Abstract
Our understanding of the pathogenesis of multiple sclerosis has increased considerably, leading to the development of novel therapeutic approaches and compounds. Several agents have undergone clinical testing and have recently received market authorization or are being evaluated for approval. Alemtuzumab is a humanized monoclonal antibody that rapidly depletes CD52+ cells of the lymphoid lineage from peripheral blood, but spares lymphoid precursor cells. Clinical efficacy and safety data from clinical phase II and III trials-all using interferon-β-1a as active comparator-are summarized and placed in perspective. This review further analyzes the differential reconstitution of T and B cells as a potential mode of action and the pathogenic link to treatment-emergent secondary autoimmune conditions. Given recent positive opinions by regulatory agencies, this new drug will be positioned for the treatment of active relapsing-remitting multiple sclerosis and enlarge our therapeutic armamentarium.
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