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Dissociatives

Smyth

Smyth

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I dont understand why not more dissociatives. PCP has all but disappeared. Im interested in that 2-MDP structure also. Kind of strange since i understand that dxm is a shit dissociative where as it has been documented that the bad rap for pcp comes from users mistakenly taken 10x the proper dosage unit.
 
one reason why there are more dissociatives is because alex shulgin doesnt like them. and he is the only chemist i know of that is continuing making new componds. if there was a person like d m turner or john lily around then that would be a different story.hehe we would haved DIKAL.
i think more dissociatives would be a good idea considering K is the only one i like, never done pcp. and dont care for dxm.
good post. informative, it got my brain thinking this morning.

btw i feel like salvia can be quite dissoiative like
 
A lot of the structures shown may well have dissociative properties, but will not substituye for ketamine/pcp for one of several reasons. A good example is MK-801. It has NMDA antagonist activity, but doesn't have the dopaminergic activity of the arylcyclohexylamines; as such it's generally reported as being like a long bout of confusion, rather than producing any moments of insight. Others such as pentazocine have kappa agonist activity (ie salvia-like activity) and because of the emotional component will not substitute for either of the two aforementioned arylcyclohexylamines.

Usable dissociatives are a bit more complex than just plain NMDA antagonists
 
I agree with illusion - dissociatives are not popular in either legitamate or "underground" drug research, probably due to the PCP stigma. Notice how, after Dizocilipine was introduced, it immediately became the NMDA antagonist of choice for legitamate researchers? It is all to circumvent the PCP stigma. Since Ketamine has become a recognized recreational drug, it, too, has become stigmatized.
 
and arylcyclohexylamines are dopaminergic in what way? RUI?

do they augment sero and epi RU as well?

and when you hear people say they cant feel pain on PCP, thats not through opioid receptors is it? Cause isnt the opioid affinity of PCP pretty damn low so as couldnt possibly have an effect on pain at a recreational dosage?
 
Can't remember how arylcyclohexylamines exert their dopaminergic effects, but as BTCP (the PCP analogue with a benzothiophene group replacing athe phenyl group) is an active reuptake inhibitor, that'd be my guess.

The lack of pain is to do with stopping external stimuli reaching the brain rather than any opiate mediated activity (it's not just pain signals, it's all external sensory input - the reason you become a disembodied conciousness with big doses of ketamine/PCP). If it was opiate mediated, you'd still get some pain perception, but ketamine allows for in situ amputations if needed.
 
From what I gather, if u want good dissociative then make PCP. Everything else is moot. Then again ketamine has the reputation for being 'aight.
 
I wonder if, in the case of BTCP in which dopaminergic activity is greatly enhanced whilst PCP-like activity diminished, if its possible from then on to bring back the NMDA antagonism it once had, via various substitutes and additions?

Perhaps investigation into SAR data on BTCP and its derivatives yields some sort of NMDA antag return, whilst maintaing the dopamine activity BTCP claimed from PCP.
 
As thiophene on its own results in a fairly potent PCP like agent (TCP - slightly more potent than PCP), I'd guess that it's a matter of steric hinderance w.r.t. the receptor. The aryl group in BTCP is simply 'too big' to fit into the PCP receptor site, but still fits into the DAT in the same way as PCP. Chances are that any 2-ring aromatic structure (eg napthalene or indole) is going to result in a reduction of NMDA antagonist activity while retaining dopaminergic activity.

A good line of enquiry would be to synth various PCP analogues with large groups attached to the benzene ring, such as phenoxy, benzyloxy and cyclohexyloxy groups. The opposite being using various 6 & 5 membered aromatic structures such as pyrrole and pyridine
 
^

A line of enquiry to acheive what? A highly dopaminergic (higher than PCP), and equally if not more potent NMDA antag?


TCP I read sumwhere was supposed to be slightly more dopaminergic than PCP, so perhaps, and I could be wrong, but couldnt you do additions to the T in the TCP? And result with compounds that are like 3-methoxy-TCP and such, OR is that what the B in BTCP is, and thus this wouldnt fit in PCP receptor?


Or were you suggestion said additions to the B in BTCP?? But if BTCP is already too big for PCP receptor, then how would adding more onto it, increase its affinity to that receptor?
 
^ I simply meant increasing the size of the aromatic group until you got a whole spectrum of activity from purely dopaminergic activity all the way through to compounds that were much more potent NMDA antagonists than PCP. That way, you'd be able to establish the 'crossover' point in terms of size of the aromatic group
 
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