What is Copaxone, really?

A board to discuss the Multiple Sclerosis modifying drug Copaxone

What is Copaxone, really?

Postby Johnnymac » Mon May 23, 2011 3:37 pm

When my wife first started taking copaxone in 2006 it was described to us as a 'protective coating' the mimics myellin and protects the damaged nerves from the immune system. Even the Teva website uses language like "COPAXONE is believed to..." which really makes me wonder.

Is there any real scientific evidence somewhere that I'm missing that can explain how this drug works and what it is supposed to be doing?

I'm not a believer in EAE as a model for MS, so that kinda throws most things out for me but Copaxone is so widely used, I would think there must be something I'm missing.


ps. I've given my wife hundreds upon hundreds of shots of this stuff, and continue to do so daily.
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Postby patientx » Mon May 23, 2011 7:37 pm

I'm not sure why someone would describe Copaxone as a "protective coating." As you probably already know, Copaxone is a synthetic polymer of 4 amino acids. Originally, I think it was believed it worked by acting as an MBP analog - that is, a "decoy" for myelin. However, after further research, this is no longer thought to be the case. From Curing MS by Howard Weiner:
Copolymer-I binds to specialized molecules on cells whose function is to then trigger T cells. The cells are called antigen presenting cells and the molecules that copolymer-I binds are called MHC class II molecules. With copolymer-I bound to its surface, the antigen presenting cells trigger human T cells to become cells with anti-inflammatory properties. The T cells then migrate to the brain, where they suppress the brain inflammation that causes MS by releasing anti-inflammatory substances such as IL-10 and TGF-beta. Copolymer-I is not simply an MBP analog, as originally described by Sela and Arnon. Although it may have some cross-reactivity with MBP, it has much broader properties. Human T cells from all individuals can be stimulated by copolymer-I, and after stimulation they shift from Th1 to Th2/Th3 type cells, which act as suppressor or regulatory cells. When they enter the brain, they suppress inflammation via bystander suppression....
Thus, the copolymer designed to cause EAE in mice ultimately worked in MS because of unique interactions with human T cells that weren't known when the molecule was synthesized.


So, copaxone causes a shift to a Th2/3 type (anti-inflammatory) T-cell response. This has been shown in both animals and humans, as in this study:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC377485/

Also, I have seen some studies that copaxone causes the release of brain-derived neurotrophic factor (BDNF), and may offer some level of neuro-protection.
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