Favipiravir (T-705) is a synthetic prodrug, first discovered while assessing the antiviral activity of chemical agents active against the influenza virus in the chemical library of Toyoma chemicals.
A lead compound, A/PR/8/34, later designated as T-1105, and its derivatives were found to have antiviral activities. Favipiravir is derived by chemical modification of the pyrazine moiety of T-1105.
Six months and more than 16 million confirmed cases later, the COVID-19 pandemic has become the worst public-health crisis in a century. Discovery of a new and specific antiviral agent against the SARS-CoV-2 would involve a long and arduous timeline. Hence, by default, repurposed drugs, already in use against other viral infections, have been pressed into quick service. One such drug is favipiravir, initially marketed as an antiinfluenza agent in Japan.
Within the tissue, the molecule undergoes phosphoribosylation to favipiravir-RTP, which is the active form of this drug. It exerts its antiviral effect through the following mechanisms:
1.This molecule acts as a substrate for the RNA-dependent RNA-polymerase (RdRp) enzyme, which is mistaken by the enzyme as a purine nucleotide,thus inhibiting its activity leading to termination of viral protein synthesis.
2.It gets incorporated in the viral RNA strand, preventing further extension.This mechanism of action, along with preservation of the catalytic domain of the RdRp enzyme across various RNA viruses, explains the broad spectrum of activity of this drug.
3.It has recently been shown that favipiravir induces lethal mutagenesis in vitro during influenza virus infection, making it a virucidal drug.Whether a similar activity is demonstrated against SARS-CoV-2 or not is uncertain.
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