Remdesivir can not only speed recovery, but may cut the chance of dying of COVID-19, preliminary data released by the drug’s maker suggest.
Among severely sick people, the antiviral drug reduced the risk of dying by 62% compared with standard care, the Foster City, Calif., drugmaker Gilead Sciences Inc. reported at a virtual scientific conference on July 10.
Hospitalized people taking remdesivir had a 7.4% death rate two weeks after treatment started, while those not taking the drug had a 12.5% mortality rate, the company reported.
The new data, along with another newly reported study in mice and human cells, add to evidence that remdesivir is effective as a treatment for the coronavirus.
In a previous clinical trial run by the U.S. National Institute of Allergy and Infectious Diseases, the drug shortened hospital stays by about four days, and showed a trend toward lower death rates that was not statistically meaningful.
The new data come from two studies: a Phase III study of 312 patients, which was aimed at studying the efficacy of the drug, and a study that retrospectively examined the effect of the drug in 818 people with COVID-19. The company also found that 74.4% of people taking remdesivir recovered by day 14, compared with 59% of those getting standard care.
Gilead also reported data on remdesivir given for “compassionate use” to children and pregnant women, meaning no other treatment was available and the individuals could not join a clinical trial. Of 77 pediatric patients taking remdesivir, 73%, or 56 kids, were released from the hospital by day 28. Twelve percent remained hospitalized but breathing on their own without needing extra oxygen, and 4% died. Among 86 infected women, the drug helped lessen the amount of extra oxygen needed in 96% of pregnant women and 89% of women who had newly given birth.
Those data were presented shortly after other good news about remdesivir emerged.
For the first time, researchers have direct evidence that the antiviral drug can halt replication of SARS-CoV-2, the coronavirus that causes COVID-19, in human lung cells grown in lab dishes, and in animals.
Researchers had tested remdesivir against other coronaviruses that infect bats or humans and shown that the drug could inhibit those viruses’ growth. “But we hadn’t actually shown that it was active against SARS-CoV-2, even though [the drug] was already in clinical trials,” says Andrea Pruijssers, a virologist at Vanderbilt University Medical Center in Nashville.
Pruijssers and colleagues grew SARS-CoV-2 in human lung cells or monkey kidney cells. Remdesivir worked better at fighting the virus in the lung cells, because those cells are better at converting the drug to an active form, the researchers report July 7 in Cell Reports. That’s good news because lung cells are among those that suffer the most damage from the virus.
In the animal part of the study, the researchers infected lab mice with a hybrid version of the original SARS coronavirus, engineered to carry an enzyme from SARS-CoV-2. (The COVID-19–causing coronavirus doesn’t typically infect lab mice, so the researchers had to engineer the hybrid SARS virus.) Rodents had about 100 viruses in each lung lobe after taking remdesivir. Mice that didn’t get the drug had thousands to millions of viruses in their lungs, the team found. In addition, lung function improved in mice taking remdesivir, Pruijssers says.
Together, the cell and animal studies “are the preclinical data that would normally be required for a drug trial to actually start,” she says. Now, with those trials already under way, the data provide support for the continued use of remdesivir in people.
Currently, remdesivir is given intravenously to people who are hospitalized with COVID-19. But many researchers think giving the drug earlier in an infection would be even better. Gilead announced July 8 that it would begin a clinical trial to test the safety of an inhaled form of the drug. If the inhaled form is safe and effective, it might be used to treat people at home. The company also announced it would begin testing the intravenous drug in children.
This story was originally published by Science News, a nonprofit independent news organization.