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The approval of natalizumab in 2004 was a major landmark for the therapy of multiple sclerosis (MS), thought to be the most common and disabling chronic inflammatory central nervous system (CNS) disease of young adults in developed countries. The history of this drug, known to block α4β1 integrin-mediated lymphocyte migration into the CNS, is unprecedented: natalizumab was the first specific MS therapy derived from a systematic bench-to-bedside approach, it was the first monoclonal antibody licensed for MS, and it showed an impressive clinical efficacy compared, albeit indirectly, with MS medications approved at that time, β-interferons and glatiramer acetate.1 However, further confirmation of therapeutic effects became less important following natalizumab withdrawal …
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