Daclizumab for the treatment of relapsing-remitting multiple sclerosis

ABSTRACT

Introduction: Multiple sclerosis (MS) is a common inflammatory disease of the central nervous system. Over the last two decades, the number of therapeutic options for the treatment of relapsing remitting MS (RRMS) has been constantly growing, providing new treatment options to patients.

Areas covered: Herein, the authors review the recently approved monoclonal antibody daclizumab for the treatment of RRMS. Based on original articles, they discuss its mode of action and evaluate its efficacy and safety profile compared to other available agents.

Expert opinion: The IL-2 receptor modulator daclizumab is a new highly effective agent for the treatment of RRMS with novel immunomodulatory properties. Compared to interferon-beta i.m., daclizumab is more effective in reducing relapse rates and MRI activity. However, its use is limited by the risk of autoimmune disorders and hepatotoxicity. Similar to other monoclonal antibodies for RRMS, therapy with daclizumab needs a strict preselection and monitoring of patients based on individual risk benefit assessment. Given its substantial effectiveness, daclizumab can be an attractive option for patients with highly active MS.

KEYWORDS:

• Antibody
• interleukin-2 receptor
• daclizumab
• disability
• multiple sclerosis
• natural killer cells
• opinion
• therapy

Declaration of interest

M Herwerth is supported by the Hertie Foundation. B Hemmer has served on scientific advisory boards for F. Hoffmann-La Roche Ltd, Novartis, Bayer Schering, and Genentech. He has served as DMSC member for AllergyCare; he or his institution have received speaker honoraria from Biogen Idec, Teva Neuroscience, Merck Serono, Medimmune, Novartis, Desitin, and F. Hoffmann-La Roche Ltd. Furthermore, his institution has received research support from Chugai Pharmaceuticals and Hoffmann-La-Roche. He also holds part of two patents; one for the detection of antibodies and T cells against KIR4.1 in a subpopulation of MS patients and one for genetic determinants of neutralizing antibodies to interferon-beta. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Additional information

Funding

B Hemmer is supported by the German Competence Network Multiple Sclerosis under grant number 01G10916 and the German Research foundation via grant CRC128.