Over the past decade, many new and effective therapies for multiple sclerosis (MS) have been approved for use, including a therapy, fingolimod, whose mechanism of action is the non-selective modulation of the sphingosine-1-phosphate receptor (S1PR).While this therapy is effective for MS, cardiac and other side effects have prompted the development of therapies in this class with reduced cardiac effects.In this article, we review the biological basis for, and clinical trials related to, one such therapy, ozanimod, a small-molecule S1PR modulator with greater selectivity for non-cardiac receptor subtypes than fingolimod.We review phase I pharmacokinetic and pharmacodynamic trials and pivotal clinical trials investigating the safety and efficacy of ozanimod.Together, these trials suggest superior efficacy over interferon beta-1a in relapsing MS and good tolerability.Future studies are needed to establish whether this agent is associated with fewer unwanted cardiac effects than its predecessor, fingolimod.
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Ciftci-Kavaklioglu et al. (2019) studied this question.
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