Fingolimod for multiple sclerosis: mechanism of action, clinical outcomes, and future directions

Curr Neurol Neurosci Rep. 2011 Oct;11(5):492-7. doi: 10.1007/s11910-011-0216-9.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Central Nervous System / drug effects
  • Central Nervous System / immunology
  • Clinical Trials as Topic
  • Fingolimod Hydrochloride
  • Humans
  • Immunosuppressive Agents / therapeutic use*
  • Multiple Sclerosis / drug therapy*
  • Multiple Sclerosis / pathology
  • Propylene Glycols / therapeutic use*
  • Sphingosine / analogs & derivatives*
  • Sphingosine / therapeutic use
  • Treatment Outcome

Substances

  • Immunosuppressive Agents
  • Propylene Glycols
  • Fingolimod Hydrochloride
  • Sphingosine