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Remdesivir and Its Combination With Repurposed Drugs as COVID-19 Therapeutics

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FRONTIERS IN IMMUNOLOGY
卷 13, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.830990

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repurposed drugs; therapeutics; COVID-19; remdesivir; baricitinib

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The SARS-CoV-2 virus uses an enzyme called RNA-dependent RNA polymerase (RdRp) for replication, which can be inhibited by Remdesivir. The combination treatment of Remdesivir with Baricitinib has shown better results in treating COVID-19, reducing recovery time and mortality rate. Simultaneously targeting virus replication enzymes and host human kinases may be the future strategy for SARS-CoV-2 therapeutics.
The SARS-CoV-2 virus needs multiple copies for its multiplication using an enzyme RNA-dependent RNA polymerase (RdRp). Remdesivir inhibits viral RdRp, controls the multiplication of the virus, and protects patients. However, treatment of COVID-19 with remdesivir involves adverse effects. Many ongoing clinical trials are exploring the potential of the combination of remdesivir with repurposed drugs by targeting multiple targets of virus and host human simultaneously. Better results were obtained with the remdesivir-baricitinib combination treatment for COVID-19 compared to the treatment with remdesivir alone. Notably, recovery from COVID-19 was found to be 8 days less via the remdesivir-baricitinib combination treatment as compared to remdesivir treatment alone. Furthermore, the mortality rate via the remdesivir-baricitinib combination treatment was lower compared to the remdesivir-only treatment. Remdesivir targets the SARS-CoV-2 enzyme while baricitinib targets the host human enzyme. Simultaneously, remdesivir and baricitinib as a combination inhibit their target viral RdRp and human Janus kinase, respectively. Ongoing trials for the combination of drugs will suggest in the future whether they may reduce the recovery time, reduce the mortality rate, and improve patient clinical status for noninvasive ventilation. In the future, simultaneously targeting virus replication enzymes and host human kinases may be the strategy for SARS-CoV-2 therapeutics.

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