Gilead Sciences’ experimental drug remdesivir has been gaining traction as a potential Covid-19 treatment, and late last week scored an emergency use authorization from federal regulators for it to be used in patients with the condition.

Preliminary data released last week from a closely watched trial run by the National Institute of Allergy and Infectious Diseases showed that Covid-19 patients who were given remdesivir recovered faster than those who received a placebo.

Remdesivir was originally created as a general antiviral and was later tested in Ebola patients, though it did not perform well in a landmark trial. Watch the explainer above to learn how remdesivir works against the SARS-CoV-2 virus, which causes Covid-19.

  • a bit confused about the drug interaction, I take the medication, (that are just remdesivir nucleotides?) Now since I have this “adenine” in my system all other transcription would be affected as well? Or would that have to do with dosage?

  • Hi Bhaskar,

    With your suggestion, it doesn’t make sense even more. Because if it was developed to specifically inhibit negative-sense RNA virus (i.e Ebola) then it should not have worked against COVID (positive-sense RNA virus). But as it stands currently, it’s other way round. That it works against positive-sense RNA virus but failed against negative-sense RNA virus (i.e Ebola) which was remdesivir primary preclinical target.

  • Remdesivir was developed to inhibit Ebola virus and its polymerase. Before carrying out expensive clinical trials in Ebola patients, I assume they would have done an enormous amount of testing in test tubes, on live cells and finally in animal models to confirm if remdesivir inhibits Ebola virus polymerase. Well, we know human trials against Ebola failed which suggests that remdesivir does not inhibit Ebola virus polymerase.
    We can rule out pharmacokinetics, bioavailability, the half-life of remdesivir in blood, as the reason that it failed against Ebola but works against COVID. As both the trials Ebola and COVID were done in humans’ differences in the factors mentioned above are nullified.

    What I cannot contemplate is that how can it work against the COVID virus polymerase but fails against its primary target Ebola virus polymerase for which it was designed in the first place.

    Note that Remdesivir is not an inhibitor of polymerase itself. But is an analogue of nucleotide. The way remdesivir works is that as soon as it gets incorporated in the viral RNA being extended, the viral polymerase cannot further extend the viral RNA. So, its primary mechanism of action is to induce an irreversible chain termination of viral RNA.

    With such a mechanism of action, it should have also inhibited Ebola virus polymerase and be successful in controlling Ebola infection, but it didn’t. Which suggest that if remdesivir is working against COVID, it may have a different mechanism of action than what is shown in this anime.

    • Ebola is a single strand negative sense RNA virus , while coronavirus is a single strand positive sense RNA virus. This could be a factor.

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