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New Findings on Copaxone

 

July 20, 2006

 

Researchers have found a new explanation for the effects of CopaxoneŽ (glatiramer acetate, Teva Pharmaceuticals), a treatment approved for relapsing-remitting multiple sclerosis. Nitin J. Karandikar, MD, PhD (University of Texas Southwestern Medical Center, Dallas), a Harry Weaver Neuroscience Scholar of the National MS Society, and colleagues report their findings in the Journal of Immunology (2006 Jun 1;176(11):7119-29).

 

Copaxone is a synthetic compound made up of four amino acids (the building blocks of proteins) that are found in myelin. This drug is thought to stimulate one type of T cell (called a CD4+ T cell) in the body’s immune system to change from pro-inflammatory agents that attack the brain and spinal cord in MS, to beneficial agents that work to reduce inflammation at sites of damage in the nervous system. Dr. Karandikar's team analyzed blood samples from seven people with MS treated with Copaxone, and compared them with those from four persons (with or without MS) who had never been treated with disease-modifying therapies. They used novel “flow cytometry” technology, in which samples are passed through a laser beam and analyzed by computer.

 

Dr. Karandikar and colleagues found that Copaxone therapy indeed induced not only CD4+ T cell change, but also induced the response of CD8+ T cells. CD8+ T cells have several functions in the immune system.  The results showed that Copaxone induced a form of CD8+ T cells that are “regulatory” in nature. These “T reg” cells are believed to play an important role in regulating inflammatory activity. CD8+ T reg cells were deficient in people with MS who had not been treated, and were significantly increased in those treated with Copaxone.

 

This study was conducted in a small group of people, the authors note, and was not meant to determine the clinical relevance of these findings. If confirmed in larger, clinical studies, however, this insight into the mechanism of Copaxone may help to develop better strategies for maximizing its beneficial effects.

-- Research & Clinical Programs Department