Alemtuzumab was first used in multiple sclerosis in 1991. It is a monoclonal 
antibody which is directed against CD52, a protein of unknown function on 
lymphocytes. Alemtuzumab causes a lymphopenia, following which homeostatic 
reconstitution leads to prolonged alteration of the immune repertoire. This 
reduces the risk of relapse and disability accumulation in multiple sclerosis; 
it is the only drug to show superiority over interferon β-1a in disability 
outcomes in a monotherapy phase III trial. It should be used with a parallel 
risk management programme to identify the principal adverse effects of 
alemtuzumab, especially secondary autoimmunity months or years later, mainly 
against the thyroid but also immune thrombocytopenia. This review charts the 
development of alemtuzumab as a drug for multiple sclerosis and summarizes the 
latest clinical trial data.