Glatiramer acetate (GA) is a synthetic amino acid copolymer that is approved for treatment of relapsing remitting multiple sclerosis (RRMS) and clinically isolated syndrome (CIS).

Groups of CAG140 knock-in and N171-82Q transgenic mice were treated with GA (0.625 mg/mouse) for up to 1 year of age (CAG140 knock-in mice) or 20 weeks (N171-82Q mice). Various behavioral assays were measured over the course of drug treatment whereby GA treatment delayed the onset and reduced the severity of HD behavioral symptoms in both mouse models. The beneficial actions of GA were associated with elevated levels of promoter I- and IV-driven brain-derived neurotrophic factor (Bdnf) expression and reduced levels of cytokines, in particular, interleukins IL4 and IL12, in the brains of HD mice. In addition, the GA-induced effects on BDNF, IL4 and IL12 levels were detected in plasma from drug-treated mice and rats, suggesting utility as a peripheral biomarker of treatment effectiveness. These preclinical studies support the use of GA as a relevant clinical therapy for HD patients[3].

147245-92-9

C25H45N5O13

623.657

glatiramer Acetate

[1]Prod'homme T, Zamvil SS. The Evolving Mechanisms of Action of Glatiramer Acetate. Cold Spring Harb Perspect Med. 2019 Feb 1;9(2):a029249. doi: 10.1101/cshperspect.a029249.[2]Arnon R, et al. Mechanism of action of glatiramer acetate in multiple sclerosis and its potential for the development of new applications. Proc Natl Acad Sci U S A. 2004;101 Suppl 2(Suppl 2):14593-14598.[3]McKeage K. Glatiramer Acetate 40 mg/mL in Relapsing-Remitting Multiple Sclerosis: A Review. CNS Drugs. 2015;29(5):425-432.[4]Corey-Bloom J, et al. Beneficial effects of glatiramer acetate in Huntington's disease mouse models: Evidence for BDNF-elevating and immunomodulatory mechanisms. Brain Res. 2017;1673:102-110.

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