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Review
. 2020 Sep 1:201:112527.
doi: 10.1016/j.ejmech.2020.112527. Epub 2020 Jun 6.

A promising antiviral candidate drug for the COVID-19 pandemic: A mini-review of remdesivir

Affiliations
Review

A promising antiviral candidate drug for the COVID-19 pandemic: A mini-review of remdesivir

Chengyuan Liang et al. Eur J Med Chem. .

Abstract

Remdesivir (GS-5734), a viral RNA-dependent RNA polymerase (RdRP) inhibitor that can be used to treat a variety of RNA virus infections, is expected to be an effective treatment for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. On May 1, 2020, The U.S. Food and Drug Administration (FDA) has granted Emergency Use Authorization (EUA) for remdesivir to treat COVID-19 patients. In light of the COVID-19 pandemic, this review presents comprehensive information on remdesivir, including information regarding the milestones, intellectual properties, anti-coronavirus mechanisms, preclinical research and clinical trials, and in particular, the chemical synthesis, pharmacology, toxicology, pharmacodynamics and pharmacokinetics of remdesivir. Furthermore, perspectives regarding the use of remdesivir for the treatment of COVID-19 are also discussed.

Keywords: Antiviral; COVID-19; Coronavirus; RdRP inhibitor; Remdesivir (GS-5734).

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Conflict of interest statement

Declaration of competing interest The authors declared that they have no conflicts of interest to this work.

Figures

Image 1
Graphical abstract
Fig. 1
Fig. 1
Map of the number of patients infected with SARS-CoV-2 worldwide (including death and recovery).
Fig. 2
Fig. 2
Remdesivir (GS-5734).
Fig. 3
Fig. 3
Mechanism of remdesivir-mediated inhibition of coronavirus replication in host cells. The blue arrows and numbers represent the following essential viral infection steps: (1) attachment of the coronavirus particle to its specific receptor ACE2 and uncoating of the virus after adsorption into host cells; (2) establishment of replication organelles at the endoplasmic reticulum, where both genome replication and gene expression occur; (3) early translation of the incoming viral genome, which results in the generation of the RdRP; and (4) viral RNA replication. The purple wireframe and arrows represent the intracellular triphosphorylation of remdesivir and the competitive binding of NTP and ATP to RdRP to terminate viral RNA replication. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 4
Fig. 4
Diastereomers of remdesivir.
Fig. 5
Fig. 5
Diagram of remdesivir synthesis.
Fig. 6
Fig. 6
Information on the clinical trials of remdesivir detailed in ClinicalTrials.gov.

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