Preclinical data from Teva's COPAXONE study on multiple sclerosis

Oct 21 2011

Teva Pharmaceutical Industries Ltd. (NASDAQ: TEVA) today announced preclinical data demonstrating reparative and neuroprotective effects of treatment with COPAXONE® (glatiramer acetate injection) in experimental autoimmune encephalomyelitis (EAE) models. In the study, researchers compared mice treated with COPAXONE® versus non-treated mice in relapsing-remitting and chronic multiple sclerosis (MS) disease models. Researchers observed both remyelination indicative of repair and a drastic reduction of demyelination and axonal loss in mice treated with COPAXONE®.

"While several previous studies, both clinical and preclinical, pointed to possible neuroprotective properties of COPAXONE® treatment, these data demonstrate a process of remyelination as a consequence of the treatment," said lead study author, Rina Aharoni, Senior Staff Scientist, Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel. "These data may also help explain why COPAXONE® continues to demonstrate efficacy in the long-term."

In addition to remyelination and neuronal preservation, the central nervous system of mice treated with COPAXONE® had smaller lesions, increased axonal density and a higher prevalence of normal appearing axons. Measurements were taken both before and after induction of EAE, showing that COPAXONE® prevented new damage and caused reversal of existing neurological degeneration. These data will be published this fall in the Journal of Autoimmunity.

A second preclinical study demonstrated that a signaling pathway for COPAXONE® deactivated white blood cells called macrophages that induce inflammation and autoimmune response.

"Data have indicated that activated damaging macrophages may contribute to axonal loss in MS, and that the deactivation of these macrophages may be a therapeutic goal of treatment," said lead study author, Nicolas Molnarfi, Researcher Neuroimmunologist, Department of Neurology and Program in Immunology, University of California, San Francisco, California. "These data showed that COPAXONE® deactivated specific macrophages, elucidating a potential mechanism for the impact of COPAXONE® treatment."

The results of both studies will be presented on October 20, 2011 at the Fifth Joint Triennial Congress of the European and Americas Committees for Treatment and Research in Multiple Sclerosis (ECTRIMS and ACTRIMS).