COVID-19 Treatment | Remdesivir | How Does Remdesivir Work And Can It Neutralise The Coronavirus?
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Now before I start I would like to put it out there that whilst a vaccine would almost solve the covid-19 problem, it’s unlikely to become a reality for a long while yet. Vaccines just take a long time to be granted approval.
Just look at the Ebola crisis that happened not too long ago. That was first declared an epidemic in West Africa in 2014. But it wasn’t actually approved in America for use until December 2019, 5 years after the outbreak was declared.
In fact the only reason some of these vaccines are pushing phase three already is because they got permission to skip the collection of safety data from testing on animals first, which brings up its own ethical concerns.
Remdesivir has originally been in development since 2009 for hepC, only first coming to light in the world during the ebola outbreak.
Remdesivir is a potent inhibitor of viral RNA polymerase, an enzyme viruses use to help replicate their RNA or genetic material, which found in many viruses.
Specifically, it is used against singled-stranded RNA viruses.
The structure of the drug itself is what is referred to as an adenine-nucleoside analogue (in its active form you may have heard it being referred to as GS-441524).
Meaning it mimics the structure of our naturally occurring adenosine base, one of four critical molecules forming both our DNA and RNA.
When the virus invades our cell via its S-protein binding to the ACE2 receptor, its RNA is normally translated in our ribosomes to produce the coronavirus a massive viral protein.
This protein is evidently then broken down into several smaller ones, with the one we want to focus on being known as RNA-dependent RNA polymerase.
This is the protein that reads the coronavirus RNA and copies it so that it can begin replicating itself over and over, preparing itself to burst from your cell and invade all the others.
If someone takes remdesivir, the cells can uptake these “different adenosine analogues” and on occasion, when the virus is replicating it will use one of these instead of a normal base.
This basically causes chain termination and prevents the viral RNA being produced.
This theoretically will help to slow the rate of infection in the body by blocking viral replication.
Generally remdesivir is given as a 200mg loading dose intravenously (injected through your veins) over 30-120 minutes, with follow up doses each day of 100mg for either a 5 or 10 day course.
Some of the side effects that have been recognised over the years are as follows:
Respiratory failure .
Organ impairment leading to anaemia, low potassium (hypokalaemia), low albumin (hypoalbumaemia), thrombocytopenia.
GI distress: nausea and vomiting.
Transaminitis; which can be due to liver damage.
Then of course its given as an IV infusion, which means depending on how the drug is administered there can be side effects from that as well.
Earlier in the year, the FDA in America issued an emergency use authorization for remdesivir, allowing it to be used in identified critically ill patients, even though its not an approved drug for actually anything.
The most notable studies have occurred from March onwards.
The largest studies currently being conducted for remdesivir are as follows:
A RCT conducted in 10 hospital in Wuham China with Gilead from Feb to March consisting of 237 patients, with no significant results.
Simple trial 1 had around 6000 participants enrolled that had severe disease, but there was also no control group.
They looked at the 5 day course vs 10 day course of remdesivir and noticed similar improvement through the course of the disease, with participants receiving treatment within 10 days of symptom onset having improved outcomes compared to other start times.
The second simple 2 trial with a control group is looking at the same outcomes with 600 participants originally, but this was extended to 1000 participants.
They were testing the efficacy of their 5 and 10 day courses of treatment vs the placebo.A higher proportion of patients in the 5-day treatment group achieved improvement in clinical status versus the standard of care group.
Finally Gilead also recently announced preliminary results of another randomised double blinded placebo trial which (with 1063 participants), showed an improvement in the median recovery time compared to the placebo that was statistically significant.
It also showed improved mortality rates with the rate being much lower at 7.1% with remdesivir vs 11.9% in the control group.
Finally the WHO has the Solidarity Trial currently underway.