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The Large and Nifty Not-quite-advanced Drug Chemistry, Pharmacology and More Thread

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How hard is 3-meo-pcp to synth? Does it take some highly skilled individual to do this? Im leaning more towards chinese 'chemists' just plain sucking? :|
 
I don't know if you can just do it the same as 4-MeO-PCP only substitute a certain brominated reagent (let's not get into specific synth discussion, it's not allowed), but I think I heard it's mostly more expensive to make - possibly because of the price of that ingredient.
 
Question: Is there a 'endogenous cannabinoid "releasing agent"'?

I'm not certain how else to state the question. From what I've understand trying to get the answer endocannabinoids aren't stored in vesicles so "releasing" might be incorrect term. Is there any drug that activates biosynthesis of endocannabinoids? Does anyone know if there are any in Cannabis?

If someone can direct me to such compounds(s) or literature discussing this I would appreciate it.
 
. . .nor did you come to make appropriate posts in here. :P
Please give Other Drugs a try, and make sure to run a search before asking your question.

ebola
 
You could inhibit the metabolization of the endogenous cannabinoids (specifically Anandamide) by using a FAAH inhibitor.

N-acylphosphatidylethanolamine (NAPE) or phosphatidylethanolamine will increase the amount of Anandamide synthesized versus using a FAAH inhibitor. Or you could do both.

But there is no such thing as an endocannabinoid releaser. Arachidonic acid is the raw basis of NAPE and it is healthy and is commonly used as a bodybuilding supplement (fatty acid).
 
Again I say "releaser" for lack of a appropriate term. I'm aware of enzymatic way of enhancing concentration but I was hoping for a "biosynth. activating" route.

I guess I'll take that answer then, thank you Slapdragonx.
 
The precursors to Anandamide (and other endogenous cannabinoids) are NAPE (as noted above) and Arachidonic acid - AA. With the precursors you would probably see a mild increase in the amount of endogenous cannabinoids produced within the body.

Unless you are speaking of something that directly stimulate the production of endocannabinoids, in which case I have no clue.
 
Yes I meant telling the brain to produce more not increasing concentration with biological precursors. I was hoping someone would know a direct or indirect (ie. activation/inhibition of non-CB receptor leading to this) method of doing this.
 
Technically you can activate CB1 via the allosteric binding sites and increase the concentration of the endocannabinoids. However at the same time they decrease the activity of the agonists.

Such as 1-(4-chlorophenyl)-3-(3-(6-pyr​rolidin-1-ylpyridin-2-yl)pheny​l)urea (PSNCBAM-1) or SR141716A (Rimonabant).

PSNCBAM-1:
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just for the record, I don't think it's a GABAergic drug, or if it is, that such activity doesn't explain the whole of it.
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Either way, it looks like it (and nevirapine, another reverse transcriptase inhibitor with a 1, 4-diazepine core; not sure if that's of any significance) has had words with some overactive NMDA receptors in a few studies. I thought this was a pretty good read:

http://eprints.ru.ac.za/1350/1/Zheve-MSc-TR08-169.pdf

Not that it's necessarily relevant - it could just as easily be a bunch of placebo-sodden, virus-free South African drug users who take desperation to darkly comical heights. One would think the side effects of megadoses of the RTIs would far outweigh a transient placebo high. I wonder if there's a hangover...

this sounds similar to the tamiflu story I read about a while ago
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Lawl, yeah. That and jenkem.
 
it could just as easily be a bunch of placebo-sodden
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No, it couldn't "just as easily" be placebo effect. I once found a document talking about placebo effect and psychoactive drugs but I can't seem to find it.

People don't become hooked on placebo. Placebo effect is invariably weaker than actual drug effect, and produces substantially different responding. People have passed off fake drugs as real all the time, and at others rumors would go around about how this or that would get you high. People realize they've been sold garbage. For short periods of time kids will start smoking oregano or grass or snort tylenol, but people try it, and realize they've been stupid, and so they never catch on.

this has caught on. So either it's an incredible outlier, or the drugs are active. No matter what though, the odds that this drug is actually not recreational are very, very small.
 
I know this has been posted before (I believe by Vecktor) but I cannot seem to find it, does anyone have a link to a key or guide or journal article of some kind that gives a rough estimate of how to extrapolate human doses from animal data, specifically mice and rats?
 
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