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1'-Oxoelemicin-PEA Trip Reports

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#41 [url]

Apr 20 10 1:25 AM

I don't think the human body can break piperidines down to diethylamines.

No diethylamine metabolite of PCP is known.

PCP, is a psychoactive piperidine, which has a metabolite called 5-(N-(1'-phenylcyclohexyl)amino)pentanoic acid. In this metabolite the piperidine ring is broken down into a long chain. The tail is then oxidized. See here:

Let's assume for a second that the piperidine metabolites are not active. This doesn't fit our tests results in which supplying piperidine rich sources like black pepper tea, or a few days of L-lysine supplementation, boosts the effects of allylbenzenes.

Rather than being prodrugs, maybe the piperidine metabolites are acting as inhibitors of some enzyme or other process that's inactivating the dimethylamine metabolites?

The facts are that we don't know which alkaloids are active. We known dimethylamines, piperidines, and pyrrolidines are found in animal urine after allylbenzene ingestion. But that doesn't mean these are active. Something else could be active. Something that's being completely destroyed before reaching the urine.

When fully activated these allylbenzens resemble the effects of mescaline, LSD, etc., so closely that they must be interacting with 5HT2A sites. These sites should require nitrogen atoms in order to be affected in a psychedelic way. All the main popular active psychedelics are either diethylamines (LSD), phenylethylamines (mescaline), dimethylamines (psilicin, DMT,etc.), or amphetamines (DOB). None of these are piperidines or pyrrolidines.

Note that DMT has the nitrogen position on the 3 carbon position of the BENZENE RING's carbon tail (other stuff is attached to the tail making a pyrrolidine section on the 1 position of the benzene ring's carbon tail). This configuration with the nitrogen tail piece attached to the 3 position of the benzene ring's carbon tail is like that of the dimethylamine metabolites found by Oswald. We know many of these kinds of DMT analogs are psychedelic.

LSD also has the nitrogen attached to the 3 position of the benzene ring's carbon tail in the same way as psilocin, but the tail also has a bunch of other things attached to it so it's no longer a tail. At that nitrogen position, it's a dimethylamine, but it's got things attached to one methyl side of the dimethylamine group, making it no longer classified as a dimethylamine. In essence, LSD completely contains DMT.

But if you look at LSD from a phenylethylamine point of view, instead of the indole point of view, you can see that the nitrogen is also attached at the 2 carbon position of the tail like it is with mescaline. In essence, LSD also completely contains dimethylphenylethylamine.

Mescaline has the nitrogen attached to the 2 carbon position of the benzene ring's carbon tail.

DOB has the nitrogen attached to the 2 carbon position of the benzene ring's carbon tail.

The 1'-oxo metabolites in their dimethylamine form are chemically more like DMT than mescaline or the others. If you took the pyrrolidine section off of the indole group of 6-methoxy-DMT and replaced it with a keto group, you would have 1'-oxoestragole-DMA, which is the dimethylamine metabolite of methyl chavicol.

Maybe only the dimethylamine metabolites are active, but the piperidine metabolites are somehow protecting them and this is fooling us?

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#42 [url]

Apr 20 10 1:53 AM

Here's methyl chavicol's dimethylamine metabolite also known as 1'-oxoestragole-DMA:

Here's 6-methoxy-DMT:

See how similar they are from the benzene ring down? If you simply remove the piperidine section on the tail of 6-methoxy-DMT and replace it with a keto group (C=O), then you have methyl chavicol's dimethylamine metabolite 1'-oxoestragole-DMA shown at the top.

6-methoxy-DMT is found here on PubChem:

What enzymes attack 6-methoxy-DMT? Does MAO-A and MAO-B attack it? DO BOTH?

6-methoxy-DMT is said to be inactive as a psychedelic, but I don't think anyone ever used it with both MAO-A and MAO-B inhibitors. 6-methoxy-DMT is proven to have binding affinity towards 5HT receptors in vitro and might be psychedelic if it's protected from MAO-A and MAO-B. If it is then this is very strong evidence that 1'-oxoestragole-DMA could be THE psychedelic metabolite if it is protected properly. The piperidine metabolite of methyl chavicol might just be protecting it from MAO or some other enzyme.

We might need to inhibit both MAO-A and MAO-B to get 1'-oxoestragole-DMA working in everyone. I think no one has tried inhibiting both have they?

Note that I have LOW LEVELS OF MAO-A in my body. I know this is a fact because very small doses of harmaline work in me to completely inhibit MAO-A, doses which don't work in most people. This is probably why I generally respond to lower doses of most psychedelics than the average person. This might be partially why allylbenzenes work better in me than in most other people. I want to look into this further.

Perhaps we need to add both MAO-A and MAO-B inhibitors to our latest Oilahuasca Activation mix, and also a good source of dimethylamine, and skip the piperidine? I recall that the piperidine metabolites did show MAO inhibition properties, if I remember corrects. I'll have to confirm that.

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#43 [url]

Apr 20 10 2:42 PM

Lammas, you never got any allylbenzene oils to work before even a little bit. Is that right?


That's right. My last test also was a failure. I'm thinking maybe I have a trouble absorbing the oils - I was still having basil burps like 6-7 hours later. I dissolved the oil in a small cup of whole milk.

But I have to say, I have gotten wonderful effects from whole nutmeg. I started experimenting with whole nutmeg (without any inhibitors) about a year ago and found that low dose (0.25-0.5 nuts) was a wonderful anti-depressant and mood lifter without any side effects. Higher doses (0,75-1 nuts) gave me very nice and long-lasting euphoria with minor side effects. Since the effects were so good, I kind of became addicted to it. I used it daily for about 6 months.

Now, when I eat whole nutmeg, all I get is sedation and/or anxiety. Maybe the problem is in the inhibitors (I have been using various inhibitors every time).

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#44 [url]

Apr 20 10 5:00 PM

There is no piperidine-type metabolite or look alike with 5-HT2A agonist properties. In fact I didn't found any 5-HT2A agonists with a piperidine. Best look-alikes are in fact antagonists of that receptor:

Butyrophenone - in this class there are such beauties of antipsychotic scene as haloperidol, most have added a fluorine atom on a para-position on the benzene, and something behind the piperidine, but the core is the same - it's not butyrophenone alone, it's a butyrophenone with attached piperidine on the nitrogen atom.
Melperone - best look-alike.

Muscle relaxants - Tolperisone, and Eperisone.

Illepcimide - anticonvulsant with seretonergic activity.

Ampakine drug - CX-546.

First antihistamine - Piperoxan.

Local anesthetic - Piperocaine.

Big group of opioids - Phenoperidine, PEPAP, Oxpheneridine, and Betahydroxyfentanyl. Fentanyl, and it's analogues are also here, though they don't have this beta-hydroxy group. Those opioids mostly have something attached back to the piperidine, so they probably don't reflect action of piperidine-type metabolites at all.

Anticholinergics - Cycrimine, Biperiden, and Trihexyphenidyl. Last one also binds to dopamine receptors. Maybe hydroxy-allylbenzenes sometimes bind piperidine, and this reflects anticholinergic-like symptoms of nutmeg poisoning? Maybe they mostly got a peripheral action, and that's why they don't cause hallucinations, and delirium?

Sigma receptor antagonist - AC927, and sigma-1-receptor agonist 4-PPBP. So far the most simple.

Maybe piperidine metabolites have low antiserotoninergic activity, but they inhibit MAO greatly so the overall effect is a potentiation of action. In the phenethylamine adduct test, I thought that the MAO-B inhibition which was for phenethylamine, was actually stopping breakout of all of the allybenzene-amine metabolites, that is why it was potentiating the effects. Maybe using MAO-B inhibitor without phenethylamine would clear this out.

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#45 [url]

Apr 20 10 5:59 PM


i have gotten this working with MC-PEA-piperidine metabolite many times in the past, not specifically with the new inhibitor set up, but when members were describing their oxoelemicin-PEA experiences i was getting flashbacks to the times i had been using PEA with MC together because of the similarity of the type of sensations they were describing to what i had felt many times.

i would really like to see you guys cycle one of these new amines in low dose (one of the short lasting ones) i find when i cycle these types of compounds the waves it gives and the extended duration and sensitivity give me profound insights into the nature of the uniqueness of the experience i am taking part in especially individually and also in relation to all other experiences, it greatly helps to map the puzzle of what receptors and systems each compound activates.

i am surprised you guys did not look at this the other angle yet, what if these are not directly effecting 5HT sites but what if instead the systems that synergize in the body with 5HT activation are being super enhanced by things like MC causing your endogenous 5HT activation to become a full on psychdealic trip, this is a very likely possibility. the experiences ive had on allylbenznes have felt so organic sometimes and somehow natural in a way more familiar to my body, its probably becsae we have been ingesting these amines in small amounts our whole life randomly from time to time in food and our body is more receptive to their interactions with us.

ibogaine may be a good candidate for CYP2D6 inhibition i think the only other major enzymatic alteration to ibogaine is done by CYP3A4.

i am fairly sure it will act as a competitive inhibitor, but at least now i have something that i KNOW should inhibit CYP2D6 without ingesting alcohol that my goldenseal extract is in combined with echinacea.

i find ibogaine more baseline and sober and meditative than alcohol or echinacea so i think this will give me a clearer idea if i am inhibiting CYP2D6 properly because i am pretty familiar with iboga now and can distinguish how it alters things fairly well.

also what are valerians actions? as far as alcohol like effects i mean? i want to take antagonists for the receptors it agonizes to attempt to suppress the GABA effects, trying to get cleaner experiences with allylbenzenes

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#46 [url]

Apr 20 10 10:25 PM

Has anyone else tried using acetaminophen who's gotten some effects from allylbenzenes before?


Acetaminophen doesn't interfere with allylbenzenes psychoactive effects. The first time I had OEV's on nutmeg was when I ate around 2 or 3 large nuts. I had been taking the maximum daily dose of acetaminophen for several days for a head cold, and I also chewed the end of cinnamon stick after dosing the nutmeg, and drank soda (possibly diet I can't remember) during the onset. I tripped pretty hard but I had a TWO DAY 'hangover' instead of one. At the time I attributed this to the fact that I slept through most of my trip and therefore didn't stay hydrated, but I imagine very low glutathione levels also contributed - alongside the fact that I had ingested a large amount of trimyristin, of course.

I haven't been able to replicate the same effects since with whole nutmeg and I imagine thats because I had so effectively knocked out my glutathinone. I don't think acetaminophen would prevent allylbenzenes from working at all, just be careful with how much you take.

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#47 [url]

Apr 25 10 9:49 AM

I did this 1'-oxoelemicin-PEA today. It totally blew me away. The euphoria was unbelievable! This blows away PEA. It is so smooth. There's no way I can say in words how amazing it was. It lasted all day. I did it first thing in the morning. I still feel it now.

How is it possible to feel so much euphoria for so long? How come my body isn't crashing from it? How does this work?

I feel like my whole body and mind is flooded with euphoria and there's no end in sight.

This is so different from PEA and elemicin. I never had anything like this before. I didn't know it was possible to feel this much euphoria without crashing.

I would like to see a thorough scientific investigation into how exactly this works. I feel like I'm peaking on PEA by 10x constantly the whole day long. There's no crash. There's no end to the peak.

This is so amazing. How many people have tried this? Does it work in everyone or is it like all the other allylbenzene tests which only work in some people?

Between the eyes and ears there lie The sounds of colour and the light of a sigh

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#48 [url]

Apr 25 10 1:05 PM

How is it possible to feel so much euphoria for so long? How come my body isn't crashing from it? How does this work?


I think someone mentioned it before on here, but it seems to me that the body is unable to metabolise 1'-oxoelemicin-PEA, or at least breaks it down very slowly. My best guess is that the PEA half of the molecule produces euphoria the same way regular PEA does, but because the body can't metabolise the compound very well the 1'-oxoelemicin-PEA is causing euphoria until it's all excreted out of the body. This, in my head, makes sense as to why the euphoria lasts so long and slowly, slowly drops off.
Not to mention that the elemicin side of the molecule will also produce some euphoria via it's own mechanism.

I want to know what Toastus makes of this.

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#49 [url]

Apr 25 10 8:44 PM

I have used PEA many times. Sometimes it causes very strong euphoria after about 45-60 minutes. The euphoria lasts 5-15 minutes and then fades pretty fast. With all the MAO-B inhibitors I tried the euphoria still doesn't last long. They make PEA stronger. But they don't extend the euphoria all that much. The euphoria isn't as strong as this 1'-oxoelemicin-PEA combo. It's a little different too.

I understand how adding 1'-oxoelemicin to the end of the PEA molecule could make it resistant to MAO and SSAO. What I don't understand is how come my body doesn't get tolerant to the euphoria. If I take PEA over and over with MAO-B inhibitors, it starts to no longer work, ie., the second dose is weaker than the first, the third is weaker than the second, etc. I get tolerance to PEA. Doesn't that happen to most people?

Between the eyes and ears there lie The sounds of colour and the light of a sigh

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#50 [url]

Apr 25 10 9:16 PM

Did we stumble upon a potent Mu-opioid receptor agonist without the typical withdrawal symptoms? I wonder if maybe 1'-oxoelemicin-PEA is a Mu-opioid receptor agonist?

Look at this:

That's PEA-PEA (aka diphenethylamine). It's a two headed PEA molecule.

Most of the double headed PEAs I looked at are active at dopamine and opioid receptors.

A derivative of PEA-PEA is a highly potent and selective κ-opioid receptor agonist. See here:

These similar compounds are D2 agonists and kappa-opioid receptor antagonists:

PubMed article on them:

Look at this:

That last link is a report titled "Morphine-Like Properties of Diphenylethylamine and Related Compounds". It talks about diphenylethylamine and several analogs with morphine-like action. It says β-hydroxy-αβ-diphenylethylamine gave complete relief from pain in doses of 200-400 mg. I can't find the exact structure of this. I think it's similar to NN-dimethyl-1,2-diphenylethylamine (see below).

This is very interesting:

"The R(-) isomer and (-) spa, NN-dimethyl-1, 2-diphenylethylamine, had mu-agonist like character."

That's from:

Here's the molecule they're talking about:

It's a little different from the others, but not by much.

The pattern here is that all of these have opiod action and everyone is talking about super amazing orgasm-like euphoria.

(Sorry I had to post twice. The SPAM filter got my first post.)

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#51 [url]

Apr 27 10 8:25 PM

Did we stumble upon a potent Mu-opioid receptor agonist without the typical withdrawal symptoms? I wonder if maybe 1'-oxoelemicin-PEA is a Mu-opioid receptor agonist?


The pattern here is that all of these have opiod action and everyone is talking about super amazing orgasm-like euphoria.


I don't think so. I don't get euphoria from Mu-opioid receptor agonists at all. I have tried many of them. Not everyone gets euphoria from them, despite what you read on-line. I know of several people that get no euphoria form even heroin. That's one reason why not every gets addicted to heroin. I get very strong euphria from this mix.

Phenylethylamine is partially responsible for the euphoria you get during orgasm. That's the reason people are describing orgasm-like euphoria. 

Elemicin itself causes euphoria when properly activated. It's a different type of euphoria from phenylethylamine. It's more of an excitement oriented euphoria.

I think the reason for the greatly increased euphoria is that both ends of this molecule are activating different euphoria producing sites simultaneously. This makes the euphoria effect more believable to the body. Normally euphoria is not just phenylethylamine being released. Its a whole bunch of different chemicals acting in symphony to produce euphoria.

The other thing is that normally phenylethylamine can't produce much euphoria because of rapid metabolism by MAO-B, MAO-A, and SSAO. Phenylethylamine, when attached to 1'-oxoelemicin, is probably nearly indestructible. So levels of phenylethylamine don't have a sharp peak as they normally would. This lack of a sharp peak will signal to the body that orgasm is still in effect, I believe, and that's what leads to the greatly extended euphoria from the phenylethylamine.

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#52 [url]

Apr 27 10 10:30 PM

GBL produces strong orgasm-like euphoria, morphine actually reduces this kind of euphoria. Morphine, and other opioids don't produce true euphoria, it's rather something like satisfaction, fullness, and bliss. It can actually induce greater euphoria when you've done something good or great moment before you have taken opiates, or during their effects.

So without dopamine, and satisfaction from it, morphine is rather a pretty dull euphoric. When using it as speedball effects are greatly enhanced though, I don't know this because I didn't take any stimulants (with or without), excluding caffeine, and tryptamines, which don't induce the right dopamine systems, it's only based on some observations.

Opiates alone are taken by people to reduce "Weltschmerz" feeling, as an escape from cruel reality into the world of blissful illusion, people with chronic depression, anxiety, and dysthymia, as an addition to psychedelics to prevent badtrips, and to further divert attention of the mind from the world. If used that way they can really lead to a complete addiction.

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#53 [url]

Jul 31 10 12:41 PM

Just food for thought. Im stil in the research phase and hav eyet to experience the bliss you discribe but feel a need to contribute to the vast weath of knowledge already accumulated

Ppl say synephrine gives psychedelics an lsd electric type feel. Synephrine is inpractical as a source of amine becuase of its active dose but METHYLsybephrine has bee used safely n doses exceedinging 200mg. Dont quote me on this but i believe its a beta adrineric agonist opposed to alpha. This fact causes it to manifest in less autonomic nervous activation (excelarated heart rate)

69ron you advise against hordinine as it could condence with the oxo metabolite, is thia nessesarily a bad thing? Is it not lipid soluable enough to cross the bbb?

As for the idea that the euphoria being described as natural, and i truely hope i dont sound pejorative when i say this, ill be the first to admit i know very little about this and my ideas should hold little weight, but i do not belisve the euphoria comes from an endegenous agmentatition of monoamine ativity. I believe that the reason mdma has the paradigm of a syntheitic high is because it realeses catecholeamines causing and infux folloeed by a deficit. If this compound binds to receptors as opposed to facilitating endegenous amine release i believe there would be little crash. To test the integrity of this idea, do any experienced trippers feel a crash off of lsd or mescaline? Beyond this more research should be done on receptor ddown regulation mechanisms for thr pertinent receptora (assuming we know what those receptors are) every receptor has a different mechanism of counterbalance (this might be wrong) and the fact that there is a tolorance proves there is downregulation although it might not have a pronounced effect on baseline mood like that which is attributed to the mdma mid week blues (speculation, this might just be catecholeamine depletion) i digress, i do not believe putting forth the paradign that this is a less synthetic euphoriant is condusive furthing our studies (please dont take this a perjorative, i will be the first to admit everyhing i say is speculation)

Back to alternative amine condenaation. I heard the idea of tryptamine has been concieved, has this been tried? What about nmethyl tryptamine? I believe that the methyl would make it better protected by destructive enzymes?

What about the amines present in any herbs used as enzyme agmenters or inhibitors? I see 69ron u say whethrr these herbs are taken in the second cap or the elemicine cap effects the trip, is it possible they are supplying their own amines? Is it possible to test this by using soly oils which i believe by definition are devoid of amines. (A side note, assuming the chems you want in the roobios or pom extract are non polar, perhaps you could make ur own eo. You ever heard of the honey hash method, passing butane through weed? U could do the same thing to make your own eo from any plant!)

Just food for thought. I am but an ignorant ant lost in a vast mound of almagalmated knowledge laying before me but together we can make a sea of insight that even the olympians will envey

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#56 [url]

Mar 22 13 9:36 PM


I've just read through this thread... WOW!

1'-Oxo*-PEA is definitely something I will try in future. I'll probably be one of the first 20 people to ever experience it haha!!

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