Copaxone, why is is not so effective?

C
I think Glatiramer acetate (at the population level) is a low efficacy treatment.

What supports this?
Besides the clinical efficacy we have this

Pavelek Z, Vyšata O, Sobíšek L, Klímová B, Andrýs C, Vokurková D, Mazurová R, Štourač P, Vališ M. Lymphocyte populations and their change during five-year glatiramer acetate treatment. Neurol Neurochir Pol. 2018 Aug 18. pii: S0028-3843(18)30179-8. doi: 10.1016/j.pjnns.2018.08.001. [Epub ahead of print]

BACKGROUND:The goal of this study was to determine the characteristics that are affected in patients treated with glatiramer acetate (GA).
METHODS:A total of 113 patients were included in this study. Patients were treated with glatiramer acetate (subcutaneous injection, 20 mg, each day). Peripheral blood samples were obtained just prior to treatment as well as 5 years after GA treatment. All the calculations were performed with the statistical system R (r-project.org).
RESULTS: After 5 years of treatment, a significant decrease was found in the absolute and relative CD3+/CD69+ counts, the absolute and relative CD69 counts, the relative CD8+/CD38+ count and the relative CD38 count. A significant increase was found in the absolute and relative CD5+/CD45RA+ counts and the absolute CD5+/CD45RO+ count after 5 years of treatment.
CONCLUSION: This study presents some parameters that were affected by long-term GA treatment.

In this study there was reduced activated (CD69+ or CD38+) T cells (CD3+) and CD8 T cells 5 years after the beginning of treatment. There was an increase in CD5 cells. CD5 has been associated with regulator cells, but perhaps the fact that an influence on memory B cells was not even examined seems to say it all.

However, the  fact that the people were treated for 5 years suggests that it was working for the people within the study, or perhaps the people were destined to have a mild disease course.

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