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1-{1-(3-Methoxiphenyl)-cyclohexyl}-piperidin

hugo24 said:
metaomega:really?A bit a surprise to me as the pyrrolidines are usually active.At least the title compound 1-{1-(3-Methoxiphenyl)-cyclohexyl}-piperidin has valid binding data out there,as does its OH cousin which has yet to be tried in humans.
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Thats about the logic I used in the first place; 3-OH shown to increase potency, the pyrro for the piper swap shown to increase potency, so it should be potent, more potent than regular PCP. Unfortunately as I learned this isnt like 4-anilidopiperidine SAR where things usually do work literally that simply, for PCP analogs its a whole different mixed-bag SAR. It didint pan out the way I had hoped. Even when marijuana was combined with it there was no effect apart from the MJ, and marijuana seriously potentiates the intoxication from regular PCP in my experiences. Im not sure what happened in the SAR that led to this being seemingly inactive, it couldve been active in a ketamine dose-range, I never got that high as it kinda got eerie that the SAR hadnt panned out at all the way I had intended so who knows what its really doing to the neurons, and it clearly wasnt more potent than PCP so the primary goal failed anyways.


PCPs a pretty beautiful molecule though, its quiet simple to produce in a clandestine facility and it seems it can be simply modded to yield a wide range of differing core pharmacologies, its like a cube that can morph into a circle or a triangle too, now thats a useful cube.


Not to wander off the original topic, but I rarely see serious PCP discussion threads so I must, has ANYONE yet tried BTCP? If it wasnt for the fact catalogs offering it want rediculous prices paid for rediculously small quantities, I probably wouldve tried this by now. It SOUNDS like a very interesting stimulant, but is it strictly dopaminergic or is it an SNDRI like cocaine? I only recall rearing about its dopaminergic activity. Also does anyone have a ballpark of what they think the RED (recreationally effective dosage) of this is gonna be (or IS if they tried it)?
 
hugo24 said:
generally, SAR/in vitro data is not too accurate in predicting subjective effects in a human and subjective effects in a human are not too accurate in predicting SAR/in vivo data.And extrapolations of existing data is dangerous.So we have to live with these dilemmas and yet advance to new frontiers
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I think it ultimately comes down to the molecules your dealing with. I think some have much more linear and predictable SAR, but they all have the odd anomaly in the SAR. PCP I think has VERY unpredictable SAR, evident by its wide range of pharmacologic effects that can be achieved with simple modifications.

If I recall correctly I even remember reading somewhere about a simple analog of PCP that wound up doing little more than destroying the shit out of neurons. My memory could be way off though. That kinda scared me, you really dont know what your gonna get when you delve into designer dissociative anesthetics based on the PCP molecule, its like reaching it an opaque bag and pulling out a random handful of various pharmacologic actions everytime you mess with that molecule.
 
I once stumbled across a PiHKAL/TiHKAL of PCP type book if you will in a large research library by a wacked out looking bunch (judging by the looks of their group photo) of French academicians replete with 60 or so molecular structures but without trip reports. I don't recall the title, but I certainly wish I had the book to peruse again today. Perhaps locating this volume would aid your knowledge of the subject?

Hammilton, after your latest lefetamine post, you have no room to criticize me at all for at least another week. :)
 
Hammilton, after your latest lefetamine post, you have no room to criticize me at all for at least another week.
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As in that I'm too busy? I should be, but I'll find the time. I thought it would be a good idea to provide an overview of the research published given that what lefetamine threads we've had have never once taken account of what the research actually said (beyond what was covered in an abstract, that is).

Anyway, I took a minute to compare the structures as mm2 minimized. If the benzylamine derivative of MDA is actually a monoamine releaser- which at this point is a HUGE if- then MDPCE might possibly have a chance.

However, Hugo, like I said, suggesting that MDPCP should be tested for MDMA like activity is nonsensical. Not only is the overlay much worse, though not so much that it would have no chance of binding to the same site, but because when you go from MDMA to N,N-Dimethyl-MDA you seem to lose all activity. (see PIHKAL #105). Of all the MDMA derivatives that are much closer in structure were tested (MDPV, among others), there's little or no 5HT releasing activity once you have a tertiary amine.

The suggestion to see what happens with the 2,5-dimethoxy pattern is actually a good idea, but given the lack of references cited, it seems fair to assume that it was based on whim, not reason.

Kapur and Seeman, Molecular Psychiatry, 7(8) 2002 pg. 837-844

I have the full copy of this is anyone wants to read it. edit: never mind, it's actually available free online. I'll still add it to the repository to make searching easier.

Unfortunately this paper doesn't seem to distinguish between 5HT2 receptor subtypes, as no mention of 2a specifically is mentioned. This is somewhat unfortunate, but I don't think it's a stretch to suspect that both PCP and Ketamine have fair 5HT2a affinity based on these results (and the HTR).

It would be interesting to see more research put into benzylamine analogues of phenethylamines. There's been high interest in non-PEA, non-Tryptamine, non-Lysergamide 5HT2a agonists. I'm surprised Shulgin's comment wasn't enough to generate some research, above- or under-ground. I do see some research on somewhat related drugs; piperonylamine has been shown to prevent MDMA-induced neurotoxicity, along with other MD-benzylamine derivatives. Piperonylamine itself is a weak 5HT reuptake inhibitor I read now.

Anyway, a topic for a different thread after I've had some time to find more published research and obtained the fuly copies.
 
Thanks for expanding and clearing some things up Hammilton .Point taken on the tertiary amine.The MD-N,N-Dimethylcathinon might be the only exception with some chance for 5-HT releasing.

Unfortunately you can't quote me on the 2,5-dimethoxi-PCP,I only cited the known 3,4-dimethoxi-PCP to illustrate reduced PCP/DAT binding.I have this from

Pharmacology Biochemistry & Behaviour Vol. 32 , 1989 , pp. 699-705.

It tested the affinity of 37 PCP compounds for PCP binding sites and Dopamin reuptake inhibition.I guess you know the paper.

I too have wondered that Shulgins benzylamine-analog didn't stirr up things more in that region,the activities appear retained which is a bit a surprise.The description of the effects is very minimal unfortunately.
 
rectify i fully agree with you pce is more desirable to me than taking the next step to pcp
 
metaomega said:
I tried 3-OH-PCPy (meta-hydroxyphenylrolicyclidine) up to 40mg with no discernable effect and if there was an effect it was close to placebo and lasted maybe 15 minutes.

Someone else tried up to 60mg with no discernable effect other than that which would be considered placebo.

Didint feel comfortable going any higher incase it was nuking neurons or someshit.

Any clue why this wasnt active or at least active anywhere near the anticipated dose range? :(
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You didn't have the chance to try 3-MeO-PCPyr metaomega? I'm assuming the phenol was made from the methoxi anyway.Just curious as the first trials with 3-HO-PCP appear as well somewhat inconclusive so far and something does not feel right.

But the title compound appears to be really a winner in regards to its recreational potential,wonderfully balanced effects (up to 10mg now).So the first guesses about its potency can be made now (somewhat less than PCP) although I have planned a reference experiment with PCP for getting directer comparisons,I had it last time maybe two years ago.
 
Can we please pur a halt on the interpersonal stuff, or I'll have to go a editing (& I'll not be happy as I'm a very lazy individual ;) )

Bravo hugo, another piece to the ovewrall dissociatives jigsaw puzzle found & fitted; one suggestion (feel free to point out gaping flaws in the following as it;s all stream of conciousmess type stuff going direct to posting) - from the point of view of all things toxicological, wouldn't it be better to carry out in vivo self assays with the ketamine like analogues rather than PCP ones as ketamine is way, way below PCP in the neurotoxicity stakes. As their SAR regarding the amine constituents is pretty much identical (same increases/decreases in potency when comparing ethylamino, methylamino etc substitutions. After all, the purpose of putting a keto oxygen on the cyclohexyl ring is to speed up metabolic fate & excretion by kidneys, it just seems that it also decreases neurotoxicity - admittedly it pays the price in terms of potency (ten fold drop from addition of oxygen to ring), but isn't the most important consideration not damaging the straight out of the wrapping paper brain nature has provided us with?

I know the ketamine series involves a more complex synthesis route, but don't considerably shortening the length of action & decreasing neurotoxicity mean that such things deserrve at least a cursory glance. Right now I've said my mother hen bit, still bloody interesting stuff from you there hugo. Have you considered the 2-chlorophenyl PCP analogues at all (a la ketamine's aromatic group)? It seems to give ketaminme a real edge over other aromatic substitutions like tiletamine (horrible drug, industrial grade ketamine. Best analogy I can think of is comparing an aged single malt with roughlu produced poteen (moonshine) - both eventually do the same thing, but one ois subjectively much more pleasant to consume (not bad from someone who doesn't drink anymore eh? =D)
 
More than a little late, the last such post was just short of a month ago.

On the issue of toxicology, I don't think ketamine derivatives are any better. You may have less neurotoxicity, but you end up damaging your kidneys (or is it bladder? I forget which now). I don't know that this is a better or worse trade-off.

Assuming one isn't binging heavily, whatever neurotoxic risk these drugs pose doesn't seem to result in much or any noticable impairment in life.

Shorter duration and more opioid receptor affinity seems to make for a superb dissociative. PCP with it's much longer duration and much strong dopaminergicity seems to make it much more prone to negative effects than the others. Somewhat akin to taking an anxious, paranoid tweaker and adding in a lack of pain and an ever odder thought process (well, I find the thought process induced by dissociatives to be weirder than psychosis, though the nature of the experience makes it difficult to objectively compare).
 
Report here.

The basics:

Dose: 6mg orally followed by 2mg insufflated 2hrs later. I have no tolerance to NMDA antagonists and I'm slightly more sensitive to ketamine and DXM than what I think of as average from reports.

Onset: first alerts in 30 minutes orally, but it really ramped up between the 1:20 and 2hr mark.

Duration: uncertain, I took a hit of LSD with the insufflated dose and then IM'd ketamine and psilocin about 1.5 hrs after that. I think at the 6mg level the peak is probably 2-3hrs with a 2hr decline to a wobbly baseline.
 
and all of that makes it rather useless. There's nothing in this report of any use. Novel substances combined with other drugs ruins the usefulness of the report.
 
I had 1.5-2hrs with fairly strong effects from it before LSD started to really influence the experience. The majority of the writing in the report is a reflection on my reaction to just 3-MeO-PCP.
 
It's still meaningless. You took another drug, it was already in your system. You can't possibly say whether or not the LSD was having an effect or not yet.
 
I'm sure you can tell when LSD starts affecting you if you're experienced enough with it, no? Although I've personally never had the chance to take any dissociatives at full dose, so I'm not sure how much in common they actually have with classical psychedelics. Also, the timeline for LSD is pretty much known and familiar to anyone who has tripped enough on it, so it shouldn't be too difficult to assess when it actually kicked in.

Thus, I wouldn't be so hasty as to completely dismiss psood0nym's report, I find that it has plenty to offer regardless, and is an enjoyable read at the very least.
 
Also, the timeline for LSD is pretty much known and familiar to anyone who has tripped enough on it, so it shouldn't be too difficult to assess when it actually kicked in.
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I'm afraid this isn't how science works. Subjective reports are useless enough already, but to add another drug in and assume that because you have x amount of time before it starts producing subjective effects alone that it won't have an affect on the subjective effects of the first drug is retarded. That's not how good science is done, I'm afraid.
 
Hammilton said:
It's still meaningless. You took another drug, it was already in your system. You can't possibly say whether or not the LSD was having an effect or not yet.
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In my original post above I state that I took the LSD with the 2mg insufflated dose of 3-MeO-PCP, which was 2hrs after the initial 6mg oral dose (I think in truth it was more like 2hrs 15min). LSD was not in my system for all of it. The majority of what is written regards the time period prior to the LSD even touching my tongue, which is to say the entire onset and some of the plateau of the 3-MeO. I can say definitively that LSD was not having an effect during that time, that is, unless it has the power to change the past! I didn't noticed subjective changes in the experience until about 30 minutes after taking the LSD (and nothing all that substantial for about an hour), so that 30 minute period seems pretty admissible for inclusion in a qualitative report on 3-MeO-PCP's effects to me as well. It's not meaningless to describe how it combines with LSD as I'm not aware of any reports of the combo; it's not meaningless or useless to report that I combined it with ketamine with no unexpected potentiation or contraindications either. I'm confused.
 
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Rectify said:
I once stumbled across a PiHKAL/TiHKAL of PCP type book if you will in a large research library by a wacked out looking bunch (judging by the looks of their group photo) of French academicians replete with 60 or so molecular structures but without trip reports. I don't recall the title, but I certainly wish I had the book to peruse again today. Perhaps locating this volume would aid your knowledge of the subject?
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Is anyone else familiar with the book rectify is talking about? i would be very interested in looking at it!
 
Compound : 1-{1-(3-Methoxiphenyl)-cyclohexyl}-piperidin.HCl , >99% (HPLC)

Description : Psychedelic Dissociative
Dosage : 4-12mg+ (not higher tested yet)
Administration : p.o.
Duration : ~4.5h +/-1h depending on dosage; after-effects not included
Typical course : First effects at 30', strong onset at 1h, peak at 2h, sudden drop at 3h

A recent reference experiment with 6mg PCP yielded the usual effects,they were comparable to 8mg or 10mg 3-MeO-PCP (depending on which effects are judged).So its about 50% less potent by weight than PCP.But PCP lacks this unique "window of transcendence" of its 3-MeO cousin.
 
The first downside is becoming apparent (well depending on which side you stand,I'm a passionate smoker of Havannah cigars),cigars the next day taste bad,like an old flannel.Its not just a taste-aversion but rather a change in taste, to be precise.

After the third cigar I tried unsuccesfully on one occasion, I thought it must be me and noted I had 3-MeO-PCP the evening before.It happened a second time,two weeks later,also the day after a 3-MeO-PCP trial.I remember another time where a cigar tasted very unusual and annoying but didn't make at that time the connections to a substance tried.

About the third day after,taste is back to normal,the second day there appears still a lingering impairment but its harder to judge.Maybe this gives a hint on how long the compound stays in your body,but I didn't yet smoke when "on" so its hard to say it really has a direct connection.And I haven't tried it out with normal cigarettes.

I know taste alterations sometimes happen from chemicals,it still feels odd when you experience it.Don't tell the fascistoid anti-smoking briade :(
 
^ Do you reckon it could have any miracle fruit type alterations in taste (ie making nasty tasting things seem much more palatable)? Plenty of compounds (although I can't bring any names to mind) that make cigarettes taste absolutely vile to addicted cigarette junkies.

Also do you reckon it's due to action at the taste receptor cell, or a centrallly mediated effect?
 
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