Author Topic: (-)( -) Pseudo, Selegiline, and YOU  (Read 9424 times)

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dwarfer

  • Guest
and the plague spreads across the land...
« Reply #20 on: May 12, 2004, 10:39:00 PM »
Some of my very bestest friends apparently have encountered this plague of double negativity: and unlike the usual minusX minus =+, this sux.

I believe that the Necromancers may back off some of their more noxious amendments, in favor of this apparently dead end route.

Thus do I project with perfect foresight, that Birchers may
be testing the strong alkaline nature of Na in -OH in the near future, just to counter-fuck the fuckers.

Of course talking about it will be counterproductive, as the appearance here of success stories rapidly conditions
the response of the fuckers.  Thus do I also predicet that the healthy and widespread use of non-public thread webbed information distribution may be appropriate.

Those familiar with DCM know what I am referring to..

==========

Meanwhile, a "better read" on Selegiline..

History of deprenyl -
the first selective inhibitor
of monoamine oxidase type B
ABSTRACT
(-)Deprenyl (Selegiline, Jumex, Eldepryl, Movergan), a close structural relative of phenylethylamine (PEA), is a drug with a unique pharmacological spectrum. Whereas PEA and its long-lasting variants, the amphetamines, are mixed-acting stimulants of the sympathetic system in the brain, they primarily enhance the impulse propagation generated release of catecholamines (catecholamine activity enhancer, CAE, effect) and displace catecholamines in higher concentration (catecholamine releasing effect). (-)Deprenyl is the first CAE substance in clinical use devoid of catecholamine releasing activity. (-)Deprenyl is a highly potent and selective, irreversible inhibitor of B-type monoamine oxidase (MAO), a predominantly glial enzyme in the brain. The activity of this enzyme significantly increases with age.

(-)Deprenyl, the first selective inhibitor of MAO-B described in the literature, has become a universally used research tool for selectively blocking B-type MAO and is still the only selective MAO-B inhibitor in world wide clinical use. In contrast to MAO inhibitors which strongly potentiate the catecholamine releasing effect of tyramine, (-)deprenyl inhibits it and is free of the 'cheese effect', which makes it a safe drug. Because its lack of the catecholamine releasing activity (-)deprenyl is devoid of amphetamine like dependence capacity. Maintenance on (-)deprenyl selectively enhances superoxide dismutase (SOD) and catalase activity in the striatum and protects the nigrostriatal dopaminergic neurons from selective neurotoxins (6-hydroxydopamine, MPTP, DSP-4).

Maintenance of an animal on (-)deprenyl prevents the characteristic age-related morphological changes in the neuromelanin granules of the neurocytes in the substantia nigra. Many other protective effects of (-)deprenyl, denoted as 'neuroprotective', 'trophiclike neurorescue', 'apoptosis reducing', etc, have been described. All the protective actions of (-)deprenyl are thought to be primarily related to the CAE effect of the drug. All in all, (-)deprenyl increases the activity of the nigrostriatal dopaminergic system and slows its age-related decline.

Maintenance of male rats (SQUEEEK) on (-)deprenyl delays the age-related loss of their capacity to ejaculate, slows the age-related decline of their learning capacity and prolongs their life.

Parkinsonian patients on levodopa plus (-)deprenyl (10 mg daily) live significantly longer than those on levodopa alone. Parkinsonian patients maintained, after diagnosis, on (-)deprenyl, need levodopa significantly later than their placebo-treated peers. Maintenance on (-)deprenyl significantly improves the performance of patients with Alzheimer's disease. It is concluded that patients developing Parkinson's or Alzheimer's disease need to be treated daily with 10 mg (-)deprenyl from diagnosis until death, irrespective of other medication. Because of the peculiar pharmacological spectrum and safety of the drug it may be advisable to combat the age-related decline of the nigrostriatal dopaminergic neurons in man by taking 10-15 mg (-)deprenyl weekly during the postdevelopmental phase of life. Prophylactic (-)deprenyl medication may improve the quality of life in the latter decades, delaying the time of natural death and decreasing the susceptibility to age-related neurological diseases.


Red_Crown

  • Guest
FDA
« Reply #21 on: May 22, 2004, 01:52:00 AM »
Where does FDA approval fall into all of this, before or after patenting?   I imagine after..

What the fuck though? For all of these years the other enantiomer of pseudo was the only one that was supposed to work. How do they get off with this new formulation? And mustn't it be tested and proven for safety and efficacy by others first? 

Also, if the patent is held by one company, is it reasonable to assume that other producers are not utilizing the method?

wareami

  • Guest
Saving Grace...
« Reply #22 on: May 22, 2004, 03:09:00 AM »

Also, if the patent is held by one company, is it reasonable to assume that other producers are not utilizing the method?



This may be the only saving grace in all this, but if (-)-pseudo's introduction is seen as a way of limiting the conversion of the product at the consumer level, it's well within the jurisdiction of the FDA to mandate it's inclusion at the manufacturer level and force all pfed makers into compliance.
I still don't see any documentation anywhere that points to what forces formulation changes across the board on all strengths, makes and models!
These gaaks are non-existant one day and a week later...BANG....everything sux!
Yeah....there's more to it than what is being disclosed to consumers!




Red_Crown

  • Guest
We are stereoselective
« Reply #23 on: May 22, 2004, 04:46:00 AM »
Our receptors are stereoselective, and if both forms work, there still must be a difference in the dose response and often certain side-effects.. Just switching from (+) to (-) would suggest a few possibilities:
1) This particular chiral center is not what is bound by the receptor, or is not 'that important' in the binding..
2) They've also secretly increased the dose of (-) to compensate.

edit: Well, not necessarily "increased" the dose, but at least changed it a little to compensate for the differences in effectiveness.


Red_Crown

  • Guest
The LWR in all this..
« Reply #24 on: May 22, 2004, 03:12:00 PM »