Drug Slows Progression of MS
Reported October 24, 2008
ORLANDO, Fla. (Ivanhoe Newswire) — A recent trial shows alemtuzumab (Campath), a drug that targets certain immune system cells, may postpone disability associated with multiple sclerosis (MS) when administered in the early stages of the disease.
During the trial, patients in the early stages of relapsing-remitting MS received either interferon beta-1a (Avonex) or alemtuzumab. Overall, alemtuzumab was more effective at treating the disease but caused some significant complications.
Over time, brain volume increased in the alemtuzumab group but decreased in the interferon beta-1a group. Compared with the control drug, alemtuzumab reduced the risk of sustained disability by 71 percent and the rate of relapse by 74 percent. Alemtuzumab also shrunk brain lesions in MS patients more than interferon beta-1a.
I think this is a message of hope to MS patients, that more effective suppression of their MS, and even potentially recovery of function, can be achieved, study co-author David Margolin, M.D., Ph.D., senior medical director of clinical research at Genzyme, told Ivanhoe.
The most serious complication resulting from alemtuzumab treatment was immune thrombocytopenic purpura (ITP), a bleeding disorder, which led to the death of one patient. Treatment with alemtuzumab was discontinued after patients developed the disorder.
The bleeding disorder had not been seen in the pilot studies, and that was a shock and a surprise, Dr. Margolin said.
Alemtuzumab for treatment of MS is now in phase III clinical trials. Dr. Margolin says participants now receive regular blood tests to screen for ITP and that the complications of ITP are preventable if caught early enough. He also says the drug is a promising treatment despite its side effects.
Approximately 85 percent of people are initially diagnosed with relapsing-remitting MS, according to the National Multiple Sclerosis Society.
SOURCE: Ivanhoe interview with David Margolin, M.D., Ph.D.; New England Journal of Medicine;359:1786-1801
