Latest research on Copaxone

Glatiramer acetate consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000-9,000 daltons. It is an immunomodulator, licensed in much of the world for reduced frequency of relapses in relapsing-remitting multiple sclerosis

Latest findings

Patients with a diagnosis of RRMS were eligible if they had been continuously treated with an approved DMT—interferon (IFN) (Avonex, Betaferon, Extavia, or Rebif) or GA (Copaxone)—for at least 30 days, and if informed consent was given prior to study inclusion. [source, 2016]
Of the twelve PP-MS patients, four were on interferon-β1a (Avonex, Biogen Idec, Cambridge, MA USA), two patients were on interferon-β1a (Rebif, Merck Serono, Rockland, MA, USA), four patients were on interferon-β1a (Betaseron, Bayer HealthCare Pharmaceuticals, Montville, NJ, USA) and two patients were on glatiramer acetate (Copaxone, Teva pharmaceuticals, North Wales, PA, USA). [source, 2015]
Copolymer-1 (Cop-1; also named glatiramer acetate) was therefore applied to treat glaucoma, based on the purposes of protective autoimmunity. [source, 2015]
Application of COP-1 in Lewis rats of chronic high IOP was beneficial to the survival rate of RGCs for 3 weeks. [source, 2015]
Vaccination with COP-1 in SD rats of acute high IOP also provided protection to RGCs over the sites of secondary degeneration, without any autoimmune disorders. [source, 2015]
Ben Simon et al obtained similar results in Lewis rats with chronic ocular hypertension 1 week after vaccination with COP-1.80 Later, Yang et al reported that vaccination with COP-1 in Wistar rats with experimental glaucoma elevated the expression of NT-3 and its cognate receptor, TrkC, in RGCs, RNFL, and IPL. [source, 2015]
Zhou et al demonstrated that vaccination with COP-1 in SD rats of chronic glaucoma showed enhancement of endogenous BDNF expression in retinas, accompanied by suppression of RGC apoptosis. [source, 2015]
These observations may provide several possible underlying molecular mechanisms for the protective autoimmunity offered by COP-1. [source, 2015]
This finding was confirmed by qRT-PCR in primary human monocytes, where CXCL10 was upregulated by Probioglat relative to Copaxone treatment with p value < 0.02 and fold change of 2.1. [source, 2015]
These included IL1RN, which is relevant to Copaxone mechanism of action. [source, 2015]