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dissociatives of the future

Thanks a lot Dred.

I've been told that 3-MeO-PCP completely lacked the anaesthetic element (full-body numbness) that PCP and Ketamine so powerfully produce. What do you guys think the reason for this is? FnB? :)
 
[tangent]Funny, F&B... since the last time I posted in the previous page, I have had several chances to try Ketamine IM after accquiring it OTC in India and Cambodia. You are absolutely right. I.M. is simply the best method of administering it. In fact, something seems "missing" when you snort it or even I.V. it. I decided that I will basically never take K any other way when using for entheogenic purposes :) [/tangent]
 
You'll get a good degree of analgesia with 3-MeO-PCP above 10mg.And it reveals more of the typical dissociatives effects,in my 15mg trial I was quite stoned almost floored and had the typical "where, is who, and what, (the fuck anyway)" yes the effects were still very great.And still therapeutically useful.

Recently had it at 17.4mg,and I can say it didn't dissapoint me ;)

Next stop 20mg.
 
PCP1-3 binding sites and its influence on subjective effects: the paper ( Eur. J. Med. Chem. 34 (1999) 125-135 ) tests several TCP analogs for their selectivities towards the mentioned sites,I'm wondering if anything is known about differing subjective qualities from this.

We know (or at least heard) of the rather unpleasant profile of TCP (as well as MK-801) - both bind rather selective to PCP1+2,whereas altering the structure leads to compounds selective for PCP3,like a beta-methylated thiophen,a 3-hydroxymethyl on the piperidine or the 2-furyl.I'm not yet convinced of the dopaminergic role responsible for unpleasantness of TCP-any chance the said selectivites are the culprit?

Don't know the different IC50's from Ketamine or PCP towards PCP1-3 binding sites,and def. not from the 3-Methoxyanalogs,if anyone could shed some light on that would be appreciable.

The paper describes also the FCP (N-[1-(2-furyl)cyclohexyl]piperidine,aka Fuceepee),this binds with 5nm to PCP3 (TCP 3716nm,MK-801 11125nm) and has only a slightly impared binding to PCP1 (47.8nm).It would be the easiest tool to "check" it out.

Any comments welcome.
 
fastandbulbous said:
Still reckon 2-(3-methoxy)-2-(N-ethylamino)cyclohexanone and N-ethylnorketamine are potential winners
Click to expand...
Dont you mean 2-(3-methoxyphenyl)-2-(N-ethylamino)cyclohexanone?


I found the following here: http://www.erowid.org/archive/rhodium/chemistry/pcp/ketamine.html
Two other ketamine analogs have been found on the black market: the compound missing the 2-chloro group on the phenyl ring, and its N-ethyl analog. Both of these compounds are most likely more potent and longer lasting than ketamine.
Click to expand...
 
No one dares to speculate on my last post? Smells like more work...
 
I think people forget the significance of the Sigma-1 binding site in all of this. I think for a useful, 'new' dissociative, it would have to have an action at both NMDA and Sigma to be worthwhile.

Also, for racemic chemicals, one cannot forget that there can be different qualities to each isomer and so that one isomer of a proposed chemical might be more favorable than the racemate.

I really wish more research was done the binding of R-isomer ketamine alone. It seems it's only been done with racemic and S-isomer.
 
I'll credit Jamshyd with the delightful piece of slang, "3-meo-angel dust".
I'mma start calling MDMA "3,4-methylenedioxy-crank". ;)

ebola
 
fencamfamine said:
Gavestinel?
Click to expand...
Gavestinel selectively targets glycin-sites, not glutamate sites in the nmda receptors. Don't think all subtypes are affected either. Doubt it's psychedelic at all. Any information appreciated ofc!

I'm really curious to see what sort of antidepressants the industry comes up with in the next yrs. They are still holding onto their ssri and tricyclics, cheap and selling exceptionally well. Once the first company releases a new gen antidepressant though we will see a lot of nmda antagonists popping up everywhere. my prognosis anyway.


edit: there u go: http://www.ionchannels.org/showabstract.php?pmid=12409996

Gavestinel (0.1-1 mg/kg per i.v. infusion) was not self-administered by rhesus monkeys that reliably self-administered PCP
Click to expand...
Makes me wish I were a rhesus monkey... Sigh
 
hugo24 said:
PCP1-3 binding sites and its influence on subjective effects: the paper ( Eur. J. Med. Chem. 34 (1999) 125-135 ) tests several TCP analogs for their selectivities towards the mentioned sites,I'm wondering if anything is known about differing subjective qualities from this.

We know (or at least heard) of the rather unpleasant profile of TCP (as well as MK-801) - both bind rather selective to PCP1+2,whereas altering the structure leads to compounds selective for PCP3,like a beta-methylated thiophen,a 3-hydroxymethyl on the piperidine or the 2-furyl.I'm not yet convinced of the dopaminergic role responsible for unpleasantness of TCP-any chance the said selectivites are the culprit?

Don't know the different IC50's from Ketamine or PCP towards PCP1-3 binding sites,and def. not from the 3-Methoxyanalogs,if anyone could shed some light on that would be appreciable.

The paper describes also the FCP (N-[1-(2-furyl)cyclohexyl]piperidine,aka Fuceepee),this binds with 5nm to PCP3 (TCP 3716nm,MK-801 11125nm) and has only a slightly impared binding to PCP1 (47.8nm).It would be the easiest tool to "check" it out.

Any comments welcome.
Click to expand...

Interesting, I'm afraid I can't really comment except that I didn't know there were different PCP receptors. Are these found in humans too? The paper you ref says that PCP1 is found in the rat forebrain, whereas PCP2 and PCP3 are found in the cerebellum.
 
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