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More MS news articles for November 2002

Researchers Discover Potential Neuroprotection Properties For Copaxone (Glatiramer Acetate Injection)

New Evidence Shows Drug could Protect Patients From Neuronal Loss

http://www.docguide.com/news/content.nsf/News/8525697700573E1885256C79004B82A9

November 21, 2002
MONTREAL, QC

European researchers have uncovered new evidence that Copaxone® (glatiramer acetate injection) not only reduces relapse rate in relapsing-remitting multiple sclerosis (MS) but also encourages the release of a factor that helps protect the brain from axonal loss.

The study, published in the November 2002 issue of Brain, showed that Copaxone stimulates T-cells to produce the neuroprotection factor BDNF (brain-derived neurotrophic factor) in tissue culture using T-cells from a Copaxone patient.

Previous research has suggested that the beneficial effects of Copaxone are the result of T-cell secretion of anti-inflammatory protective cytokines that suppress the damaging inflammation associated with MS. Based on this study, an additional mechanism of action is suggested based on the stimulation of BDNF production. BDNF is one of the most potent factors that encourages nerve tissue survival and regulates neurotransmitter release and nerve growth. Several previous studies have shown that BDNF can rescue injured or degenerating neurons and encourage axonal outgrowth, remyelinations and nerve regeneration. It also can protect axons from elimination during the course of degenerative diseases.

"This study clearly shows that Copaxone (glatiramer acetate injection) stimulated T-cells produce the neurotrophic factor BDNF. Because we know BDNF plays an important role in protecting and healing axonal damage, it is an important finding and may be an additional mechanism of action for Copaxone," said Tjalf Ziemssen, Department of Neuroimmunology, Max Planck Institute of Neurobiology, Martinsried, Germany.

The new findings in Brain were highlighted by an editorial, "The Janus face of CNS-directed autoimmune response: a therapeutic challenge," by Ludwig Kappos and Petra Duda of the Departments of Neurology and Research, University Hospitals, Kantonsspital, Basel, Switzerland. The editorial reviewed current literature on neuroprotection and the potential implications of this study.

"These findings would have major therapeutic implications if it were possible to obtain T-cells which react with CNS antigens and exert such protective effects without the destructive potential of CNS autoimmunity. Glatiramer acetate should be a logical candidate for the induction of such cells, as it is non-pathogenic, capable of inducing a protective immune response in EAE (the animal model of MS) and partially beneficial in relapsing-remitting multiple sclerosis," the editorial said.

The editorial further stated that recent neuroimaging findings from secondary (post hoc) analyses of clinical trials with MS patients treated with Copaxone seem to further support an anti-degenerative role for the drug.

The study in Brain was conducted by researchers from the Max Planck Institute of Neurobiology in Martinsried, Germany; the Institute for Clinical Neuroimmunology and Department of Neurology, Maximilians University in Munich, and the Department of Neurology, Karl-Franzens-University, Graz, Austria. Based on the results of this study, researchers believe that Copaxone not only provides anti-inflammatory cytokines at the MS lesion sites, but through T-cell stimulated BDNF release, also provides supportive neurotrophic effects in the multiple sclerosis target tissue. Further study is needed to determine the extent to which the release of BDNF in MS lesions not only provides protection for the neurons but can encourage repair and remyelination.

Copaxone is indicated for the reduction of the frequency of relapses in relapsing-remitting MS. In controlled clinical trials, the most commonly observed adverse events associated with the use of Copaxone which occurred at a higher frequency than in placebo treated patients were: injection site reactions, vasodilation, chest pain, asthenia, infection, pain, nausea, arthralgia, anxiety and hypertonia.

Copaxone is now approved in 41 countries worldwide, including Canada, the U.S., Australia, Israel and all the European countries. In Europe, Copaxone is marketed by Teva Pharmaceutical Industries Ltd. and Aventis Pharma. In North America Copaxone is marketed by Teva Neuroscience.

Teva Pharmaceutical Industries Ltd., headquartered in Israel, is among the top 35 pharmaceutical companies in the world. More than 80 percent of Teva's sales are in North America and Europe. The company develops, manufactures and markets generic and branded human pharmaceuticals and active pharmaceutical ingredients. Teva's innovative R&D focuses on developing novel drugs for diseases of the central nervous system.

Copaxone® (glatiramer acetate for injection) is a registered trademark of Teva Pharmaceutical Industries Ltd.

This release contains forward-looking statements, which express the current beliefs and expectations of management. Such statements are based on current expectations and involve a number of known and unknown risks and uncertainties that could cause Teva's future results, performance or achievements to differ significantly from the results, performance or achievements expressed or implied by such forward-looking statements. Important factors that could cause or contribute to such differences include Teva's ability to successfully develop and commercialize additional pharmaceutical products, the introduction of competitive generic products, the impact of competition from brand-name companies that sell their own generic products or successfully extend the exclusivity period of their branded products, Teva's ability to rapidly integrate the operations of acquired businesses, the availability of product liability coverage in the current insurance market, the impact of pharmaceutical industry regulation and pending legislation that could affect the pharmaceutical industry, the difficulty of predicting U.S. Food and Drug Administration ("FDA") and other regulatory authority approvals, the regulatory environment and changes in the health policies and structure of various countries, acceptance and demand for new pharmaceutical products and new therapies, uncertainties regarding market acceptance of innovative products newly launched, currently being sold or in development, the impact of restructuring of clients, reliance on strategic alliances, exposure to product liability claims, dependence on patent and other protections for innovative products, fluctuations in currency, exchange and interest rates, operating results and other factors that are discussed in Teva's Annual Report on Form 20-F and its other filings with the U.S. Securities and Exchange Commission ("SEC"). Forward-looking statements speak only as of the date on which they are made, and the Company undertakes no obligation to update publicly or revise any forward-looking statement, whether as a result of new information, future developments or otherwise.

SOURCE: Teva Pharmaceutical Industries Ltd
 

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