Immunotherapy Drug Gammagard May Stop Alzheimer's
Early study results indicate that an immunotherapy drug known as Gammagard may stop shrinkage of the brain associated with Alzheimer’s disease and help maintain memory. The drug is currently being studied in a large trial.
Potential Alzheimer’s drug is derived from human plasma
In April 2010, the pharmaceutical company Baxter International, which is currently working with Weill Cornell Medical Center in New York in a trial to confirm early test results on Gammagard, announced a Phase III clinical trial regarding the immunotherapy drug. At that time, Baxter said it hoped to complete enrolling patients by the end of 2010, and that patients were expected to remain in the trial for 18 months.
That announcement came after the company had garnered positive results from a Phase II clinical trial in patients who had mild to moderate Alzheimer’s disease. Generally, the Food and Drug Administration (FDA) requires two Phase III trials before it approves a drug for a specific condition. Gammagard is already being used to treat various immune disorders.
The new trial involves 360 individuals who have early symptoms of Alzheimer’s disease. In an earlier trial, the results of which were published in the journal Neurology, researchers found that previous treatment with intravenous Gammagard was associated with a 42 percent reduced risk of developing Alzheimer’s disease and related disorders.
Gammagard is a combination of antibodies derived from human plasma, and these antibodies can be used against beta-amyloid, a protein that is highly suspected to play a major role in the progression of Alzheimer’s disease. The drug is administered intravenously, although it is also available as a liquid.
Gammagard, which is referred to generically as immune globulin, is currently approved to treat primary immunodeficiency disorders including but not limited to congenital X-linked agammaglobulinemia and severe combined immunodeficiencies. Could it be used some day soon to treat Alzheimer’s disease? The trials may tell.
Fillit H et al. Neurology 2009 Jul 21; 73(3): 180-85