PlumX Metrics
Embed PlumX Metrics

Oral Fingolimod or Intramuscular Interferon for Relapsing Multiple Sclerosis

The New England Journal of Medicine [NEJM], ISSN: 0028-4793, Vol: 362, Issue: 5, Page: 402-415
2010
  • 1,991
    Citations
  • 0
    Usage
  • 1,174
    Captures
  • 12
    Mentions
  • 23
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    1,991
    • Citation Indexes
      1,968
    • Policy Citations
      16
      • Policy Citation
        16
    • Clinical Citations
      5
      • PubMed Guidelines
        5
    • Patent Family Citations
      2
      • Patent Families
        2
  • Captures
    1,174
  • Mentions
    12
    • References
      8
      • Wikipedia
        8
    • Blog Mentions
      2
      • Blog
        2
    • News Mentions
      2
      • News
        2
  • Social Media
    23
    • Shares, Likes & Comments
      23
      • Facebook
        23

Most Recent News

Fingolimod vs Glatiramer Acetate in RRMS: We Have a Winner

SEATTLE -- Fingolimod (Gilenya) bested glatiramer acetate (Copaxone) at lowering relapses and disease activity in relapsing-remitting MS patients, the phase IIIb ASSESS trial showed. Over

Article Description

Fingolimod (FTY720), a sphingosine-1-phosphate–receptor modulator that prevents lymphocyte egress from lymph nodes, showed clinical efficacy and improvement on imaging in a phase 2 study involving patients with multiple sclerosis. In this 12-month, double-blind, double-dummy study, we randomly assigned 1292 patients with relapsing–remitting multiple sclerosis who had a recent history of at least one relapse to receive either oral fingolimod at a daily dose of either 1.25 or 0.5 mg or intramuscular interferon beta-1a (an established therapy for multiple sclerosis) at a weekly dose of 30 μg. The primary end point was the annualized relapse rate. Key secondary end points were the number of new or enlarged lesions on T 2 -weighted magnetic resonance imaging (MRI) scans at 12 months and progression of disability that was sustained for at least 3 months. A total of 1153 patients (89%) completed the study. The annualized relapse rate was significantly lower in both groups receiving fingolimod — 0.20 (95% confidence interval [CI], 0.16 to 0.26) in the 1.25-mg group and 0.16 (95% CI, 0.12 to 0.21) in the 0.5-mg group — than in the interferon group (0.33; 95% CI, 0.26 to 0.42; P<0.001 for both comparisons). MRI findings supported the primary results. No significant differences were seen among the study groups with respect to progression of disability. Two fatal infections occurred in the group that received the 1.25-mg dose of fingolimod: disseminated primary varicella zoster and herpes simplex encephalitis. Other adverse events among patients receiving fingolimod were nonfatal herpesvirus infections, bradycardia and atrioventricular block, hypertension, macular edema, skin cancer, and elevated liver-enzyme levels. This trial showed the superior efficacy of oral fingolimod with respect to relapse rates and MRI outcomes in patients with multiple sclerosis, as compared with intramuscular interferon beta-1a. Longer studies are needed to assess the safety and efficacy of treatment beyond 1 year. ( ClinicalTrials.gov number, NCT00340834.) In this 12-month trial involving patients with relapsing–remitting multiple sclerosis, oral fingolimod was more effective than intramuscular interferon beta-1a in reducing relapse rates. Adverse events associated with fingolimod included herpesvirus infections (two fatal infections), atrioventricular block, macular edema, skin cancer, and liver-enzyme elevation. In patients with relapsing–remitting multiple sclerosis, oral fingolimod was more effective than intramuscular interferon beta-1a in reducing relapse rates. Adverse events included herpesvirus infections (two fatal infections), atrioventricular block, macular edema, skin cancer, and liver-enzyme elevation. Oral fingolimod (FTY720) is a sphingosine-1-phosphate–receptor modulator. After phosphorylation, fingolimod acts as a functional antagonist of the sphingosine-1-phosphate type 1 receptor, inducing receptor internalization and rendering T and B cells insensitive to a signal necessary for egress from secondary lymphoid tissues. 1, 2 The resulting redistribution to lymph nodes reduces recirculation of autoaggressive lymphocytes to the central nervous system. 3–5 Also, fingolimod is lipophilic, readily crosses the blood–brain barrier, and is phosphorylated within the central nervous system. 6 Through interaction with sphingosine-1-phosphate receptors on neural cells, fingolimod may have neuroprotective or reparative effects. 6–9 Fingolimod effectively treats experimental autoimmune encephalomyelitis, an animal. . .

Bibliographic Details

Cohen, Jeffrey A; Barkhof, Frederik; Comi, Giancarlo; Hartung, Hans-Peter; Khatri, Bhupendra O; Montalban, Xavier; Pelletier, Jean; Capra, Ruggero; Gallo, Paolo; Izquierdo, Guillermo; Tiel-Wilck, Klaus; de Vera, Ana; Jin, James; Stites, Tracy; Wu, Stacy; Aradhye, Shreeram; Kappos, Ludwig; TRANSFORMS Study Group

Faculty Opinions Ltd

Medicine

Provide Feedback

Have ideas for a new metric? Would you like to see something else here?Let us know