There is no approved drug against COVID19, but more than 600 interventional clinical trials are ongoing as of beginning of May 2020. Recently the malaria drug chloroquine received widespread attention after a briefing by the US-president Trump and some Lupus patients in the US reported problems as their drug was sold out. For this therapeutic anecdotal evidence from France indicates it could alleviate COVID-19 symptoms in combination with an antibiotic.
However, there are further drugs for which already the evidence is a bit more solid. Remdesivir is an antiviral drug developed for influenza and other RNA viruses. Similarly Favirpiravir, is a nucleoside analogues which interferes with the replication of RNA viruses. Studies in China show both drugs are effective at early stages of COVID19, but patients with severe pneumonia appear not to benefit. It is currently not clear whether their efficacy could be somehow improved.
Another idea is using antibodies produced by patients whose immune system successfully fought off COVID19. Therefore convalescent plasma is explored, a product derived from donated blood of recovered individuals containing anti SARS-CoV-2 antibodies. This plasma could be transfused into patients with severe symptoms, without sufficient immune response. The virus would be decorated with transfused antibodies and unable to enter cells. While this is a promising option in the short term, it has also limitations which include price and availability.
Many RNA viruses require proteases, specific enzymes cleaving proteins. For HIV the protease inhibitor Liponavir has been approved, and it might help also to inhibit the protease of SARS-CoV-2. Also Ritonavir is a protease inhibitor which have been used to treat AIDS and both inhibitors were tested in China with encouraging results. Coincidentally the protease inhibitor CAMOSTAT inhibits the cellular protease TMPRSS2, which has been found essential for viral entry.
The viral spike protein on the surface responsible for the crown like protrusions mediates viral entry. It binds ACE2, which serves as viral receptor on the cell surface. After spike and ACE2 have bound, the protease TMPRSS2 joins, which primes the virus for entry by cleaving the spike protein. Only this primed spike protein adopts the right conformation to trigger fusion of the virus with the cellular membrane.
Interestingly, ACE2 protein has been developed as therapeutic against acute lung injury and delivering soluble ACE2 to the lung may inhibit viral entry by blocking the essential interaction of the virions with the target cell. Clinical trials have been initiated in China to test whether soluble ACE2 can help COVID-19 patients, presumably similar to antibodies they would decorate the virus and prevent the essential interaction with the target cell.
This completes our cursory overview of the many different leads researchers and clinicians currently follow up to provide hopefully soon relief to those patients badly affected by COVID-19. This is only a cursory overview of the many different leads researchers and clinicians follow up to provide hopefully soon relief to those patients badly affected by COVID-19: Let’s hope some of these approaches will soon help to stem the enormous numbers of patients requiring ventilators and intensive care with the threat to overburden health care systems. In the meantime however, we should all follow the local instructions to avoid unnecessary contacts. As medical research is a slow and sometimes tedious process, we really need to buy some more time by flattening the curve. Currently it is still the virus which makes the timeline, as American physician Anthony Fauci recently said.
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Review on drugs currently explored for COVID-19
Therapeutic strategies in an outbreak scenario to treat the novel coronavirus originating in Wuhan, China
Currently there are 186 interventional clinical trials listed addressing COVID-19 at Clinicaltrials.gov:
