Contributions
Abstract: P617
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
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 (р = 0,000034 and р = 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 (р = 0,00114) and in Copaxon®
(р = 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.
Trial registration:
Russia 346 06/10/13
Ukraine 151/KD 02/07/14
Disclosure: This study was sponsored by JSC Biocad.
Abstract: P617
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
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 (р = 0,000034 and р = 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 (р = 0,00114) and in Copaxon®
(р = 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.
Trial registration:
Russia 346 06/10/13
Ukraine 151/KD 02/07/14
Disclosure: This study was sponsored by JSC Biocad.