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Viral RdRp inhibitor
Remdesivir, also known as GS-5734, is a 1’-cyano-substituted adenosine nucleotide analog prodrug that shows broad-spectrum antiviral activity. Remdesivir was originally developed as an anti-viral against Ebola virus , but since has been shown to attenuate viral loads of a number of RNA viruses including respiratory syncytial virus (RSV) and β-coronaviruses such as SARS-CoV, MERS-CoV, and the causative agent of COVID-19, SARS-CoV-2 [2-3].
Remdesivir specifically inhibits the activity of the viral RNA-dependent RNA-polymerase (RdRp), essential in viral replication [3-5]. Upon entry into the cell, Remdesivir is rapidly metabolized into a nucleoside monophosphate (GS-441542 MP), which is then further processed into an active triphosphate form (GS-441524). GS-441524 is an adenosine triphosphate (ATP) analog and is thus, able to be used as a substrate by viral RdRp. GS-441524 outcompetes ATP for incorporation into the newly synthesized RNA strand, ultimately causing premature termination of the RNA product. However, unlike classic chain-terminators, the incorporation of GS-441524 causes delayed chain-termination downstream of this site [3, 4]. Importantly, it has been established that GS-441524 evades proofreading by the viral exoribonuclease (ExoN) .
Remdesivir has been shown to have no significant inhibitory activity on human RNA Pol II and mitochondrial RNA polymerase (h-mtRNAP) . Recently, Remdesivir has been shown to exhibit protective effects in vitro against non-alcoholic fatty liver disease (NAFLD), by inhibiting pro‑inflammatory signaling mediated by STING .
Key features of Remdesivir:
- Metabolized intracellularly into an active adenosine triphosphate analog (GS-441524)
- Potent inhibitor of viral RdRp function
- Highly pure (≥ 95%) and the absence of bacterial contamination has been confirmed in cellular assays.
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1. Warren, T.K. et al. 2016. Therapeutic efficacy of the small molecule GS-5734 against Ebola virus in rhesus monkeys. Nature 531, 381-385.
2. Gordon, C.J. et al. 2020. The antiviral compound remdesivir potently inhibits RNA-dependent RNA polymerase from Middle East respiratory syndrome coronavirus. J Biol Chem
3. Gordon, C.J. et al. 2020. Remdesivir is a direct-acting antiviral that inhibits RNA-dependent RNA polymerase from severe acute respiratory syndrome coronavirus 2 with high potency. J Biol Chem 295, 6785-6797.
4. Tchesnokov, E.P. et al. 2019. Mechanism of Inhibition of Ebola Virus RNA-Dependent RNA Polymerase by Remdesivir. Viruses 11
5. Agostini, M.L. et al. 2018. Coronavirus Susceptibility to the Antiviral Remdesivir (GS-5734) Is Mediated by the Viral Polymerase and the Proofreading Exoribonuclease. mBio 9
6. Li, Y.N. & Su, Y. 2020. Remdesivir attenuates high fat diet (HFD)-induced NAFLD by regulating hepatocyte dyslipidemia and inflammation via the suppression of STING. Biochem Biophys Res Commun 526, 381-388.
CAS number: 1809249-37-3
Molecular weight: 602.58 g/mol
Solubility: 100 mg/ml (165.95 mM) in DMSO and 25 mg/ml (41.48 mM) in ethanol
- 0.01 - 1 µM (viral RdRp inhibition in published cell culture assays) 
Note: Cellular cytotoxicity is observed at concentrations greater than 10 µM (CC50 > 10µM) 
- Purity: ≥95% (UHPLC)
- The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ hTLR2 and HEK-Blue™ hTLR4 cells.
- 1 mg Remdesivir (provided as a dried powder)
Remdesivir is shipped at room temperature.
Upon receipt, store Remdesivir at -20 °C. Upon resuspension of Remdesivir in DMSO, prepare aliquots and store at -20 °C.
Resuspended product is stable for at least 3 months when properly stored.
Avoid repeated freeze-thaw cycles.Back to the top
Chemical structure of Remdesivir
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