[Blackfeather]

My neuro has prescribed azilect for me but am wondering why it doesn't seem to get mentioned much on this forum. Is it not very effective, too expensive? Is it prescribed mainly for early stage pwp?

[olsen]

Hello, If you research the topic "Azilect, Rasagaline" on this forum you will uncover numerous postings concerning Azilect, starting with 2007. Since the newest studies disproved its neuroprotective status the drug has fallen out of favor, I think. MAO-B inhibitors have been used in first line therapy for PD for many yrs, with the intention of deceasing the breakdown of dopamine, thus keeping dopamine around for a longer period of time. Selegiline or Eldepryl was first utilized, supplanted by Azilect, which was very expensive (i have no idea its cost now). My husband used it for several years. Did it help? who knows. There are an incredible number of drug interactions which can occur with the MAO-B inhibitors, and these are drugs that are often used, such as the fluroquinolone antibiotics--ie Cipro. There are lists stating which drugs result in interactions with MAO-B inhibitors. I think it more than prudent to keep a listing of those drugs to which one can easily refer.
There was much hope that this drug would be neuroprotective. I am unsure if my husband would take it now that this action has been disproven.

[johnt]

Good question.

I think the relatively low rate of mention in this forum of rasagiline as compared to Sinemet, say, is due to:
- fewer of us are on it, so there's naturally fewer people posting about it;
- it has a limited effect: 1mg has a levodopa equivalent dose of about 100mg, which, although welcome, is a small part of the 1000mg levodopa equivalent daily dose that many of us take;
- its method of working means that its effect is almost constant through the day, so you just don't notice it.

I thought the claim of neuroprotection has not been proven. This is not the same as saying it has been proven not to be neuroprotective. I think we can view the results of the trials as indicating that, at best, there may be a small neuroprotective effect.

It seems to me that if you buy into the theory that changes in dopamine levels due to the drugs we take should be minimized as far as possible then rasagiline has a part, albeit a small part, to play.

John

[soccertese]

in the u.s it can be very expensive, no generic. copays can be as high as $400.00
it only reduces the breakdown of dopamine in the brain so what is there lasts longer. so if someone isn't doing well on it or feels no affect, they just stop taking it rather than struggle to "adapt" to it, neuro's likely aren't going to urge you to just stick with it and see if you get used to it like they might with an agonist and surely with C/L.
the possibility that it could slow progression has likely influenced doctor's decisions to write RX's for it since it has only a small benefit, the study by TEVA to test that wasn't statistically significant but it was "a close call". strangely, those receiving 2mg did worse than those receiving 1mg.

selegiline is similar and when it first came out it was thought to slow progression but was later proven not to. same with agonists when they first came out.

[zanpar321]

Originally Posted by soccertese

in the u.s it can be very expensive, no generic. copays can be as high as $400.00
it only reduces the breakdown of dopamine in the brain so what is there lasts longer. so if someone isn't doing well on it or feels no affect, they just stop taking it rather than struggle to "adapt" to it, neuro's likely aren't going to urge you to just stick with it and see if you get used to it like they might with an agonist and surely with C/L.
the possibility that it could slow progression has likely influenced doctor's decisions to write RX's for it since it has only a small benefit, the study by TEVA to test that wasn't statistically significant but it was "a close call". strangely, those receiving 2mg did worse than those receiving 1mg.

selegiline is similar and when it first came out it was thought to slow progression but was later proven not to. same with agonists when they first came out.

The Israeli drugmaker has asked the Food and Drug Administration to expand approval so that Azilect can be prescribed to slow the underlying disease. Currently no treatments are approved for that use.

But the FDA's panel of outside experts voted 17-0 against recommending approval for that use, saying the company's clinical study results were not convincing.

"I believe the drug shows signs of effectiveness for symptomatic use, for which it is already approved. But the higher bar is whether it does anything for disease modification, and it did not meet that standard," said Dr. Justin Zivin of the University of California, San Diego.

http://www.huffingtonpost.com/2011/1...n_1016612.html

[bigguyclyde]

About 9 years ago my wife and I met a lady who was on the clinical trial for Azilect as a neuroprotective agent She seemed to have no PD symptoms even though she had been diagnosed quite a long time. However one anecdotal case doesn't prove anything. There must have been quite a few people like this woman to convince Teva to give the drug a shot at neuroprotection. It turned out to be a longshot that did not deliver the goods.