Glatiramer acetate, formerly known as copolymer 1, is a mixture of synthetic
polypeptides composed of four
amino acids.
Glatiramer acetate has been shown to be effective in preventing and suppressing experimental
autoimmune encephalitis (EAE), the animal model of
multiple sclerosis (MS). Therefore it was tested in several clinical studies, where it was found to slow the progression of disability and to reduce the relapse rate and the magnetic resonance imaging (MRI)-defined disease activity and burden in relapsing-remitting MS. As a daily standard dose, 20mg of
glatiramer acetate is injected subcutaneously. After injection,
glatiramer acetate undergoes rapid degradation to
amino acids and shorter
peptides; so it is not possible to measure any systemic plasma concentrations or excretion rates. Two major mechanisms have been proposed to explain the effects of
glatiramer acetate in EAE and MS: the induction of
glatiramer acetate-reactive T helper 2 (Th2)-like regulatory suppressive cells and the interference with T cell activation as an altered
peptide ligand. The most common adverse effects were mild
injection site reactions (
erythema,
inflammation and induration). The most remarkable adverse event is the acute and transient immediate postinjection reaction manifested by
flushing, chest tightness, palpitations and dyspnoea. Other reported adverse effects are transient
chest pain and
lymphadenopathy.
Antibodies to
glatiramer acetate induced during treatment do not interfere with its clinical effects. In several controlled clinical studies,
glatiramer acetate has been shown to provide consistent, reproducible clinical benefits in the target population of patients with relapsing-remitting MS. The safety profile and risk-benefit ratio are excellent. Overall,
glatiramer acetate is very well tolerated and has an excellent risk-benefit profile in patients with relapsing-remitting MS.