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

doi:10.1073/pnas.0402653101

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

^*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, Charité, Humboldt-University Berlin, Schumannstrasse 20/21, D-10117 Berlin, Germany; and ^§Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892

Contributed by Thomas A. Waldmann, April 14, 2004

Abstract

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-β 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.

Footnotes

↵ ¶ To whom correspondence should be addressed at: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive, MSC 1400, Bethesda, MD 20892. E-mail: martinr{at}ninds.nih.gov.
Abbreviations: CEL, contrast-enhancing lesions; EDSS, expanded disability status scale; IVMP, intravenous methylprednisolone; MS, multiple sclerosis; NRS, neurological rating scale.
↵ ∥ Rose, J. W. (2003) in Proceedings of the 55th Annual Meeting of the American Academy of Neurology, 60, Suppl. 1, A478–A479 (abstr.).