The drug remdesivir appears to help patients recover faster from the coronavirus, according to highly anticipated study results announced Wednesday by the U.S. government.

Except maybe not, according to a second study published the same day in the Lancet, a British medical journal.

A contradiction? Not at all, say those who follow clinical trials for a living. Taken together, the two studies suggest that the drug has a modest benefit and is far from a cure. Neither study found that the drug improved a person’s chance of survival.

Yet amid the world’s thirst for answers to a deadly pandemic, the news is reason for cautious optimism, said Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases.

“It is a very important proof of concept,” he said, announcing the results of the U.S. study at the White House alongside President Donald Trump. “What it has proven is that a drug can block this virus.”

Fauci said the news reminded him of when a drug was developed for a different epidemic more than 30 years ago: AIDS. That drug, called AZT, was a first step that had to be combined with other therapies to manage the disease long term.

The details of why the two remdesivir studies arrived at different results take a bit of explaining.

That the drug would work at all was far from certain. Made by Gilead Sciences of Foster City, Calif., the drug was originally designed to treat the Ebola virus, which is not closely related to the coronavirus. It wasn’t effective for Ebola.

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In the study that found evidence of a faster COVID recovery — sponsored by the institute Fauci directs — the median recovery time for hospitalized patients treated with remdesivir was 11 days, meaning half of them recovered faster than that and half took longer. Those who were given a placebo, on the other hand, generally needed four more days to get better, with a median recovery time of 15 days. (Among the 400 coronavirus patients enrolled to date were 20 participants at the University of Pennsylvania’s Perelman School of Medicine.)

Yet the Lancet study, conducted in China, was inconclusive — possibly because the researchers were unable to enroll enough patients to draw firm statistical conclusions. The study had to be stopped early because the epidemic had passed its peak; Chinese officials said the ebbing infection rate meant too few patients met eligibility criteria for the study.

Still, the partial results left open the possibility that the drug was helping, said John Norrie, chair of medical statistics and trial methodology at the University of Edinburgh, who was not involved with the research.

The recovery times for Chinese patients who got the drug appeared slightly shorter than for those who did not, though the difference was not statistically significant — meaning that it could have occurred by chance. Taken together with the U.S. results, “it looks like there’s a benefit,” Norrie said.

Derek Lowe, a medicinal chemist and drug researcher who blogs for the journal Science Translational Medicine, said remdesivir “is not a game-changer.”

“Based on what we’ve seen, the drug may be kind of useful. But the effect size is not huge. This is just going to help take the edge off” if given relatively early in the course of severe COVID-19, he said.

Norrie also cautioned that the U.S. study, though appearing to show a benefit, has yet to be reviewed for publication — which is the usual process of independent reviewers assessing any side effects and scrutinizing the results in “subgroups” of patients with different medical histories.

But the devastation of the coronavirus has accelerated research to a pace that is unprecedented in modern drug development.

“There is such urgency here that they’ve announced the headline results,” Norrie said. “It’s very unusual to hear the results announced like this. I think we’re in extraordinary times.”

The apparent benefit in the U.S. study was sufficient that for the remainder of the trial, all patients will be given remdesivir, Fauci said. Some will be randomly selected to receive an additional drug to combat inflammation.

A combination treatment is likely to be useful, said infectious-diseases specialist William R. Short, who is overseeing the portion of the trial at Penn.

“We need an antiviral,” he said. “We need something else to control all the inflammation that’s going on in the lungs at a later stage.”

The early results were enough to spark optimism both among patients and investors, who boosted Gilead’s stock price by 5.7% Wednesday.

Still, Norrie cautioned that complete data will be needed to see if the initial “headline results” stand up.

“We need to find something that actually works,” he said. “Just because we want drugs to work, that is not enough.”