-- Study published in Nature Medicine --
-- DR6 antagonist may play dual role in preventing axonal demyelination --
WESTON, Mass.--(BUSINESS WIRE)--Biogen Idec (NASDAQ: BIIB), a leader in the research and development of treatments for people with multiple sclerosis (MS), today announced results from a study that suggest that inhibiting death receptor-6 (DR6) function may represent a novel approach in the treatment of multiple sclerosis by blocking autoimmune response while promoting remyelination. Data from in vitro and in vivo models were published online today and will be published in the July print issue of Nature Medicine.
“Our approach to finding new treatments for this complex disease looks beyond known pathways affected by current MS treatments,” said Sha Mi, Ph.D., distinguished investigator, neurobiology research, Biogen Idec. “Our in vivo and in vitro studies demonstrate that inhibiting or blocking DR6 function results in robust axonal remyelination. These data provide strong evidence that this targeted approach warrants further research and ultimately may lead to an important new way of treating demyelinating diseases, including MS.”
MS affects each person differently, and more treatment options that target multiple pathways are needed in order to meet the various needs of patients. This study is the first-ever to demonstrate the negative role that DR6 plays in regulating remyelination within the central nervous system. Equally important, the data support the development of DR6 antagonist as a treatment for MS, a neurodegenerative disease that contains both autoimmune and demyelination components. The dual role of DR6 antagonists in promoting remyelination and inhibiting autoimmune activation represents a novel approach for the treatment of multiple sclerosis and other central nervous system diseases that result from demyelination.
“Until we find a cure, Biogen Idec is dedicated to driving ground-breaking research and pursuing highly differentiated therapies for the treatment and management of MS and other central nervous system diseases,” said Douglas E. Williams, executive vice president, research & development, Biogen Idec. “No currently approved MS treatment targets DR6, and the identification of the potential role of this receptor illustrates the breadth of our ongoing commitment to using cutting-edge science to discover of potential new treatment options for the MS community.”
About Biogen Idec
Biogen Idec uses cutting-edge science to discover, develop, manufacture and market therapies for serious diseases with a focus on neurology, immunology and hemophilia. Founded in 1978, Biogen Idec is the world’s oldest independent biotechnology company. Patients worldwide benefit from its leading multiple sclerosis therapies, and the company generates more than $4 billion in annual revenues. For product labeling, press releases and additional information about the company, please visit www.biogenidec.com.
Safe Harbor
This press release contains forward-looking statements, including statements about the development of potential new treatments for demyelination diseases such as MS. These statements may be identified by words such as "believe," "expect," "may," "plan," "will" and similar expressions, and are based on our current beliefs and expectations. Drug development involves a high degree of risk. Factors which could cause actual results to differ materially from our current expectations include the risk that unexpected concerns may arise from additional data or analysis, regulatory authorities may require additional information or may fail to approve any potential new therapy, or we may encounter other unexpected hurdles. For more detailed information on the risks and uncertainties associated with our drug development and other activities, please read the Risk Factors section of our most recent annual or quarterly report and in other reports we have filed with the SEC. Any forward-looking statements speak only as of the date of this press release and we assume no obligation to update any forward-looking statements.
