Scientists at the University of Alberta have shown that the drug remdesivir is highly effective in stopping the replication mechanism of the coronavirus that causes COVID-19, according to new research published today in the Journal of Biological Chemistry.

The paper follows closely on research published by the same lab in late February that demonstrated how the drug worked against the Middle East Respiratory Syndrome (MERS) virus, a related coronavirus.

Image/Hannah A Bullock; Azaibi Tamin

“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 U of A.

“We obtained almost identical results as we reported previously with MERS, so we see that remdesivir is a very potent inhibitor for coronavirus polymerases.”

Götte’s new paper demonstrates how remdesivir, developed in 2014 to fight the Ebola epidemic, works in detail. He likens the polymerase to the engine of the virus, responsible for synthesizing the virus’ genome.

“If you target the polymerase, the virus cannot spread, so it’s a very logical target for treatment,” Götte said.

The lab’s work shows how remdesivir tricks the virus by mimicking its building blocks.

“These coronavirus polymerases are sloppy and they get fooled, so the inhibitor gets incorporated many times and the virus can no longer replicate,” Götte explained.

He said the evidence from his group, 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.

He said 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.

While Götte said the evidence justifies clinical trials, he cautioned that the results obtained in the lab cannot be used to predict how the drug will work with people.

Read more at University of Alberta