biosynthesizing cannibinoids

[(zonk)]

So something along the lines of the tryptamine thread...
Anandamide is metabolized into 2-aminoethanol and arachidonic acid, these are also starting ingredients in syntheticly made anandamide
p-aminophenol is metabolized into AM-404 (anandamide with a phenyl in place of the ethyl) by the reaction of arachidonic acid under FAAH

So... Could taking aminoethanol be like a prodrug of anandamide? And if so, could potentially stronger anandamide analogs be made by things like aminoethanol analogs like 2-chloroethylamine or 2-aminobutanol?

 

[Hammilton]

Are you sure about p-Aminophenol being metabolized to AM404? I don't think that's accurate. APAP is, but p-Aminophenol isn't the same as APAP. It seems unlikely, because of the acetyl group that's not present in PAP.

anyway, PAP is nephrotoxic, not a viable.

Also, why would 2-AE be a prodrug for anandamide? If AN is metabolized to 2-AE, it seems unlikely that the reverse will occur in any relevant amount. If it did, your body wouldn't have a viable way to remove the AN.

that makes the rest rather unlikely.

And AM404 is entirely devoid of recreational value. Of the anandamide analogues I've tried, they're almost completely without value, and all I got was a headache.

 

[late show wdl]

N-acetyl 2-aminoethanol would be the candidate for an anandamide precursor, I'm betting that for whatever reason it might transesterify (or transamideify I guess) with arachidonic acid to make acetic acid and anandamide. Not certain, since a phenylamine is quite unlike an ethylamine. I do not know why this method is the main metabolism for APAP instead of glucorinidation of the hydroxy.

 

[(zonk)]

APAP is 1st deacetylated then it metabolizes into all the other compounds including am404, I dont believe APAP has any real effect before metabolizing, maybe PAP is metabolized too quickly which is why it's acetylated, I really dont know, I'm just going by what I've read.
Whether or not the phenyl could be replaced with an ethyl and still go through the same metabolic process as PAP/APAP is what I'm totally in the dark about. Whether or not that could go 1 step further and be able to replace the hydroxyl with chloro, who knows. But If these analogs are really without value maybe it's a moot point.

Hey Hamm.. Do you have any trip or should I say non-trip reports about these analogs. What doses, how did you take them. I saw one postive report along time ago for IV anandamide. That report said 2-AG was not active though.

 

[Hammilton]

I've talked about it here, probably as Ham-milton, before my isomerization. Anyway, I administered them IV primarily, dissolved in ethanol which was extremely painful and may account for the headache.

PAP itself is pretty nephrotoxic, which APAP isn't, which is why I'm not sure about it being de-acetylated (and also because at least one paper shows a route different than you describe). Are you absolutely certain about this? I could be definitely be wrong, but the lack of nephrotoxicity is hard to explain.

 

[(zonk)]

yeah, upon more searching i saw the nephrotox stuff, it said PAP is a minor toxic metabolite of APAP. I don't remember what the links were to the data PAP being the primary metabolite and that PAP is the precursor to AM404, and honestly I dont feel like looking for them(got better things todo), But I'm inclined to believe you in this case cause I see the data on PAP toxicity now.

One interesting thing i found was IBUPROFEN has data on being a powerfull blocker of anandamide deaminase and even some data on it being a possible FAAHI, it's probly the deaminase (not sure the difference). Perhaps combining APAP+Ibuprofen might be a usefull endocannibinoid booster.

here... fou nd it in yer thread...

metabolically:
AM404 simply arises due to FAAH removing the acetyl function and replacing it with arachidonic acid.
chemically it is a straight forward synth, especially as arachidonic acid is becoming more readily available commercially.
it is my opinion that only a few of the many potential long chain fatty acid amides have any recreational potential at all. On the whole they smell awful have very poor adme being chewed extremely rapidly by FAAH and other amidases. I would like to see someone prove me wrong

Now that rings a bell, FAAH was necessary to convert APAP to AM404 so taking it while on a FAAHI would be pointless. Maybe the deacetylation+arachidonoylation happen simmultaniously so there's no real formation of PAP

 

[(zonk)]

HAMM
searched could not find anything related to what AEA type compounds you've tried and at what doses/what effects. Could you please atleast give a quick re-rundown for me.
I've read that substitutions at the hydroxy and ethyl positions greatly enhance activity/potency/affinity/stability/resistance to enzymetic degradation
perhaps something like arachidonoyl-chlorobutylamide