Response to "Dose Rationale for Favipiravir Use in Patients Infected With SARS‐CoV‐2"

CLINICAL PHARMACOLOGY & THERAPEUTICS(2020)

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摘要
: We appreciate the letter by Eloy P., et al for their comments and complement regarding our review1-2 . Two independent in vitro studies indicated that favipiravir (T-705) inhibited SARS-CoV-2 replication in Vero E6 cells with EC50 values of 61.88 μM (9.4 μg/mL)3 and \u003e100 μM (15.7 μg/mL)4 , respectively. Data from the authors\u0027 group suggests an EC50 value in the range 40-80 µg/mL (X. de Lamballerie \u0026 F. Touret, unpublished results). I agree with the authors\u0027 assumption that favipiravir shows similar EC50 against SARS-CoV-2 and EBOV. As favipiravir is a prodrug that requires metabolic activation through ribosylation and phosphorylation in the host cells to form its triphosphate form (favipiravir-RTP), we think that variation in favipiravir activation by the cultured cells may, at least partially, contribute to the difference in the in vitro EC50 among studies.
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COVID-19,Favipiravir,pharmacokinetics
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