The drug showing promise against Covid-19
From almost 200 treatments being investigated for their effectiveness against Covid-19, one is showing promise and it’s not bleach
Despite the upbeat headlines about clinical results of a treatment tested on people with Covid-19, scientists warn it’s no “magic bullet”.
The antiviral medicine remdesivir, originally intended for use against Ebola, appears to reduce the length of time a person with Covid-19 is ill from 15 to 11 days.
Only preliminary results have been published, but these have excited Dr Anthony Fauci, the US director of the National Institute of Allergy and Infectious Diseases.
"The data shows that remdesivir has a clear-cut, significant, positive effect in diminishing the time to recovery," he said at a White House briefing.
The study of 1000 people has been halted because the results were so promising it was considered unethical to continue giving the control group in the study a placebo drug. The preliminary results say only 8 percent of the patients receiving remdesivir died, compared to 11.6 percent receiving the placebo.
Our own Director-General of Health Ashley Bloomfield has said he’s aware of Fauci’s enthusiasm and is interested in seeing the final study with the full data shared.
“Two earlier studies, one of which is published in The Lancet done in Wuhan, didn’t show any impact of the drug and neither did the other one. I’m very interested to see this one.”
He also pointed out the remdesivir is not licensed for treatment in any country.
Created in the mid 2010s, remdesivir was designed to slow infection by creating a roadblock between the Ebola virus and healthy cells.
University of Otago’s professor Kurt Krause describes it as a small molecule that “gums up the works”.
“If enough remdesivir is around, the virus just can’t replicate and stops dead in its tracks.”
Human trials of remdesivir in Ebola patients in the Democratic Republic of Congo showed the initial promise shown in animal tests didn’t play out as strongly in human trials. Other treatments worked better. For a while the drug sat on the pharmaceutical scrap heap.
When SARS and MERS arrived it was tested again in human cell cultures and mice to see if it worked against coronavirus, again early test results showed promise.
The two studies referred to by Bloomfield include a study done in Wuhan that struggled to find enough participants. Only 237 of the intended 453 patients were recruited because by the time the study started the local outbreak was coming to an end.
The study found no statistically significant benefit in using the drug.
The other study was conducted by the drug’s maker, Gilead Sciences. It found patients treated with both five and 10-day courses of remdesivir had similar improvements. This study was done without a control group receiving a placebo. Full results of this study have not been released, and without a control group it will be hard to assess what improvement was due to the drug, or a patient recovering on their own.
Krause sums up that the varying outcomes suggested there’s reason for caution.
“There are lots of confounding variables in these studies, numbers of patients, how sick they are, how much and how early the tested drug is given and for how long, etc. It will be important to watch this space for further studies on remdesivir and other drugs in the same category in the future.”
Other scientists share similar views. The devil will be in the detail.
Dr Babak Javid, from the Tsingshua University School of Medicine and infectious disease consultant at Cambridge University, said the data is promising and could lead to remdesivir getting fast-tracked for approval.
“However, it also shows that remdesivir is not a magic bullet in this context: the overall benefit in survival was 30 percent. It would be interesting to see if there were differences according to underlying health conditions or other variables.”
Another factor is when the best time to give a patient the drug is. If remdesivir is most effective given early in an infection, then its need to be injected could pose a problem.
“... selecting the optimal patient population that will most likely benefit the most from remdesivir may still need to be evaluated.”
Krause thinks the drug would be reserved for sicker patients, to potentially lower mortality and shorten hospital stays.
“I’m not quite ready to call it a game changer yet, but it looks more positive than some of the earlier drugs we’ve read about which have petered out."
He wonders if the true power of remdesivir will come from being teamed up with other antiviral drugs in a “cocktail” approach.
“People would also be looking to combine remdesivir with another antiviral that would target a different target in the virus, a different protein, then, usually together they get stronger.”
Protease inhibitors are another group of drugs Krause thinks may prove to be useful against Covid-19. These are not yet approved for use in humans and if found to be helpful would need to go through an approval process.
Another drug, camostat mesylate, which might block the processing of the spike protein, has been approved in use for humans for pancreatitis. Should tests show it’s effective, it could be rolled out as a treatment straight away. It’s among a number of potential treatments that have been approved for use in other conditions being investigated.
Krause, who recently published an article in New Zealand Medical Journal, has suggested New Zealand officials prepare to deal with post-lockdown outbreaks by either stockpiling potential medicines, or by being prepared to manufacture medicines locally.
The article points out the wait for a successful vaccine could be longer than hoped and puts the risk of the virus being reintroduced to New Zealand as a "virtual certainty".
"It's a marathon, not a sprint, but I'm cautiously optimistic that we will be able to put together a cocktail that will work together to really knock the virus down."
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