An effective treatment would allow countries to loosen some of the restrictions that are strangling their economies. They would be able to risk more people catching the virus in the knowledge that they could be cured.
This hope has energised the hunt for a drug against covid-19 since the early days of the pandemic. President Donald Trump, for one, has touted hydroxychloroquine, an anti-malarial drug. But it is remdesivir, an experimental antiviral drug, that is proving the most exciting. The share price of its maker, Gilead Sciences, shot up by 12% on April 17th after a leak in STAT, an online medical publication, of a discussion suggesting impressive results of a trial with the drug.
Unlike drugs like hydroxychloroquine, which were made to treat other conditions but might have antiviral effects, remdesivir was designed from the outset to kill viruses. It is a molecule known as a “nucleotide analogue”. Its structure mimics the letters that are used to make up the RNA sequences of the virus. The idea is that when viruses try to use these pseudo-letters it gums up their works. Gilead, a drugmaker from California, developed remdesivir to treat Ebola. Although it performed poorly in this, laboratory tests have shown it to be effective against a range of viruses. Thus there is a reasonable hope that it will work against the new coronavirus, called SARS-CoV-2.
Yet science remains equivocal about whether this drug actually works for covid-19 sufferers. Two trials in China have already failed, because of lack of enrolment. (China started its trials relatively late in its epidemic, so it was hard to recruit sufficient numbers of patients.) The recent publication in the New England Journal of Medicine, of a study of remdesivir given to 53 severely afflicted patients, reported that 68% of them improved. However the study has proven divisive among scientists. To begin with, errors can be large given the small number of patients. Moreover, the trial was not “randomised”, so there is no way of knowing whether the sample properly reflects the population of severely afflicted patients. Last, there was no comparison group that was given a placebo, ie, a substance with no therapeutic effect, to establish the real effectiveness of the drug.
For all the excitement it generated, the STAT report was little more than a leaked conversation between doctors. It revolved around a trial at the University of Chicago with 125 patients, mostly severely ill with covid-19. One of the doctors is reported as saying that most of the patients had been discharged and only two had died. But even if this is correct, the lack of a placebo group makes it hard to assess the real worth of the drug. The University of Chicago itself warned that drawing any conclusions was "premature and scientifically unsound".
Stephen Evans, a professor of pharmacoepidemiology at the London School of Hygiene and Tropical Medicine, warns that medicine is littered with instances where treatments were incorrectly believed to have strong benefits based on non-randomised data. Luckily, there are some gold-standard trials under way. One global effort, under the auspices of the World Health Organisation, began in mid-March but results are not expected until after June. Another by the National Institute of Allergy and Infectious Diseases in America could come in late May.
Even if the drug proves successful, it is still experimental, and only limited quantities of such drugs are usually available. Gilead has increased production to meet demand for use in trials. On April 5th, it said it had enough to supply more than 140,000 patients. These sorts of numbers are larger than would be required by clinical trials, so suggest that Gilead is ramping up production for clinical use. The firm also said it was hoping to increase output again as raw materials became available. Looking further ahead, at even broader use, the firm has set an “ambitious goal” of producing more than 500,000 treatment courses by October, and 1m by the end of the year, from a geographically diverse group of suppliers.
The best solution to the pandemic is still a vaccine against SARS-CoV-2; it would prevent people from catching it rather than curing them after they fall ill. But an effective medicine, even in small quantities, would make a huge difference—not least because it would speed up the development of a vaccine. The quickest way to test whether a vaccine works is to give it to a group of volunteers (and a placebo to another), and then expose them to the coronavirus. This is ethically dubious for a disease that has no known cure. A good treatment, though, would make such “human challenge” trials much more likely to go ahead.