Why Remdesivir only helps to a limited extent – healing practice

Effect of Remdesivir deciphered

In the search for effective drugs against the SARS-CoV-2 coronavirus, attention was drawn to the Ebola drug Remdesivir early on, and in July this was the first drug approved in the EU for COVID-19. However, the remedy only helps to a limited extent and a recent study has now made it clear why Remdesivir cannot completely prevent the virus from multiplying.

Researchers from the Max Planck Institute (MPI) for Biophysical Chemistry in Göttingen and the University of Würzburg have investigated the effect of Remdesivir against the coronavirus and deciphered how the drug influences the replication of the virus and why it cannot be stopped entirely. The corresponding study results were published in the specialist magazine “Nature Communications“.

Virus replication is inhibited

As the first drug against COVID-19, Remdesivir was approved subject to conditions in Europe. “The active ingredient is supposed to suppress the rapid multiplication of the SARS-CoV-2 pathogen in human cells by stopping the viral copying machine, known as RNA polymerase,” explains the Max Planck Institute (MPI) for Biophysical Chemistry in a press release to the current study results.

In the study, the researchers were able to show how Remdesivir disrupts the viral polymerase during copying, but it also became clear that it does not completely inhibit the replication of the virus. This explains why the drug works rather weakly, reports the MPI.

“After complicated investigations, we come to a simple conclusion: Remdesivir hinders the work of the polymerase, but only after a certain delay. And the drug doesn’t completely stop the enzyme, ”summarizes Max Planck Director Patrick Cramer.

Incorporation into the RNA chain

“Remdesivir is similar in structure to RNA building blocks,” explains Professor Claudia Höbartner from the University of Würzburg. This can mislead the virus’s polymerase and incorporate the substance into the growing RNA chain. What happens next, the researchers examined using biochemical methods and cryo-electron microscopy. They found out that the copying process pauses exactly when the RNA chain has lengthened by three more RNA building blocks after incorporating Remdesivir.

“The polymerase no longer allows a fourth building block. This is due to only two atoms in the structure of Remdesivir that get stuck at a certain point on the polymerase, ”reports Goran Kokic from the MPI. However, Remdesivir does not completely block RNA production. “The polymerase often continues to work after an error has been corrected,” says Kokic.

Hope for better active ingredients

According to the researchers, understanding the mechanism of action of remdesivir against SARS-CoV-2 also opens up new opportunities in the fight against the virus. “Now that we know how Remdesivir inhibits corona polymerase, we can work on improving the substance and its effects,” emphasizes Cramer. The vaccinations that have been started are essential to bring the pandemic under control, “but we must also continue to develop effective drugs that, in the event of infections, alleviate the course of COVID-19,” concluded the MPI director. (fp)

Author and source information

This text corresponds to the requirements of the medical literature, medical guidelines and current studies and has been checked by medical professionals.

Author:

Dipl. Geogr. Fabian Peters

Swell:

  • Goran Kokic, Hauke ​​S. Hillen, Dimitry Tegunov, Christian Dienemann, Florian Seitz, Jana Schmitzova, Lucas Farnung, Aaron Siewert, Claudia Höbartner, Patrick Cramer: Mechanism of SARS-CoV-2 polymerase stalling by remdesivir; in: Nature Communications (published January 12, 2021), nature.com
  • Max Planck Institute (MPI) for Biophysical Chemistry: Why Remdesivir does not completely switch off the coronavirus (published January 13, 2021), mpibpc.mpg.de

Important NOTE:
This article is for general guidance only and is not intended to be used for self-diagnosis or self-treatment. He can not substitute a visit at the doctor.

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