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Deprenyl drug testing.

drug testing deprenyl

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9 replies to this topic

#1 Reformed-Redan

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Posted 15 July 2013 - 09:31 PM


I'm wondering if anyone would like to find out at what amount does Deprenyl taken sublingually or swallowed trigger a false positive drug test. Would anyone be willing to procure a commercailly available drug test kit and see this? Do law enforcement officials use urine analysis or take actual samples of blood on the road?

If anyone can calculate the amount of methamphetamine metabolites, per units cubed, produced by say 1.5/5/10 mg of deprenyl taken orally (swallowed) and then see how accurate a typical drug test kit used by law enforcement officials is that should suffice too.
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#2 protoject

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Posted 15 July 2013 - 11:41 PM

I had the same question... was hoping i could get away with 1mg without any issues

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#3 NeuroNootropic

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Posted 16 July 2013 - 01:37 AM

The methamphetamine metabolite of Selegiline is L-Methamphetamine, which is not the same as D-Methamphetamine. It is also the main ingredient in Vick's Inhaler, something available OTC. You could just say that you used the Inhaler if your drug test was positive.

Also, doesn't sublingual Selegiline bypass liver metabolism? If so, you shouldn't have a problem with drug tests.

#4 Reformed-Redan

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Posted 16 July 2013 - 03:56 AM

The methamphetamine metabolite of Selegiline is L-Methamphetamine, which is not the same as D-Methamphetamine. It is also the main ingredient in Vick's Inhaler, something available OTC. You could just say that you used the Inhaler if your drug test was positive.

Also, doesn't sublingual Selegiline bypass liver metabolism? If so, you shouldn't have a problem with drug tests.

Not sure, about that. Don't think it would be difficult to check and see if deprenyl triggers a false positive.

#5 brainslugged

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Posted 16 July 2013 - 04:08 AM

Rasagiline could be an alternative.

But as long as you list it on a test as a med you are taking, I think it is okay.

They can test to see if it is l-meth or d-meth, and d-meth is the primary one used recreationally (most recreational meth doesn't even have any levo, I think). That combined with the fact that it is going to be in very low concentrations, I doubt you would get in trouble. It would be easy to prove that you aren't smoking meth theoretically.

The only exception I could see is if you get fired on the spot or there is some sort of zero tolerance thing and they don't even let you appeal.

But that is suing grounds, methinks.

#6 Reformed-Redan

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Posted 16 July 2013 - 04:12 AM

If I list it wouldn't they ask to see a prescription given from a doctor for it?

I'd still like to know for my personal knowledge if it shows up at 1.5mg sub-lingual or swallowed (sometimes I don't have the time to hold it under my tongue for 15min.)

#7 Reformed-Redan

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Posted 16 July 2013 - 04:17 AM

Forgot to mention that Rasagiline doesn't have the pro-longevity effects of deprenyl.

#8 Reformed-Redan

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Posted 16 July 2013 - 04:22 AM

I would be willing to purchase the most popular commercially available drug tests and do a comprehensive test on deprenyl (1/1.5/5/10mg) sublingual and swallowed. Then take a urine sample during peak plasma 3 intervals -30 min from peak plasma 0 min during peak plasma and +30min after peak plasma. Any thoughts?
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#9 LexLux

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Posted 23 February 2014 - 11:59 AM

Forgot to mention that Rasagiline doesn't have the pro-longevity effects of deprenyl.


where did you find that???

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#10 LexLux

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Posted 23 February 2014 - 02:45 PM

Plus I am pretty sure that this study contradicts what you said:

http://www.ncbi.nlm....pubmed/23739004
Revelation in the neuroprotective functions of rasagiline and selegiline: the induction of distinct genes by different mechanisms.


Abstract


In Parkinson's disease, cell death of dopamine neurons in the substantia nigra progresses and neuroprotective therapy is required to halt neuronal loss. In cellular and animal models, selegiline [(-)deprenyl] and rasagiline, inhibitors of type B monoamine oxidase (MAO)-B, protect neuronal cells from programmed cell death. In this paper, the authors review their recent results on the molecular mechanisms by which MAO inhibitors prevent the cell death through the induction of antiapoptotic, prosurvival genes. MAO-A mediates the induction of antiapoptotic bcl-2 and mao-a itself by rasagiline, whereas a different mechanism is associated with selegiline. Rasagiline and selegiline preferentially increase GDNF and BDNF in nonhuman primates and Parkinsonian patients, respectively. Enhanced neurotrophic factors might be applicable to monitor the neurorescuing activity of neuroprotection.
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