Glatiramer acetate is a synthetic copolymer composed of a random mixture of four
amino acids that modifies the immune response that results in the CNS
inflammation,
demyelination and axonal loss characteristic of
relapsing-remitting multiple sclerosis (RRMS). In three randomised, double-blind trials in patients with RRMS, subcutaneous
glatiramer acetate 20 mg/day was significantly more effective than placebo for the primary outcome measure of each trial (mean relapse rate, proportion of relapse-free patients and number of
gadolinium-enhancing lesions on magnetic resonance imaging [MRI] scans). The mean relapse rate was significantly reduced at endpoint (approximately one-third less) in the two larger trials (the US pivotal trial [primary endpoint] and the European/Canadian study [tertiary endpoint]) in patients receiving
glatiramer acetate compared with those receiving placebo. The rate was 78% less for
glatiramer acetate than placebo patients in the pilot trial that investigated a slightly different patient population.
Glatiramer acetate significantly decreased disease activity and burden of disease, as assessed in the European/Canadian study using a range of MRI measures. Patients with RRMS treated with
glatiramer acetate in the US trial were significantly more likely to experience improved disability (whereas placebo recipients were more likely to experience worsening disability) and their overall disability status was significantly improved compared with placebo recipients. Data from the active-treatment extension of the US trial suggest that
glatiramer acetate has sustained clinical benefits up to 8 years.
Glatiramer acetate was generally well tolerated; the most commonly reported treatment-related adverse events were localised
injection-site reactions and transient post-injection systemic reactions. Both reactions were generally mild and self limiting but were responsible for the majority of withdrawals from treatment (up to 6.5 and 3.5%, respectively).
Glatiramer acetate is not associated with the
influenza-like syndrome or neutralising
antibodies that are reported in patients treated with
interferon-beta for RRMS. The cost effectiveness of
glatiramer acetate has yet to be definitively determined as assessment of available data is confounded by very different models, data sources and assumptions.
CONCLUSION:
Glatiramer acetate has shown efficacy in well controlled clinical trials in patients with RRMS; it reduces relapse rate and decreases MRI-assessed disease activity and burden. It is generally well tolerated and is not associated with the
influenza-like symptoms and formation of neutralising
antibodies seen with the
interferons-beta. Based on available data and current management guidelines,
glatiramer acetate is a valuable first-line treatment option for patients with RRMS.