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Copaxone's mechanism of action?
Posted: Mon Jun 08, 2009 9:05 am
by cheerleader
Most copaxone users know about the dreaded heart racing, flushing, blood rushing side effect. Even if you've never had this reaction, you're told to look out for it. Jeff had it once after taking his injection after exercising. Guess what causes it? vasodilation.
Vasodilation is listed as one of the major side effects of Copaxone. Could it be that this side effect is the mechanism of action for this drug? Researchers have told us they don't really know exactly what makes Copaxone effective. Huh....
from the Copaxone website:
The mechanism(s) by which glatiramer acetate exerts its effects in patients with MS are not fully understood. However, glatiramer acetate is thought to act by modifying immune processes that are believed to be responsible for the pathogenesis of MS.
That's alot of unknowns for 2 sentences. not fully understood, thought to act, believed to be...
I think vitamin B12/niacin can give you the same "rush" for alot less.
cheer
Posted: Mon Jun 08, 2009 9:17 am
by notasperfectasyou
This is really impressive. Somewhere I have read, long ago, in a comparision with the INF's, that the INF's were thought to help tighten up the BBB and that Copaxone was thought to sway the Th1 v/s Th2 balance. I recall a diagram with the IFN's showing a more solid BBB and a more free flowing BBB in the Copaxone diagram. Has me wondering if the IFN's are vasoconstricting, I speculate IFN-y is - just guessing. Ken
Re: Copaxone's method of action
Posted: Mon Jun 08, 2009 2:54 pm
by NHE
notasperfectasyou wrote:Copaxone was thought to sway the Th1 v/s Th2 balance.
After I was diagnosed, I did extensive reading of the published literature on the ABC drugs available at the time. To the best of my understanding, Ifn-B is believed to induce a Th1 to Th2 shift. In contrast, if I remember correctly, Copaxone acts through an effect via binding to the MHC.
NHE
Posted: Mon Jun 08, 2009 3:27 pm
by mrhodes40
Copaxone mechanism from
HERE
Glatiramer acetate (GA; copolymer-1, Copaxone) suppresses the induction of experimental autoimmune encephalomyelitis and reduces the relapse frequency in relapsing-remitting multiple sclerosis. Although it has become clear that GA induces protective degenerate Th2/IL-10 responses, its precise mode of action remains elusive. Because the cytokine profile of Th cells is often regulated by dendritic cells (DC), we studied the modulatory effects of GA on the T cell regulatory function of human DC. This study shows the novel selective inhibitory effect of GA on the production of DC-derived inflammatory mediators without affecting DC maturation or DC immunostimulatory potential. DC exposed to GA have an impaired capacity to secrete the major Th1 polarizing factor IL-12p70 in response to LPS and CD40 ligand triggering. DC exposed to GA induce effector IL-4-secreting Th2 cells and enhanced levels of the anti-inflammatory cytokine IL-10. The anti-inflammatory effect of GA is mediated via DC as GA does not affect the polarization patterns of naive Th cells activated in an APC-free system. Together, these results reveal that APC are essential for the GA-mediated shift in the Th cell profiles and indicate that DC are a prime target for the immunomodulatory effects of GA.
Re: Copaxone's mechanism of action?
Posted: Mon Jun 08, 2009 9:24 pm
by NHE
Thanks for posting that paper. It lends support to what I initially wrote. Copaxone binds to the MHC on the antigen presenting cells. Here's another paper, the full version of which is available for free.
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 Oct 5;101 Suppl 2:14593-8.
The mode of action of GA is by initial strong promiscuous binding to MHC molecules and consequent competition with various myelin antigens for their presentation to T cells.
NHE