Remdesivir is the first drug against Covid-19 to be conditionally approved in Europe and the United States. The drug is designed to suppress the rapid replication of the SARS-CoV-2 virus in human cells by blocking the viral copying machine, called RNA polymerase. Researchers at the Max Planck Institute (MPI) for Biophysical Chemistry in Göttingen and the University of Würzburg have now elucidated how remdesivir interferes with the viral polymerase during copying and why it does not inhibit it completely. Their results explain why the drug has a rather weak effect. (Nature Communications, January 12, 2021)
“After complicated studies, we come to a simple conclusion,” Max Planck Director Patrick Cramer says. “Remdesivir does interfere with the polymerase while doing its work, but only after some delay. And the drug does not fully stop the enzyme.”
At the pandemic’s beginning, Cramer’s team at the MPI for Biophysical Chemistry had elucidated how the coronavirus duplicates its RNA genome. For the pathogen this is a colossal task as its genome…
