Multiple sclerosis (MS) is an autoimmune disorder that destroys the myelin sheath, a critical insulator surrounding axons, in the central nervous system. While MS affects more than 2.3 million individuals globally, current therapeutic options are limited.
Discovery of the G-protein coupled receptor sphingosine 1-phosphate receptor 1 (S1PR1) evoked interest in the scientific community as a possible therapeutic target for MS and other autoimmune disorders. S1PR1 activation has been linked to myelin production, astrocyte migration, neurite outgrowth, and neurogenesis. The link between S1PR1 and myelin-producing oligodendrocytes is of particular interest because new oligodendrocytes could potentially reverse early demyelination.
A study recently published in Lancet Neurology discusses amiselimod, a novel oral selective modulator of the S1PR1 receptor.4 In the double-blind phase II clinical trial, patients from Europe and Canada with relapsing MS were randomly assigned to a range of daily doses of amiselimod or placebo for 24 weeks. From weeks 8-24, researchers monitored axonal damage and used advanced magnetic resonance to locate lesions.
Doses of 0.2 mg and 0.4 mg of amiselimod were found to significantly reduce the number of lesions. Amiselimod was safe, well-tolerated, and efficacious, reducing disease activity in a dose-dependent manner. The selective S1PR1 modulator is the first to be investigated for treatment of MS in phase II studies without adverse cardiac events. However, amiselimod warrants further investigation to determine if it is a feasible long-term treatment for MS and other autoimmune-mediated diseases.
By Devin Roshan
References may be found in the journal.