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Kendra L Furber,1–3 Marina Van Agten,1–3 Charity Evans,2,4 Azita Haddadi,2 J Ronald Doucette,3–5,† Adil J Nazarali1–4 1Laboratory of Molecular Cell Biology, 2College of Pharmacy and Nutrition, 3Neuroscience Research Cluster, University of Saskatchewan, 4Cameco Multiple Sclerosis Neuroscience Research Center, City Hospital, 5Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada †Dr. J Ronald Doucette passed away on May 15, 2016 Abstract: Multiple sclerosis (MS) is a progressive, neurodegenerative disease with unpredictable phases of relapse and remission. The cause of MS is unknown, but the pathology is characterized by infiltration of auto-reactive immune cells into the central nervous system (CNS) resulting in widespread neuroinflammation and neurodegeneration. Immunomodulatory-based therapies emerged in the 1990s and have been a cornerstone of disease management ever since. Interferon β (IFNβ) was the first biologic approved after demonstrating decreased relapse rates, disease activity and progression of disability in clinical trials. However, frequent dosing schedules have limited patient acceptance for long-term therapy. Pegylation, the process by which molecules of polyethylene glycol are covalently linked to a compound, has been utilized to increase the half-life of IFNβ and decrease the frequency of administration required. To date, there has been one clinical trial evaluating the efficacy of pegylated IFN. The purpose of this article is to provide an overview of the role of IFN in the treatment of MS and evaluate the available evidence for pegylated IFN therapy in MS. Keywords: interferon, pegylation, multiple sclerosis, relapsing–remitting, disease-modifying therapy |
