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Re: Anyone still finding benefits from Selegiline ? Craig Allen

Posted by wingedcat on February 16, 2003, at 18:12:46

In reply to Re: Anyone still finding benefits from Selegiline ? wingedcat, posted by Craig Allen on February 15, 2003, at 19:08:38

> hello. i'm thinking about a trial on selegeline, if my doctor will go for it. can you tell me about DL-phenylalanine? i saw that you were augmenting the selegeline with it. i'm not familiar with this item. what is it, what does it do? thanks.

It is the precursor to some neurotransmitters, including phenylethylamine and dopamine. Because selegiline increases the level of these two in the brain (mostly by taking away the enzyme which destroys them), DLpa speeds up the buildup of them. It lets you take a lower dose of selegiline. You should take the DLpa on an empty stomach, and then take the selegiline with food. 5mg a day was enough for me with 400 mg DLpa.

Like I said, it did make me more anxious, that is why I am stopping it now, until I can get on something for the anxiety. BUT... it has helped concentration, get rid of anhedonia(lack of pleasure) and banishing the suicidal thoughts faster and better than Wellbutrin, Paxil, or Buspar did for me. Also, I had faster orgasms while I was on selegiline than any other time in my life!!!

Deprenyl plus L-phenylalanine in the treatment of depression.
Birkmayer W, Riederer P, Linauer W, Knoll J.

The antidepressive efficacy of 1-deprenyl (5-10 mg daily) plus 1-phenylalanine (250 mg/day) has been evaluated in 155 unipolar depressed patients. Both oral and intravenous administration showed beneficial effects in 90% of outpatients and 80.5% of inpatients. It is concluded that this combined treatment has a potent antidepressive action based on the accumulation of 1-phenylethylamine in the brain.

Sustained antidepressant effect of PEA replacement.
Sabelli H, Fink P, Fawcett J, Tom C.
Rush University and the Center for Creative Development, Chicago, Illinois, USA.

Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day, with 10 mg/day selegiline to prevent rapid PEA destruction) were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments. PEA improves mood as rapidly as amphetamine but does not produce tolerance.
History of deprenyl--the first selective inhibitor of monoamine oxidase type B
Knoll J.

(-)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.
Are metabolites of l-deprenyl (selegiline) useful or harmful?
Yasar S, Goldberg JP, Goldberg SR
Department of Anesthesiology
and Critical Care Medicine,
Johns Hopkins University,
Medical School, Baltimore, MD, USA.

A frequent topic of controversy has been whether metabolism of l-deprenyl (selegiline) to active metabolites is a detriment to clinical use. This paper reviews possible roles of the metabolites of l-deprenyl in producing unwanted adverse side effects or in augmenting or mediating its clinically useful actions. Levels of l-amphetamine and l-methamphetamine likely to be reached, even with excessive intake of l-deprenyl, would be unlikely to produce neurotoxicity and there is no preclinical or clinical evidence of abuse liability of l-deprenyl. In contrast, there is evidence that l-amphetamine and l-methamphetamine have some qualitatively different actions than their d-isomer counterparts on EEG and cognitive functioning which might result in beneficial clinical effects and complement beneficial clinical actions of l-deprenyl itself.
Metabolism of deprenyl to amphetamine and methamphetamine may be responsible for deprenyl's therapeutic benefit: a biochemical assessment.
Karoum F, Chuang LW, Eisler T, Calne DB, Liebowitz MR, Quitkin FM, Klein DF, Wyatt RJ.

The urinary excretion of some important phenylethylamines, catecholamines, their metabolites, amphetamine, and methamphetamine were measured in parkinsonian patients on Sinemet (L-dopa plus carbidopa, a peripheral dopadecarboxylase inhibitor) and depressed patients after chronic (-) deprenyl treatment. Deprenyl was efficiently metabolized to amphetamine and methamphetamine. It increased the excretion of phenylethylamine and of m- and p-tyramine, and reduced the output of norepinephrine metabolites, but failed to alter the excretion of dopamine-deaminated metabolites. These changes were attributed more to amphetamine and methamphetamine than to inhibition of monoamine oxidase type B. Sinemet treatment alone increased the excretion of dopamine, 3-methoxytyramine, and their respective deaminated metabolites, 3, 4-dihydroxyphenylacetic acid and homovanillic acid. It is concluded that conversion of deprenyl to amphetamine and methamphetamine may contribute to some of the therapeutic benefits of deprenyl.
Selegiline-Transdermal - Somerset: Emsam.

Adis CommentsSomerset Pharmaceuticals, a 50/50 joint venture between Watson Pharmaceuticals and Mylan Laboratories, is developing a transdermal formulation of the monoamine oxidase type B inhibitor selegiline [Emsam] for the treatment of depression, Alzheimer's disease and Parkinson's disease. Somerset have filed an NDA with the US FDA for the use of the transdermal formulation of selegiline in depression. However, the FDA has deemed the application 'not approvable' and is requesting additional efficacy data. The product is also undergoing phase III development in the US for Alzheimer's disease and Parkinson's disease. However, initial results in Alzheimer's disease have not been promising. Somerset Pharmaceuticals is also investigating the utility of the selegiline transdermal formulation in patients with attention-deficit hyperactivity disorder (ADHD) and has conducted an 8-week fixed-dose study in adolescent patients in the US.
Selegiline transdermal system Somerset.

Mahmood I.

Division of Clinical Trial Design and Analysis, Center for Biologics Evaluation and Research, Food & Drug Administration, MD 20852, USA.

Somerset is developing a selegiline transdermal system (STS) for potential use in the treatment of depression. It has also been developed for Alzheimer's disease (AD), Parkinson's disease and attention-deficit hyperactivity disorder (ADHD) [182121], although no development has been reported for AD or ADHD in recent years. Somerset claims the transdermal system could be more effective than the oral formulation of selegiline already marketed [250573]. In May 2001, Somerset filed an NDA with the US FDA for STS for the treatment of depression [410848], however, in March 2002, the company received a 'non-approvable' letter from the FDA requesting additional efficacy data. At this time, Somerset had scheduled a meeting with the FDA to review and clarify their comments [456735]. Selegiline will be co-promoted in the US by Watson, under the terms of a previous agreement [275389].




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