Fingolimod therapy for multiple sclerosis.

@article{Willis2013FingolimodTF,
  title={Fingolimod therapy for multiple sclerosis.},
  author={Mary Alissa Willis and Jeffrey A. Cohen},
  journal={Seminars in neurology},
  year={2013},
  volume={33 1},
  pages={
          37-44
        }
}
Because of its potent efficacy and oral route of administration, the approval of fingolimod as treatment for relapsing-remitting multiple sclerosis (MS) was highly anticipated. The therapeutic and adverse effects are mediated by modulation of sphingosine 1-phosphate receptors. Fingolimod inhibits the egress of lymphocytes from lymph nodes and may also have direct effects on the central nervous system. The clinical trials that led to the approval of fingolimod demonstrated benefit on relapses… 
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Multiple sclerosis rebound after fingolimod discontinuation for lymphopenia
A Caucasian 36-year-old woman was affected by RRMS of 17 years duration. Interferon beta treatment was interrupted on April 2012 for lack of efficacy (3 relapses over the last 2 years). The patient
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References

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TLDR
Findings suggest that S1PR modulation by fingolimod in both the immune system and CNS, producing a combination of beneficial anti‐inflammatory and possibly neuroprotective/reparative effects, may contribute to its efficacy in MS.
Fingolimod for Multiple Sclerosis: Mechanism of Action, Clinical Outcomes, and Future Directions
TLDR
Overall, in clinical studies fingolimod was well tolerated and had a favorable safety profile, and in follow-up studies with continuous fingolIMod, treatment showed sustained efficacy while being well tolerated.
Fingolimod (FTY720): discovery and development of an oral drug to treat multiple sclerosis
TLDR
The discovery and development of fingolimod is described, which was approved by the US Food and Drug Administration in September 2010 as a first-line treatment for relapsing forms of multiple sclerosis, thereby becoming the first oral disease-modifying therapy to be approved for multiple sclerosis in the United States.
Critical appraisal of the role of fingolimod in the treatment of multiple sclerosis
TLDR
The authors conclude that only long-term safety data from post-marketing surveillance plans, together with additional head-to-head studies, would allow evidence-based treatment decisions and that a close dialog with the well-informed patient, secured by effective risk mitigation plans, is required to choose the compound.
Severe multiple sclerosis relapse under fingolimod therapy: Incident or coincidence?
TLDR
Fingolimod is the first orally administered disease-modifying drug that has been approved for treatment of relapsing-remitting multiple sclerosis and acts as a nonselective functional antagonist of the sphingosine-1-phosphate receptor family, trapping B and T lymphocytes in secondary lymphoid tissues.
Rebound of disease activity after withdrawal of fingolimod (FTY720) treatment.
TLDR
Two aspects relevant to any newly approved multiple sclerosis treatment with immunomodulatory properties are highlighted with this case: possible rebound of disease activity after discontinuation; second, the occurrence of a tumor as a possible treatment-related complication.
CRITICAL VASOSPASM DURING FINGOLIMOD (FTY720) TREATMENT IN A PATIENT WITH MULTIPLE SCLEROSIS
We report on a woman who developed critical arterial vasospasm of the left arm within 7 days after having started treatment with Fingolimod (FTY720). Fingolimod is an orally administered modulator of
Mechanism of Action of Oral Fingolimod (FTY720) in Multiple Sclerosis
TLDR
Fingolimod crosses the blood-brain barrier and may therefore have direct CNS effects, distinguishing it from immunologically targeted MS therapies, andTherapeutic efficacy observed in animal studies has been substantiated in phase 2 and 3 trials involving patients with relapsesing or relapsing-remitting MS.
Clinical immunology of the sphingosine 1-phosphate receptor modulator fingolimod (FTY720) in multiple sclerosis
TLDR
Functional antagonism of S1P1 by fingolimod results in a reduction in peripheral lymphocyte counts by inhibiting egress of lymphocytes, including potentially encephalitogenic T cells and their naïve progenitors that would otherwise be present within the circulation.
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