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Drug Evaluation

Glatiramer acetate in the treatment of multiple sclerosis

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Pages 1149-1165 | Published online: 24 Feb 2005

Bibliography

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  • •The first Phase II trial of glatiramer acetate.
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  • ••Phase III trial that led to FDA approval.
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  • ••Oral glatiramer acetate suppressed EAE inanimals, a study which led to a clinical study in humans.
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  • ••Glatiramer acetate binds to various MHCclass II molecules - the first step in its mechanism of action.
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  • •Proof of binding, using purified human MHC class II molecules.
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  • •Possible mechanism of action of glatiramer acetate at the level of competition for the specific TCR.
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  • ••Cross-reaction between glatiramer acetateand MBP at the level of Th2 cells - possibly the main mechanism of glatiramer acetate activity.
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  • •Suppression of EAE by Th2 cells, regardless of the inducing antigen.
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  • •Glatiramer acetate protects the damaged optic nerve due to T-cell immunity.
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  • ••Hopes for therapy by glatiramer acetate ofglaucoma and of acute and chronic degenerative disorders.
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  • •Describes in humans shift from Thl to Th2.
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