NDLI: Alemtuzumab in Multiple Sclerosis: Mechanism of Action and Beyond

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Alemtuzumab in Multiple Sclerosis: Mechanism of Action and Beyond

Content Provider	MDPI
Author	Ruck, Tobias Bittner, Stefan Wiendl, Heinz Meuth, Sven
Abstract	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.
File Size	739328
Ending Page	16439
Page Count	26
Starting Page	16414
File Format	PDF
e-ISSN	14220067
DOI	10.3390/ijms160716414
Journal	International Journal of Molecular Sciences
Issue Number	7
Volume Number	16
Language	English
Publisher Date	2015-07-20
Access Restriction	Open
Subject Keyword	alemtuzumab CD52 mechanism of action secondary autoimmune disease multiple sclerosis experimental autoimmune encephalomyelitis (EAE)
Content Type	Text
Resource Type	Article

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