Remdesivir has emerged as a potential treatment option for SARS-CoV-2 and continues to demonstrate positive outcomes. It works by disrupting the ability of SARS-CoV-2 to replicate, however, how this occurs has been unknown. Recently, researchers at the University of Chicago have revealed Remdesivir’s mechanism of action. Their results are published in the journal, ACS Central Science.
"It's important to understand how remdesivir works at a molecular level," said Prof. Juan de Pablo, who led the research. "Now that we see that it is effective, and other drugs are not as effective, it can guide future efforts for treating COVID-19."
Remdesivir disrupts SARS-CoV-2's RNA polymerase, a key enzyme needed for replication. When this enzyme is disrupted, the virus cannot spread. Clinical trials have yielded varied results with Remdesivir, with some demonstrating faster recovery rates and improved mortaility rates, while others showed no significant improvement.
Two other treatments were analyzed, ribavirin and favilavir. Researchers found that remdesivir binds stronger to the virus, compared to ribavirin and favilavir. They also found that remdesivir destabilizes the virus's protein complex, also reducing its ability to replicate.
"We've seen that the virus is not going away and is in fact starting to mutate," de Pablo said. "Efforts to find the best therapies, and the best ways to administer them, have to continue."