Two drugs being studied by Bay Area doctors for use in fighting coronavirus infections may keep more COVID-19 patients alive and out of the hospital if proved effective.

One of the drugs, colchicine, is a cheap and common anti-inflammatory treatment for gout. UCSF is using it in a clinical trial of COVID-19 patients that is occurring entirely remotely. Patients receive colchicine or placebo pills in the mail and do not need to be seen in person.

The other drug, leronlimab, is a newer experimental treatment that was originally developed for use on HIV patients before being tested more recently on some people with breast cancer. Leronlimab is a monoclonal antibody made by the Vancouver, Wash., company CytoDyn, whose chief science officer is based in San Francisco.

Doctors have already seen success in using the drug on some coronavirus patients. It is administered through shots similar to how patients get insulin. Researchers are conducting clinical trials to further test how leronlimab affects people with COVID-19.

Both drugs seek to reduce deaths and hospital stays associated with the pandemic by preventing or alleviating the cytokine storm, a medical term describing how a person’s immune system goes into overdrive and begins attacking the body’s healthy cells. Cytokine storms are believed to play a major role in deaths from COVID-19.

It’s too early to say if either drug will make a decisive dent in the severity of the pandemic, but local doctors involved with studying them are hopeful.

In the case of colchicine, the drug’s low cost and widespread availability would make it an attractive treatment option if it is shown to work well on coronavirus patients.

Dr. Priscilla Hsue, a UCSF cardiologist and professor of medicine who is overseeing the California portion of the trial, said colchicine could be readily used in countries with “limited access to very sophisticated health care systems.” The drug has no major safety issues and it could help doctors everywhere intervene early, she said.

“By the time a patient with COVID-19 makes it into the hospital, they’re already quite sick,” Hsue said. “Anything that’s going to prevent patients from getting sicker and needing to go the hospital is going to have a huge, tremendous impact.”

The colchicine trial is primarily being led by the Montreal Heart Institute in Canada, but UCSF and the New York University School of Medicine are serving as the first two U.S. sites. Researchers are hoping to enroll 6,000 people to see how the drug affects deaths and hospital stays over the 30 days they take the pills.

A major benefit to colchicine is that it would not be hard to manufacture on a large scale. Unlike more complex drugs that are “very, very specific to one inflammatory mechanism,” colchicine is “easy to make,” said Dr. David Waters, another UCSF cardiologist involved in the colchicine trial.

But Waters cautioned against setting expectations too high.

“There’s no magic bullet that’s going to come along, I would bet, that you just give it to everybody and three days later, they’ve gone back to work,” he said.

Leronlimab has already shown promise in treating some people suffering from COVID-19. The drug was authorized by the U.S. Food and Drug Administration as an emergency investigational new drug, meaning doctors can seek approval to use it on a case-by-case basis. CytoDyn, the drugmaker, has sought to have the drug approved for compassionate use, which would allow it to be prescribed more widely for patients in intensive care units.

Results from the first 36 coronavirus patients who took leronlimab have been broadly promising, said Dr. Jay Lalezari, a San Francisco physician who is CytoDyn’s chief science officer. About 30 more patients have been enrolled in clinical trials that Lalezari hopes will eventually grow to nearly 400 people.

Lalezari said he believes that leronlimab can effectively treat COVID-19.

“I don’t know if this is a double, a triple or a home run,” he told reporters in an interview on Tuesday. Based on his research, he said the drug restores immune balance and lowers the cytokine storm.

One of the patients who has already been treated with the drug is Samantha Mottet, a 55-year-old resident of Seal Beach (Orange County). She fell ill, primarily with exhaustion, shortly after her husband returned from a trip to the East Coast last month. She was eventually admitted to the hospital at UCLA, where she received an organ transplant 14 years ago, after testing positive for the coronavirus.

Her condition worsened in the hospital and she was placed on a ventilator. The first round of drugs Mottet was given did not improve her COVID-19 symptoms. Then, with her husband’s approval, her doctor administered leronlimab.

Mottet told The Chronicle that the drug was her “last hope” — and it worked. Within 24 hours, she needed less oxygen, and she was taken off the ventilator a few days later. She said she has experienced no side effects.

“All I know is I’m just thankful to be here today,” Mottet said. “This drug worked for me and I hope it works for other people.”

Dr. Warner Greene, a senior investigator with the Gladstone Institutes who has been studying the coronavirus, said leronlimab appears to be “more surgical in its effect.” Colchicine, though well known and widely used, “seems like a blunt instrument for the job at hand,” he said.

Greene said leronlimab is a more targeted kind of drug that would be “interfering with a fundamental part of the process that is causing the trouble.”

“Colchicine may be doing that, but it’s having its effect all over the body,” he said. “That said, if it blocked the cytokine storm ... that would be wonderful.”

Doctors studying leronlimab think it could be broadly effective. While CytoDyn would like to use the drug on ICU patients, its greatest benefit will likely be on patients in earlier stages of COVID-19 — hospitalized people with symptoms more severe than mild shortness of breath, said Lalezari of CytoDyn.

Dr. Bruce Patterson, CEO of the San Carlos single-cell diagnostic company IncellDx that has been working on leronlimab, said the drug is exciting because it appears to impact some of the most essential elements of the viral disease, “not just a piece of what COVID is all about.”

“This is the ideal drug to meet everybody’s needs about reopening the country,” Patterson said. “If we had something that we could say we can treat the severe (patients) and we can keep the mild-to-moderates from getting severe, then it becomes the flu. Then we’re not so scared of people getting infected.”

J.D. Morris is a San Francisco Chronicle staff writer. Email: jd.morris@sfchronicle.com Twitter: @thejdmorris