Here is the germane citation:
Calvin J Gordon, Egor P Tchesnokov, Emma Woolner, Jason K Perry, Joy Y. Feng, Danielle P Porter, Matthias Gotte. Remdesivir is a direct-acting antiviral that inhibits RNA-dependent RNA polymerase from severe acute respiratory syndrome coronavirus 2 with high potency. Journal of Biological Chemistry, April 13, 2020; DOI: 10.1074/jbc.RA120.013679
Should this development be a breakthrough , does it call for a 'celebration' or is it merely a red herring? Thanks and stay safe!!
Clinical trials with Remdesivir are ongoing; you can find all trials at ClinicalTrials.gov
Clinical trials with Remdesivir are ongoing; you can find all trials at ClinicalTrials.gov
Clinical trial is at phase III which includes human trial. Several countries under WHO agreed for this and they are going to try three other drugs also.
Please see the link below.
https://www.nejm.org/doi/pdf/10.1056/NEJMoa2007016?articleTools=true
With about 15% of COVID-19 patients suffering from severe disease and hospitals being overwhelmed, treatments are desperately needed. So rather than coming up with compounds from scratch that may take years to develop and test, researchers and public health agencies are looking to repurpose drugs already approved for other diseases and known to be largely safe. They’re also looking at unapproved drugs that have performed well in animal studies with the other two deadly coronaviruses, which cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS).
SARS-CoV-2; Effective treatments; Remdesivir(development code GS-5734) etc.
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Article Inhibition of SARS-CoV-2 (previously 2019-nCoV) infection by...https://www.nature.com/articles/s41422-020-0305-
xhttps://zhuanlan.zhihu.com/p/120337020
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https://www.researchgate.net/post/What_is_a_new_idea_How_are_new_ideas_born_in_science_art_and_politics
https://www.jbc.org/content/early/2020/04/13/jbc.RA120.013679.abstract
Remdesivir is a direct-acting antiviral that inhibits RNA-dependent RNA polymerase from severe acute respiratory syndrome coronavirus 2 with high potency
Abstract
Effective treatments for coronavirus disease 2019 (COVID-19) are urgently needed to control this current pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Replication of SARS-CoV-2 depends on the viral RNA-dependent RNA polymerase (RdRp), which is the likely target of the investigational nucleotide analogue remdesivir (RDV). RDV shows broad-spectrum antiviral activity against RNA viruses, and previous studies with RdRps from Ebola virus (EBOV) and Middle East respiratory syndrome coronavirus (MERS-CoV) have revealed that delayed chain-termination is RDV’s plausible mechanism of action. Here, we expressed and purified active SARS-CoV-2 RdRp composed of the non-structural proteins nsp8 and nsp12. Enzyme kinetics indicated that this RdRp efficiently incorporates the active triphosphate form of RDV (RDV-TP) into RNA. Incorporation of RDV-TP at position i caused termination of RNA synthesis at position i+3. We obtained almost identical results with SARS-CoV, MERS-CoV, and SARS-CoV-2 RdRps. A unique property of RDV-TP is its high selectivity over incorporation of its natural nucleotide counterpart ATP. In this regard, the triphosphate forms of 2’-C–methylated compounds, including sofosbuvir, approved for the management of hepatitis C virus infection, and the broad-acting antivirals favipiravir and ribavirin, exhibited significant deficits. Furthermore, we provide evidence for the target specificity of RDV, as RDV-TP was less efficiently incorporated by the distantly related Lassa virus RdRp, and termination of RNA synthesis was not observed. These results collectively provide a unifying, refined mechanism of RDV-mediated RNA synthesis inhibition in coronaviruses and define this nucleotide analogue as a direct-acting antiviral (DAA).
Remdesivir (development code GS-5734) is an antiviral medication being studied during 2020 as a possible post-infection treatment for COVID-19 illness.[1] Remdesivir is a nucleotide analog, specifically an adenosine analogue, which inserts into viral RNA chains, causing their premature termination.Contents
- 1Research
- 1.1COVID-19
- 1.2Ebola virus
- 2Mechanism of action and resistance
- 3Synthesis
- 4Access
- 5Other animals
- 6References
- 7External links
ResearchRemdesivir was developed by Gilead Sciences as a treatment for Ebola virus disease and Marburg virus infections.[2] There is some evidence that it may have activity against other single stranded RNA viruses.[3]Mechanism of action and resistanceRemdesivir is a prodrug that metabolizes into its active form GS-441524. An adenosine nucleotide analog, GS-441524 interferes with the action of viral RNA-dependent RNA polymerase and evades proofreading by viral exoribonuclease (ExoN), causing a decrease in viral RNA production. It was unknown whether it terminates RNA chains or causes mutations in them.[22] However, it has been learned that the RNA-dependent RNA polymerase of Ebola virus is inhibited for the most part by delayed chain termination.[23]Mutations in the mouse hepatitis virus RNA replicase that cause partial resistance to remdesivir were identified in 2018. These mutations make the viruses less effective in nature, and the researchers believe they will likely not persist where the drug is not being used.[22]
https://en.wikipedia.org/wiki/Remdesivir
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https://www.medscape.com/viewarticle/924964Remdesivir Under Study as Treatment for Novel CoronavirusDoug BrunkFebruary 07, 2020
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Pol...
https://www.cbsnews.com/news/gilead-sciences-coronavirus-drug-remdesivir-overwhelming-demand/
See; https://www.researchgate.net/post/What_is_a_new_idea_How_are_new_ideas_born_in_science_art_and_politics
SARS-CoV-2. COVID-19. - Cytokine Storm. Proinflammatory cytokines. Cholinergic anti-inflammatory pathway
https://en.wikipedia.org/wiki/Cytokine_release_syndrome
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What works well in the test tube often does not work in test animals (mice). And mice are not men, "Safe and Effective" is the ultimate criteria in human trials. The Chinese have abandoned using it on COVID-19.
The WHO has fast-tracked remdesivir into clinical trials and is among several drugs being compared as potential treatments for hospitalized COVID-19 patients in a dozen countries @ Ijaz Durrani
https://www.clinicaltrialsarena.com/analysis/coronavirus-mers-cov-drugs/
When it comes to try efficacy of a medicine in very acute case/s of COVID-19, I would suggest a homoeopathic medicine that I have clinically observed its capacity in repair of bronchi/ decayed - tubercular cavities and complete bioregeneration of lung tissue, a perfect healthy lung with no trace of tubeculosis in the year 1972-3. Ofcourse there was a whole protocol of medication but this being the major component.
The medicine is Bacilinum-200c. One drop dose directly on toung in the morning, noon and evening. If the response is favourable pl do not repeat the medicine till the improved symptoms start relapsing, keep repeating in the same fashion till the patient feels quite comfortable.
Good news for remdesivir, the company stock soar 8% yesterday.
Reported yesterday (CNN; 4/16/20):
In a trial, Covid-19 patients receiving the experimental drug remdesivir have been recovering quickly, with most going home in days.
The patients taking part in a clinical trial of the drug have all had severe respiratory symptoms and fever, but were able to leave the hospital after less than a week of treatment, STAT quoted the doctor leading the trial as saying.
https://www.cnn.com/2020/04/16/health/coronavirus-remdesivir-trial/index.html
test tube data is not animal data, and mice are also not men. Remdesivir failed against Eboli
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