[DizzyDean]

Hi, I'm a new poster to this board. Have had RRMS for a long time, its been fairly mild but even with LDN I've had a relapse, first in 4 yrs, but still a relapse. Thinking hard about Copaxone, possibly in addition to LDN. But does Copaxone really work, that is the question.

I am researching this, trying to form an opinion. Teva of course has lots of press releases touting studies which appear to show efficacy of C, but other resources I've consulted aren't so sure.

For example the Cochrane Review did a scathing article in 2004 about efficacy of the ABC's generally, and concluded C's efficacy was the lowest of them all, and in fact so low that it wasn't even recommended for routine use in the article's conclusion.

I guess another thing I wonder about is Teva's recent release of "26 years" of safety and efficacy data. Riddle me this, if the drug has only been on market since 1996 or so (~11 years) and yet Teva has some "26 years" of data on it, why did it take so long to get C to an FDA approved status and on-market???

I gather that there is some fairly interesting story behind the development of C. It is NOT an interferon, it was serendipitiously discovered when a combination of amino acids that were thought might INDUCE EAE in mice actually had the opposite effect on the mice's myelin.

My neuro keeps trying to push me this way, he has indicated its the least "harsh" of the ABCR choices in terms of side effects, and that "it seems to work well for milder forms of MS" at least in his practice, which is what I have.

I've heard different rumblings of whether or not C actually works, and want to get the collective wisdom of the group, many of whom (I assume) have actually taken copaxone at one time or another.

Appreciate any thoughts, again, I am aware of the fact that C hasn't been shown to help progressive MS, only RRMS. I'm just asking "for RRMS, do we really think this stuff works"?