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Alemtuzumab in Multiple Sclerosis: Mechanism of Action and Beyond

Department of Neurology, University of Muenster, Muenster 48149, Germany
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Katalin Prokai-Tatrai
Int. J. Mol. Sci. 2015, 16(7), 16414-16439;
Received: 16 June 2015 / Revised: 12 July 2015 / Accepted: 13 July 2015 / Published: 20 July 2015
(This article belongs to the Special Issue Advances in Multiple Sclerosis)
PDF [722 KB, uploaded 20 July 2015]


Alemtuzumab is a humanized monoclonal antibody against CD52 (cluster of differentiation 52) and is approved for the therapy of relapsing-remitting multiple sclerosis. The application of alemtuzumab leads to a rapid, but long-lasting depletion predominantly of CD52-bearing B and T cells with reprogramming effects on immune cell composition resulting in the restoration of tolerogenic networks. Alemtuzumab has proven high efficacy in clinical phase II and III trials, where interferon β-1a was used as active comparator. However, alemtuzumab is associated with frequent and considerable risks. Most importantly secondary autoimmune disease affects 30%–40% of patients, predominantly impairing thyroid function. Extensive monitoring and early intervention allow for an appropriate risk management. However, new and reliable biomarkers for individual risk stratification and treatment response to improve patient selection and therapy guidance are a significant unmet need. Only a deeper understanding of the underlying mechanisms of action (MOA) will reveal such markers, maximizing the best potential risk-benefit ratio for the individual patient. This review provides and analyses the current knowledge on the MOA of alemtuzumab. Most recent data on efficacy and safety of alemtuzumab are presented and future research opportunities are discussed. View Full-Text
Keywords: alemtuzumab; CD52; mechanism of action; secondary autoimmune disease; multiple sclerosis; experimental autoimmune encephalomyelitis (EAE) alemtuzumab; CD52; mechanism of action; secondary autoimmune disease; multiple sclerosis; experimental autoimmune encephalomyelitis (EAE)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Ruck, T.; Bittner, S.; Wiendl, H.; Meuth, S.G. Alemtuzumab in Multiple Sclerosis: Mechanism of Action and Beyond. Int. J. Mol. Sci. 2015, 16, 16414-16439.

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