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Treatment of multiple sclerosis with glatiramer acetate - new information about its mechanisms of action, pharmacokinetics, adverse effects and clinical studies

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Ziemssen,  T.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Farina,  C.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Hohlfeld,  R.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Citation

Ziemssen, T., Neuhaus, O., Farina, C., Hartung, H. P., & Hohlfeld, R. (2002). Treatment of multiple sclerosis with glatiramer acetate - new information about its mechanisms of action, pharmacokinetics, adverse effects and clinical studies. Nervenarzt, 73(4), 321-331. doi:10.1007/s00115-001-1257-0.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0012-2378-7
Abstract
Glatiramer acetate (GA, Copaxone((R))), a standardized mixture of synthetic polypeptides, has now been approved also in Germany for the treatment of relapsing-remitting multiple sclerosis (RR-MS). After it had been shown effective in suppression of experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS), it was evaluated in several clinical studies. In these studies, GA could alter the natural history of MS by both reducing the relapse rate and affecting disability. The clinical therapeutic effect of GA was consistent with the effect on magnetic resonance imaging- defined disease activity and burden in a recent multicenter study. As a daily standard dose, 20 mg of GA is injected subcutaneously. The induction of GA-reactive T-helper 2-like regulatory suppressor cells is thought to be the main mechanism of action. The most common adverse effects are mild injection site reactions. A remarkable but rare adverse effect is the only transient immediate post-injection systemic reaction manifested by flushing, chest tightness, palpitations, and dyspnea. Antibodies to GA which are induced during GA treatment do not interfere with its clinical effects.