An experimental new drug designed to shut down the body’s misguided assault on its own joints is showing promise against rheumatoid arthritis, relieving its crippling effects with few if any side effects.
The drug, still in testing, neutralizes the immune system T cells that help direct the assault.
It could give doctors another weapon in their arsenal of drugs against rheumatoid arthritis, which afflicts 2.1 million Americans.
Other drugs target some of the processes that underlie rheumatoid arthritis, but this is the first to attack the disease in precisely this way.
In a study of 339 patients, CTLA4Ig was added to methotrexate — the standard drug — in arthritis sufferers who had not gotten enough relief from methotrexate and still had many swollen and painful joints.
After six months, 60 percent of these patients were feeling better — some of them dramatically so. Only 35 percent of the patients on methotrexate alone reported some relief.
“I’m very excited about it. But there’s still a considerable amount of work to be done,” said Dr. Gary Firestein, chief of rheumatology, allergy and immunology at the University of California at San Diego and chairman of the Food and Drug Administration’s arthritis advisory committee.
Bristol-Myers Squibb Co. said it expects to apply to the FDA some time next year for approval to sell the drug.
More than 2,000 patients are taking part in the final round of tests needed to win FDA approval.
The findings were published in Thursday’s New England Journal of Medicine. The study was led by Dr. Joel M. Kremer, director of research at the Center for Rheumatology in Albany, N.Y., and clinical professor of medicine at Albany Medical College.
The drug cannot be taken by mouth; it must be given by an intravenous infusion. In the study, it was given three times in one month, then once every month after that for five months. People who received it with methotrexate had no more side effects than those who got only methotrexate.
CTLA4Ig is one of many drugs on the market or in development that take advantage of scientists’ clearer understanding of the complicated processes of inflammation and autoimmune diseases. Different drugs take aim at different parts of the process.
TNF inhibitors, for example, target an inflammation-causing protein called tumor necrosis factor, or TNF.
Methotrexate, originally developed to fight cancer, replaced gold salts — which helped fewer than one-third of all patients — as the standard drug against rheumatoid arthritis in the late 1980s. But two-thirds of all patients still hurt. TNF inhibitors have helped some of them.
Firestein said there is a good chance that people who do not respond to TNF inhibitors will respond to the new drug.
“Each time, the slice of the pie of people who do not respond gets thinner and thinner,” he said.