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More MS news articles for May 2004

Humanized anti-CD25 (daclizumab) inhibits disease activity in multiple sclerosis patients failing to respond to interferon {beta}

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15161974

Proc Natl Acad Sci U S A. 2004 May 25
Bielekova B, Richert N, Howard T, Blevins G, Markovic-Plese S, McCartin J, Wurfel J, Ohayon J, Waldmann TA, McFarland HF, Martin R.
Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; Department of Neurology, University of North Carolina at Chapel Hill, 6109 Neuroscience Research Building, Chapel Hill, NC 27599; Institute of Neuroimmunology, Charite, Humboldt-University Berlin, Schumannstrasse 20/21, D-10117 Berlin, Germany.

Identifying effective treatment combinations for MS patients failing standard therapy is an important goal.

We report the results of a phase II open label baseline-to-treatment trial of a humanized monoclonal antibody against CD25 (daclizumab) in 10 multiple sclerosis patients with incomplete response to IFN-beta therapy and high brain inflammatory and clinical disease activity.

Daclizumab was very well tolerated and led to a 78% reduction in new contrast-enhancing lesions and to a significant improvement in several clinical outcome measures.