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

Copaxone indications

As well as the injectable therapies that have a long history of use as first-line treatments (Betaseron, Rebif, Avonex, Copaxone, Extavia––‘BRACE’), several intravenous or oral therapy options have become available in recent years: natalizumab (Tysabri®; Biogen Idec, initially 2004, then 2006 following temporary withdrawal for safety review); alemtuzumab [Lemtrada®; Sanofi, 2013––European Union (EU) only]; fingolimod (Gilenya®; Novartis, 2010––different indications in the USA and the EU); teriflunomide (Aubagio®; Sanofi, 2012), and dimethyl fumarate (DMF; Tecfidera®; Biogen Idec, 2013) [14]. [source, 2014]
Subcutaneous immunization with COP-1 has pleiotropic properties, among them are: i) an inhibitory effect on monocyte reactivity limiting their production of tumor necrosis factor α (TNFα) and interleukin-12 (IL-12), and increasing IL-10 and transforming growth factor β (TGFβ); ii) activation of Th2/3 and regulatory T cells (Treg); iii) COP-1-specific Th2/3 cells cross the blood-brain barrier and secrete neurotrophins and anti-inflammatory cytokines; iv) elevated proliferation of neural precursor cells (NPC), proliferation and recruitment into the injury site [13]. [source, 2015]
However, two separate studies have suggested that GA (Copaxone) is ineffective in treating murine models of MCAo [14,15]. [source, 2015]
The aim of this study was to evaluate the effect of COP-1 on neurogenesis and neurological recovery during the acute phase (7 days) and the chronic phase of stroke (60 days) in a rat model of tMCAo. [source, 2015]
The exact effect of in vivo COP-1 immunization on neurotrophin production should be further clarified. [source, 2015]
The present study corroborated the beneficial effect COP-1 after tMCAo by demonstrating that it significantly improves neurological deficit 60 days after. [source, 2015]
It is important to mention that we had previously demonstrated the beneficial effect of COP-1 on the outcome of infarct volume [4]. [source, 2015]
All the aforementioned data strongly suggests the beneficial effects of COP-1 in the treatment of acute ischemic stroke but larger multi-center confirmatory preclinical studies are required. [source, 2015]
Poittevin et al. also had a follow-up period of 7 days, which according to our present study is not enough to truly appreciate the beneficial effects of COP-1 treatment. [source, 2015]
Copaxone produced a dose-dependent increase in IL-4 release from these Th2-polarized T cells (Fig 2B); a similar dose effect was seen with the other cytokines (data not shown). [source, 2015]