COVID-19 Drugs: Studies Identify That Anti-Inflammatory Drugs Carprofen and Celecoxib Could Also Have Antiviral Properties Against COVID-19
Source: COVID-19 Drugs May 28, 2020 4 years, 5 months, 2 weeks, 3 days, 4 hours, 16 minutes ago
COVID-19 Drugs: Spanish researchers from the Rovira i Virgili University Department of Cheminformatics and Nutrition have identified that the anti-inflammatory drugs carprofen and celecoxib could have antiviral properties against the SARS-CoV-2 coronavirus that causes the deadly COVID-19 disease, by inhibiting replication of the virus.
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The research study has been published by the International Journal of Molecular Sciences (IJMS).
https://www.mdpi.com/1422-0067/21/11/3793
The outbreak of the COVID-19 pandemic and its rapid spread has resulted in the medical and scientific community working on developing an effective treatment for the COVID-19 disease. To date there are still no effective drugs to treat the disease. It is extremely critical to find drugs that can either suppress the activity of the virus or to eradicate it, as the possibility of an effective vaccine materializing to prevent COVID-19 seems actually remote day by day despite the “hot-air’ being spewed by unscrupulous government authorities and greedy pharmaceutical companies.
As a result of this urgency, the Spanish URV's Cheminformatics and Nutrition research group has carried out a computational screening to predict whether there is a medicine authorized for treating another pathology that can inhibit the main protease of the virus (M-pro). This is critical to the whole process because this enzyme plays an essential role in the replication of the virus.
The research demonstrates that a human and a veterinary anti-inflammatory drug Celecoxib and Carprofen can inhibit a key enzyme in the replication and transcription of the virus responsible for COVID-19.
The drug repurposing research study used computer techniques to analyze whether 6,466 drugs authorized by various drug agencies for both human and veterinary use could be used to inhibit the M-pro enzyme.
The M-pro enzyme is a protease that is responsible for cutting two polypeptides (generated by the virus itself) and generating a number of proteins that are essential for the reproduction of the virus. Some of the trials coordinated by the WHO against the COVID-19 pandemic also aim to inhibit M-pro using two antiretrovirals such as lopinavir and ritonavir (drugs initially designed to treat HIV).
The research study findings indicated that 7 of these 6,466 drugs may inhibit M-pro. The results have been shared with the international initiative COVID Moonshot which has selected 2 of these 7 compounds (i.e., Carprofen and Celecoxib) in order to test their ability to inhibit M-pro in vitro.
Further research showed that show that at a concentration of 50 μM of Celecoxib or Carprofen, the inhibition of the in vitro activity of M-pro is 11.90 and 4.0%, respectively. Therefore, both molecules could be used as a starting point for further lead optimization to obtain even more potent derivatives.
The research by the Cheminformatics and Nutrition research group from the Biochemistry and Biotechnology Department of the URV has been led by Drs. Gerard Pujadas and Santi Garcia-Vallvé with the collaboration of Dr Aleix Gimeno, Dr María José Ojeda-Montes and Dr Adri&a
mp;agrave; Cereto-Massagué, the Ph.D. students Guillem Macip and Bryan Saldivar-Espinoza and student Júlia Mestres-Truyol (double degree student in Biotechnology and in Biochemistry and Molecular Biology at the URV).
The research study is the first to be published worldwide on drug repositioning as inhibitors of SARS-CoV-2 M-pro where computational predictions are experimentally corroborated. The remaining 5 molecules are expected to be selected soon by COVID Moonshot so that their bioactivity can be tested as well.
Another Chinese that has yet to be peer-reviewed showed that Celecoxib (Celebrex) also demonstrated the ability to inhibit the cytokine storms in patients with COVID-19.
https://www.medrxiv.org/content/10.1101/2020.05.05.20077610v1
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