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Fingolimod for Multiple Sclerosis: Mechanism of Action, Clinical Outcomes, and Future Directions

Mehling, Matthias ; Kappos, Ludwig ; Derfuss, Tobias

In: Current Neurology and Neuroscience Reports, 2011, vol. 11, no. 5, p. 492-497

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    Title
    • Fingolimod for Multiple Sclerosis: Mechanism of Action, Clinical Outcomes, and Future Directions
    Author
    • Mehling, Matthias. Department of Neurology and Department of Biomedicine, University Hospital Basel, Petersgraben 4, CH-4031, Basel, Switzerland
    • Kappos, Ludwig. Department of Neurology and Department of Biomedicine, University Hospital Basel, Petersgraben 4, CH-4031, Basel, Switzerland
    • Derfuss, Tobias. Department of Neurology and Department of Biomedicine, University Hospital Basel, Petersgraben 4, CH-4031, Basel, Switzerland
    Document Type
    • Postprint
    Language
    • English
    Published in
    • Current Neurology and Neuroscience Reports, 2011, vol. 11, no. 5, p. 492-497. Current Science Inc.
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:319262
    Summary
    The oral sphingosine 1-phosphate receptor (S1PR) modulator fingolimod functionally antagonizes S1PR hereby blocking lymphocyte egress from secondary lymphoid organs to the peripheral blood circulation. This results in a reduction in peripheral lymphocyte counts, including potentially encephalitogenic T cells. In patients with relapsing multiple sclerosis fingolimod has been shown to be an effective treatment. In phase 2 and phase 3 studies fingolimod-treated patients had reduced disease activity clinically and in MRI. Although severe infectious complications occurred in single cases treated with fingolimod, the frequency of overall infections was comparable in fingolimod-treated patients and controls. Overall, in clinical studies fingolimod was well tolerated and had a favorable safety profile. In follow-up studies with continuous fingolimod, treatment showed sustained efficacy while being well tolerated