Anyone tried Cb-25 Cb-52

[ZeuSSS]

Anyone tried Cb-25 or Cb-52?

They're both new analogues of THC and anandamide (AEA). Synthesised in 2005 and currently undergoing studies in rats. I have yet to see any human reports, but I expect it will be similar to Cp 55,940, but probably not as long in duration. An 18 hour trip is all very good if you like the buzz, but for me THC analogues dont seem to go down very well, my Cp 55,940 trip was not done in the right environment, and your likely to wake up the next day still fukt. But if it turns out to be a substance that has all the good effects of cannabis but disgards any of the negatives, it has the potential to be an awesome compound. Though as its only an analogue of two constituents of MJ, so its unlikely to produce extremely similar effects.

These are both available to buy from various places, for quite a high cost, but I dont think that anyone has tried it yet. Unless I'm mistaken? I might get some if people think its safe or would be worthwhile.

Heres the relevant publication with all the info, its a very detailed full text on the studies with mice, which I haven't had the time to read through fully yet:

In vitro and in vivo pharmacology of synthetic olivetol- or resorcinol-derived cannabinoid receptor ligands

For those technical chem junkies that think in IUPAC and not english, heres the info:

Drugs
CB-25 (11-(3-hydroxy-5-pentyl-phenoxy)-undecanoic acid cyclopropylamide) and CB-52 (11-(5-hydroxy-2-pentyl-phenoxy)-undecanoic acid cyclopropylamide) (Figure 1) were synthesized in our laboratory as described previously (Brizzi et al., 2005). AM251 (N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide), capsazepine (N-[2-(4-chlorophenyl)ethyl]-1,3,4,5-tetrahydro-7,8-dihydroxy-2H-2-benzazepine-2-carbothioamide, CP-55,940 ((−)-cis-3-[2-hydroxy-4-(1,1-dimethylheptyl)-phenyl]-trans-4-(3-hydroxy-propyl)-cyclohexanol), WIN55,212-2 ((R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate) and AM630 (6-iodo-2-methyl-1-[2-(4-morpholinyl) ethyl]-1-H-indol-3-yl](4-methoxyphenyl)methanone) were purchased from Tocris Cookson Ltd (Bristol, UK). SR141716A (N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazolearboxamide) was generously provided by Sanofi-Synthelabo Recherche (France).

Anyone want to hazard a guess at the human effects they may cause? You think they'll be worthwhile?

 

[Limpet_Chicken]

Both are antagonists/inverse agonists.

 

[Sturnam]

there was a post very recently on CB-52 here

product insert says partial agonist at CB1 and neutral antagonist at CB2.

which brings up my question from the other thread that wasn't answered:
what's a neutral antagonist?

 

[vecktor]

there was a post very recently on CB-52 here

product insert says partial agonist at CB1 and neutral antagonist at CB2.

which brings up my question from the other thread that wasn't answered:
what's a neutral antagonist?

neutral antagonists block normal or inverse agonists but on their own they don't cause any change in the activity of the receptor.

 

[Sturnam]

^ but isn't that pretty much the definition of an antagonist?

so then the neutral part is repetitive? Or do 'positive' or 'negative' antagonists exist?

and i suppose this one might have recreational value considering its a partial agonist at CB1. CB2 doesn't contribute to the psychoactive effects, but screwing with that might do some nasty things to your immune system. they think CB2 agonists might be helpful with inflammation and pain, so CB2 antagonists....might increase pain?

 

[vecktor]

^ Agreed the terminology can be vague or confusing at times, not helped by the fact we really don't understand GPCR's. the more we learn the less we know.

a functional antagonist can be an inverse agonist, or neutral (silent) the difference might seem insignificant but it is much more important in vivo than in vitro. the whole thing is a lot more complex than this as there are GPCR modulators as well.

The identification of constitutive, or intrinsic, activity of G-protein coupled receptors has had major impact on receptor theory, the identification of agents that inhibit this ligand-independent receptor activity has led, in turn, to the concept of inverse agonism. It has subsequently emerged that the majority, around 85%, of all known G-protein coupled receptor antagonists are, in fact, inverse agonists. Agents that affect only ligand-dependent receptor activation, i.e. have no effect on constitutive receptor signalling, are termed neutral antagonists and turn out to be relatively rare in pharmacology. Is this relevant for medicinal chemistry? That question is difficult to answer with certainty because there has been little or no effort to understand the structure activity relationships of neutral antagonist vs. inverse agonist molecules. In this review, we suggest that these pharmacological differences may well be translated to differential effects in the whole animal and in medicine. We argue that having either option to inhibit a particular receptor may reveal differences in efficacy and tolerability thus increasing the potential value of a G-protein coupled receptor inhibitor programme. However, since inverse agonists appear to constitute a default inhibitor mode, a systematic survey of the structure activity relationships around what makes a neutral antagonist will be an essential first step towards this goal.

http://dx.doi.org/10.1016/j.ejphar.2006.09.032