• N&PD Moderators: Skorpio

Possible ultra potent GHB analog

A couple of things I don't get about that molecule (HOCPrCA):
- is it a double radical, cause if those are two free adjacent electrons, isn't that just a bond? Is there like a chaperone molecule to stablize it normally, otherwise it all seems ridiculously reactive.
- its R,R-isomer is stereochemically made .. selectively, but how is it even a chiral molecule cause it looks planar trigonal?

A radical is denoted with a dot. The star means it's chiral. And yes two electrons would pair up.

It's chiral. With two enantiomers and a meso.
 
Just me, but I don't think an ultrapotent GHB analog can come to anything good.
Likely as not, it will be toxic, and a convulsant to boot.
 
Hmmmm, yeah I think I agree with you there.

Making GHB ultra potent, morally, isn't such a good idea. It would be lovely for us fiends but fiends we would become. I think sticking with GHB as it is is the best idea, however I am interested in more potent GABAb agonists such as SKF-97541. They could be used for numerous purposes, in a similar way to benzodiazepines. I have to say Phenibut has been wonderful to me but you can go over the edge very easily, 24hr+ intoxication is not as fun as it sounds. Making more potent compounds would only induce alcoholism-esque problems and we really don't need more of them. It may be slightly better to your liver but addiction and social consequences are bound to be present if such a compound arises. This is not the way we want the human organism to progress into.

Instead we should be striving for nootropics and cognition enhancement. Done are the days of layabout drunks and sordid societies.
 
Because of the date rape thing? Good NaGHB is already pretty much tasteless in drinks with a taste of their own + you have benzos that can be used for the same purpose and are active in the mg range. I don't think a stronger version of GHB would change much..
 
No I'm saying that as human beings we shouldn't be indulging ourselves with such CNS depressants lest we become vegetables.

However there are such drugs and I really don't think we need more potency as a moral standpoint. We have alcohol and GHB and benzos, lets just leave it at that.

I realise that's not the way we should go about things if we are to evolve our knowledge base but these compounds are harmful...ah but fuck, I do 'em everyday the same, so I'm a hell of a hypocrite.

I guess I'm trying to say there shouldn't be more intoxicating compounds such as these or as a society we'll destroy ourselves.

And I'm still a hypocrite.
 
I don't really see the problem. If it's like ghb, the dose range would still be narrow. The only difference would be that instead of 1-5g you'd take (for example) 1-5mg. Taking more wouldn't do anything good, same as taking 10g of ghb doesn't do anything good. And I'm pretty sure the price would reflect potency so you couldn't get 1g of this super potent analogue for the same price as 1g of ghb.
 
Apparently they cause seizures.

Also, HOCPCA is a radical?...
Even besides that, it is a direct - sort of constrained kinda - T-HCA analogue and that one is toxic methinks.

Combine it with a GABA-B agonist, then? For that matter, just use HOCPCA and SKF-97541?

Also I am thinking that the reason phosphonate thioesters are such potent alkylating agents (= VX nerve gas) has to do with the sulfur-phosphorus bond having the "perfect" shape and electronic structure to react only when activated by cholinesterase. I don't think typical phosphonates are acetylcholinesterase inhibitors.

blueberries said:
No I'm saying that as human beings we shouldn't be indulging ourselves with such CNS depressants lest we become vegetables.
Likely so. GHB is not known for safety. A precisely controlled ratio of two selective agonists could be safer.
 
Part of the reason the phosphonate thioesters are so potent as AChE inhibitors is that after phosporylating a serine residue in the active site of the enzyme, they can then undergo a rearrangement, which if I remember, splits off a phosphate group, permanently inactivating the cholinesterase enzyme. It varies in terms of time taken to do so with the agent, but its at least 24 hours for VX, soman is the really nasty one, as it 'ages' once bonded to cholinesterase within minutes, rendering oxime agents useless.
 
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