DX41 Efficacy of Glatiramer Acetate 40-mg Injection Three Times Weekly

Thursday, May 30, 2013
Omar Khan, MD , Neurology, Wayne State University, Detroit, MI
Peter Reckmann, MD, FRCPC , Neurology, University of Erlangen, Bamberg, Germany
Alexey Boyko, MD , Moscow MS Center at RSMU, Moscow, Russia, Moscow, Russia
Krzysztof Selmaj, MD, PhD , Medical University of Lodz, Lodz, Poland, Lodz, Poland
Robert Zvadinov, MD, PhD , Neurology, SUNY Buffalo, Buffalo, NY


Background: The 20-mg/day regimen for glatiramer acetate (GA) reduces relapse frequency and delays disability progression in patients with RRMS. The Glatiramer Acetate Low Frequency Administration (GALA) study was conducted to investigate the efficacy and safety of GA 40-mg subcutaneous injection, administered 3 times weekly (t.i.w.).

Objectives: To assess the efficacy and safety of 40-mg GA administered t.i.w. in patients with relapsing-remitting multiple sclerosis (RRMS).

Methods: RRMS patients (= 1404) were randomized in a 2:1 ratio to receive GA (= 943) 40mg t.i.w. s.c. injection or matched placebo (= 461) for 12 months. Neurological examinations occurred at screening, baseline, 1, 3, 6, 9, and 12 months or early discontinuation. MRI scans were obtained at baseline and months 6 and 12. Study endpoints included annualized relapse rate (ARR) and MRI markers of disease pathology.

Results: Compared with placebo, treatment with GA 40mg t.i.w. led to a 34.4% reduction (P < .001) in annualized relapse rate (ARR). At 12 months, the cumulative number of new or enlarging T2 lesions (34.7% reduction, < .001) and gadolinium-enhancing (GdE) lesions (44.8% reduction, < .001) were significantly lower in GA patients. Post-hoc assessments indicated that a greater proportion of patients receiving GA were disease free (no relapses, GdE or T2 lesions, or progression on Expanded Disability Status Scale [EDSS] at months 6 or 12) relative to placebo (GA 23.3%, placebo 15.2%, < .001). A greater proportion of patients in the GA 40mg t.i.w. group were also free of MRI disease activity (no GdE or T2 lesions at months 6 and 12; GA 29.8%, placebo 21.5%, = .001) and clinical disease activity (no relapses, no EDSS progression; GA 74.7%, placebo 63.9%, < .001).

Conclusions: Glatiramer acetate at 40mg t.i.w. significantly reduced the ARR as well as the cumulative number of new/enlarging T2 and GdE lesions. It also significantly increased the proportion of patients free of disease markers. At a dose of 40 mg t.i.w., GA may provide an alternative therapeutic option of a higher dose of GA at a reduced injection frequency.