Coronavirus remains to cause chaos globally, and there is no drug found or produced that can cope with it. Some individuals have been advocating the "possible" value of hydroxychloroquine, such as US President Donald Trump, but another drug attracts medical interest-Favipiravir.
Favipiravir (CAS No.259793-96-9, 6-fluoro-3-hydroxy-2-pyrazine carboxamide, T-705) is indeed a particular type of RNA polymerase blocker working on the prevention of reproduction through viral genetic copying. It was approved for marketing in Japan in March 2014, as another tool for antiviral treatment of influenza A and B. Studies have shown that Favipiravir may also exhibit good antiviral effects on a variety of RNA viruses as well as influenza viruses, such as Ebola virus, sand virus, Bunia virus, and rabies virus, etc. The COVID-19 is a coronavirus, a positive-stranded single-stranded RNA virus with a cover, and Favipiravir also has a possible antibacterial effect though from a mechanical perspective.
The process for which Favipiravir exercises a broad-spectrum antiviral activity has not been fully elucidated. Still, the current evidence supports that it can inhibit RNA - dependent polymerase (RdRp) of RNA viruses selectively and potently. Favipiravir undergoes an active form of intracellular phosphoribosylation, Favipiravir-RTP (Favipiravir ribofuranosyl-5′-triphosphate), which RdRp recognizes as a substrate and inhibits the activity of RNA polymerase. Favipiravir RTP's structure is similar to that of purine, which can compete with purine for viral RNA RNA polymerase. Making it mistakenly recognized by viral RNA RNA polymerase and inserted into the viral RNA chain or combined with the viral RNA polymerase domain to induce fatal mutations, thus preventing the incorporation of nucleotides for viral RNA replication and transcription.
There have been two published COVID-19-treatment trials for Favipiravir:
An open-label, non-randomized Shenzhen (N=80)5 trial examined the efficacy of Favipiravir (259793-96-9) versus lopinavir/ritonavir (n=45) for COVID-19 treatment. Viral clearance time (primary endpoint) for Favipiravir versus lopinavir/ritonavir was significantly shorter (median four days versus 11 days; p<0.001). Patients receiving Favipiravir also reported substantial changes in chest imaging relative to those receiving lopinavir/ritonavir, with an improvement rate of 91.43 percent versus 62.22 percent (p = 0.004). Favipiravir was reported to have less adverse reactions (11.43 percent ) compared to lopinavir/ritonavir (55.56 percent) (p><0.01).
An open-label, randomized trial in Wuhan (N=240)6 examined the efficacy of Favipiravir (n=120) versus Arbidol (n=120) for COVID-19 treatment. There was no difference in the general population in Favipiravir's 7-day clinical recovery rate (primary endpoint) versus Arbidol (61.21 percent versus 51.67 percent; p=0.14). However, the 7-day clinical recovery rate was slightly higher with Favipiravir (71.43 percent; 70/98) versus Arbidol (55.86 percent; 62/111) for a sub-population of non-critical patients without hypertension or diabetes (p = 0.02).