polymerase, the virus cannot spread, so it's a very logical target for treatment. These coronavirus polymerases are sloppy and they get fooled, so the inhibitor gets incorporated many times and the virus can no longer replicate.”

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University of Alberta