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Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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Glatitramer acetate is a mixture of synthetic polypeptides composed of four aminoacids.

The mechanism of action is not known but it may:

  • inhibit the binding of myelin basic protein antigens to the T-cell receptor (1)
  • modulate the phenotype of myelin-autoreactive T-cells

The treatment is well tolerated although a self-limiting systemic reaction (with symptoms such as flushes, palpitations, chest tightness and dyspneoa) was experienced by 48% of patients on glatiramer acetate (vs. 29% on placebo) starting within minutes of injection and lasting up to 30 minutes (2,3). Injection site reactions (including redness, pain, swelling, itching, oedema) were reported in 82% of patients on glatiramer acetate (vs. 48% on placebo).

Subcutaneous administration has been shown to result in approximately 30% reduction in relapse frequency (4). However a review by Drug and Therapeutics bulletin states that "in our view, the published clinical evidence suggesting glatiramer acetate reduces rate of relapse in patients with relapsing-remitting multiple sclerosis is both limited and compelling evidence that the drug prevents or slows progression or disability (5)".

The summary of product characteristics should be consulted before prescribing this drug.


  • (1) Neuhaus O et al (2001). Mechanisms of action of glatiramer acetate in multiple sclerosis. Neurology, 56, 702-8.
  • (2) Copaxone. Summary of Product Characteristics, UK. Teva Pharmaceuticals Ltd, April 2001.
  • (3) Johnson KP et al (2000). Sustained clinical benefits of glatiramer acetate in relaping multiple sclerosis patients observed for 6 years. Mult Scler, 6, 255-66.
  • (4) Bornstein MB et al (1987). A pilot trial of Cop1 in exacerbating-remitting multiple sclerosis. NEJM, 317, 408-14.
  • (5) Drugs and Therapeutics Bulletin (2001), 39 (6), 41-2.

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