Effects of generic glatiramer acetate (BCD-063) on magnetic resonance imaging outcomes in patients with relapsing multiple sclerosis. A randomized double-blind 48 weeks clinical trial

OBJECTIVE: To evaluate whether generic glatiramer acetate (BCD-063) is equivalent to the originator brand glatiramer acetate product (Copaxone®-Teva), as measured by imaging endpoints. DESIGN, SETTING AND PARTICIPANTS: Randomized, multicenter, double-blind, active and placebo-controlled phase 3 trial. Participants were patients with confirmed relapsing-remitting multiple sclerosis (McDonald 2005 criteria) 18 to 55 years old with at least 1 relapse or 1 gadolinium-enhancing MRI lesion in the prior year, with Expanded Disability Status Scale (EDSS) score 0-5.5 and relapse-free > 4 weeks. INTERVENTIONS: Participants were randomized 2:2:1 to receive BCD-063 (20 mg), Copaxone® (20 mg), or placebo by daily subcutaneous injection for 48 weeks. MRI OUTCOMES AND MEASURES: MRI outcomes included the number of combined unique active (CUA) lesions at week 48 as well as other magnetic resonance imaging parameters. RESULTS: 121 participants were included in analysis of MRI outcomes in three groups: BCD-063 (n = 48), Copaxone® (n = 51), or placebo (n = 22). CUA lesions at week 48 were (M±sd) 0.89±1.43 in BCD-063 group, 1.06±1.69 in Copaxone® group, 2.71±3.3 in placebo group. No statistical difference was observed when CUA lesion numbers were compared in BCD-063 and Copaxone® groups (p=0.7189); paired difference test for both groups in comparison with placebo was statistically significant (p=0.0195 for BCD-063, p=0.0346 for Copaxone®). CUA lesions decrease (week 48 vs. week 24) was statistically significant in BCD-063 group, as well as in Copaxone® group (p = 0.000034 and p = 0.002547, respectively), unlike in placebo group, where change in CUA lesion number was non-significant. The number of Gd+ T1 lesions at week 48 decreased in BCD-063 (p = 0.00114) and in Copaxone® (p = 0.00036) groups, but statistically significant dynamics in placebo group was not observed (p=0.21157), which was expected. There were no statistically significant differences between glatiramer acetate groups. The number of new T2 lesions at week 48 did not have significant differences in BCD-063 and Copaxone® groups, with statistically significant differences between the groups of glatiramer acetate and placebo (p = 0.00002 for BCD-063 vs. placebo and p = 0.024 for Copaxone® vs. placebo). CONCLUSIONS AND RELEVANCE: BCD-063 and Copaxone® have equivalent effects on MRI disease activity and similar safety profile in patients with RR-MS.