Drugs: Remdesivir, Camostat and Recombinant Human TMPRSS2 Protein
In the last post, I described the genetic machinery of human cells and that of COVID-19 . Recall that Sars-Cov-2 is a single stranded ‘positive’ sense virus which means it has an RNA polymerase enzyme that helps it replicate inside the cell. The virus has a spike protein that binds the ACE-2 receptor of human lung cells. Now, one more fact you should know is that there is a protein called TMPRSS2 which facilitates that binding.
So now if you are a scientist trying to block this virus, you have three targets to work on. The first is the viral RNA polymerase. That is where the drug Remdesivir comes into play. The drug Remdesivir is a inhibitor of RNA polymerase. A randomized double blind placebo controlled trial published in New England Journal of Medicine this may described a study of 1000 hospitalized patients half of whom received the drug. Remdesivir was superior to placebo in shortening the time to recovery regardless of age, sex, race, and comorbid conditions such as diabetes or hypertension. Mortality was numerically lower in the Remdesivir group but because the number of patients were small it did not reach statistical significance ( 7% vs 11%).
The human TMPRSS2 which helps the virus enter the cell is also a target for treatment. The drug Camostat is a TMPRSS2 inhibitor and currently being studied. It was successful in animal models. Scientists have also made a recombinant human TMPRSS2 protein that can act as a dummy particle and fool the virus to bind it in lieu of the real protein. Both have been successful in animals trial and currently being studied. You can visit clinicaltrials.gov and search the names of the drugs and see the ongoing trials.
I promised to tell you how the virus escapes detection of our immune system.