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Review
. 2021 Mar;71(3):166-170.
doi: 10.1055/a-1296-7935. Epub 2020 Nov 11.

Favipiravir and COVID-19: A Simplified Summary

Affiliations
Review

Favipiravir and COVID-19: A Simplified Summary

Morteza Ghasemnejad-Berenji et al. Drug Res (Stuttg). 2021 Mar.

Abstract

A recent outbreak of coronavirus disease 2019 (COVID-19) caused by the novel coronavirus designated as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) started in Wuhan, China, at the end of 2019 and then spread rapidly all over the world. However, there are no specific antiviral therapies for COVID-19, using the agents which approved or in development for other viral infections is one of the potentially quickest ways to find treatment for this new viral infection. Favipiravir is an effective agent that acts as a nucleotide analog that selectively inhibits the viral RNA dependent RNA polymerase or causes lethal mutagenesis upon incorporation into the virus RNA. In view of recent studies and discussion on favipiravir, in this mini review we aimed to summarize the clinical trials studying the efficacy and safety of favipiravir in patients with COVID-19.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Chemical structure of favipiravir (T-705) .
Fig. 2
Fig. 2
Schematic representation of the activation mechanism of favipiravir (Based on Furuta et al. 22 ). Favipiravir is incorporated into cells and converted to favipiravir ribofuranosyl phosphates by host cell enzymes. The triphosphate form, favipiravir-RTP, inhibits the influenza viral RNA polymerase activity.

References

    1. Lai C-C et al. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and corona virus disease-2019 (COVID-19): The epidemic and the challenges. International Journal of Antimicrobial Agents. 2020:105924. - PMC - PubMed
    1. Li G, De Clercq E. Therapeutic options for the 2019 novel coronavirus (2019-nCoV). 2020, Nature Publishing Group - PubMed
    1. Furuta Y et al. In vitro and in vivo activities of anti-influenza virus compound T-705. Antimicrobial Agents and Chemotherapy. 2002;46:977–981. - PMC - PubMed
    1. Dong L, Hu S, Gao J. Discovering drugs to treat coronavirus disease 2019 (COVID-19) Drug Discoveries & Therapeutics. 2020;14:58–60. - PubMed
    1. Baranovich T et al. T-705 (favipiravir) induces lethal mutagenesis in influenza A H1N1 viruses in vitro. Journal of Virology. 2013;87:3741–3751. - PMC - PubMed