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Synthetic Cannabinoid Drugs

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9353392
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9060042
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9989926
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=12505688

Well you were asking about the subjective effects of increasing anandamide by inhibiting uptake or degredation. You can try yourself: just take some ibuprofen. Maybe the data explain why ibuprofen makes you a bit drowsy and aspirin and paracetamol hardly do so.
Also cannabidiol might inhibit uptake and degredation. I have done a little experiment where i left cannabis (up to a year or more), in a closed container, in an open container, or in and open container in sunlight. I did this to let the delta 9 thc degrade in to various cannabinoids. I wasn't completely systematic in my approach, but the effect of the air and sun exposed material ( maybe three months exposure) made me relaxed and drowsy, but not stoned or high. If i would add this material to a normal joint it would inhibit the high or stonedness of the joint. I was looking for a way to drease the paranoia from thc, it worked, but the remaining effect was not really worth it. Leaving it airtight for two years even did still get me high, but thc must still have been present since it degrades slowly.

So i think just because somethindg effects a certain transmitter system, certainly does not make it recreational. Allthough there will probably be some recreational thc ananlogs, uptake inhibitors etc out there. I think cannabidiol might be valuable in the treatment of cannabis over-use, since it might decrease tension etc from withdrawal, and decrease pleasure from relapse-smoking.
 
smartshop said:
I have done a little experiment where i left cannabis (up to a year or more), in a closed container, in an open container, or in and open container in sunlight. I did this to let the delta 9 thc degrade in to various cannabinoids.
Click to expand...

Well, looks like you were trying to convert your THC into CBD, what's NOT going to happen.. THC breaks down into CBN when exposed to heat, air, light, etc. Btw, I don't see how CBN can inhibit the high of THC, it potentiates it. Or you are just referring to the effects of CBN, they dissappear quite rapidly..
 
Rimonabant has become known in the popular media recently and I'm wondering what effect it will have on marijuana's illegal status. I wonder what the long term effects of a CB antagonist will be, if any. The popular press are promoting the drug as a pancea for 1) cardiovascular health- blood pressure, cholesterol, diabetes; 2) drug abuse- esp alcohol, marijuana, cocaine, nicotine; 3) obesity.

This is a little off topic but I am going to get some of Sanofi's stock :)
 
Blowmonkey, somebody borrowed the book i have this information from but it said that thc converts both to cbd and cbn and light exposure increasing the conversion to one of both. When i have the text i can be more specific. Untill then maybe try yourself. I was really surprised by the outcome. But you might be right that in reality thc was broken down into cbn and that the material had high initial amounts of cbd, wich inhibited the high. I have no tests to prove what my sample contained, although it did come from a high-cbd plant (durban poison).
 
CBD significantly decreases anxiety and it increases "mental sedation", partly because it slows down heartrate. I was always under the impression that CBN wasn't capable of alleviating anxiety, but rather it contributed to THC induced anxiety/paranoia by increasing heart rate. There is no doubt about your sample containing CBD, but the following parts led me to believe that what you have is mostly CBN, not CBD; "made me relaxed and drowsy, but not stoned or high" and "the remaining effect was not really worth it" which is a strong indicator of high amounts of CBN as opposed to CBD.

it said that thc converts both to cbd and cbn and light exposure increasing the conversion to one of both.
Click to expand...

You're right in saying that CBD is also a degradation product of THC, but the main chemical THC degrades into is CBN. Loss of THC after exposure to light does not lead to a significant increase in CBN, but air oxidation in the dark does. Still, the main chemical degradation product is CBN in most old marijuana samples.

If you want to discuss this further, let's do so somewhere else.
 
published analogous compounds

This particular compound, drawn by f&b is not known at scifinder, but huge amounts of similar ones. The refs and abstracts are added. Have a closer look at the authors names.;)

Soft cannabinoid analogues as potential anti-glaucoma agents. Buchwald, A.; Browne, C. E.; Wu, W.-M.; Ji, F.; Bodor, N. Center for Drug Discovery, College of Pharmacy, University of Florida, Gainesville, FL, USA. Pharmazie (2000), 55(3), 196-201. Publisher: Govi-Verlag Pharmazeutischer Verlag, CODEN: PHARAT ISSN: 0031-7144. Journal written in English. CAN 133:4811 AN 2000:192084 CAPLUS

Abstract

Cannabinoids have intraocular pressure (IOP) lowering effects, thus, they have a therapeutic potential in the treatment of glaucoma. Unfortunately, in the same time, they show CNS and cardiovascular effects as well. Our aim was to develop a safer, cannabinoid type anti-glaucoma agent, a topically applied soft analog, that has local, but no systemic effect. The lead compd. chosen was a nitrogen-contg. cannabinoid analog that was shown to have IOP lowering activity. A full library of possible soft drugs was generated and the structures were ranked based on the closeness of calcd. properties to those of the lead compd. I. The lead compd. I has been synthesized, and a preliminary pharmacol. study was performed. The structure-activity relationship and pharmacol. results indicate a good possibility for the development of a safe, soft anti-glaucoma agent.



1,2,3,4-Tetrahydro-5H-[1]benzopyrano[3,4-d]pyridines and 1,2,3,4,13,14-hexahydro-5H-[1]benzopyrano[3,4-d]pyridines. Shulgin, Alexander T. (Dow Chemical Co.). U.S. (1970), 9 pp. Division of U.S. 3429889. CODEN: USXXAM US 3522260 19700728 Patent written in English. Application: US 68-717061 19680219. Priority: . CAN 74:3599 AN 1971:3599 CAPLUS




8-Alkyl (and 8-cycloalkyl-lower-alkyl)-10-hydroxy-5-oxo-1,2,3,4-tetrahydro-5H-[1]benzopyrano[3,4-d]pyridines. Shulgin, Alexander T. (Dow Chemical Co.). U.S. (1969), 8 pp. CODEN: USXXAM US 3429889 19690225 Patent written in English. Application: US 65-490667 19650927. Priority: . CAN 70:87787 AN 1969:87787 CAPLUS


Citations, abstracts and formulae are attached!
 

Attachments

  • cbs.doc
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You know what shits me? There are still no commercially available water soluble CB1 agonists! What a fucking joke.
 
^ I'm pretty certain that the nitrogenous THC analogue I mentioned previously (even if I got the side chain group wrong) is a CB1 agonist that's water soluble. It may also have activity at the CB2 receptor as well, but considering the water solubility of the salt, you'd think somewhere like Tocris would carry it, wouldn't you?
 
I tried WIN55212-2 a while back, its active at a dose of around 1-3mg (nasal insufflation as it doesn't dissolve in water)

Feels much like THC but milder and shorter lasting, quite pleasant really. Gets you kinda stoned but without the sleepy fuzzy headed effects that cannabis has. The maximal effect is less than that of THC; WIN55212-2 is more potent than THC but a weaker partial agonist, so you can feel effects from even 0.5mg, but then they don't get much stronger even if you have 6mg.

I've known someone else who tried taking HU210 by IV, they said it was sedative and very long lasting, compared it to a 12-hour k hole. Don't think they enjoyed it really, wheras personally I liked WIN55212-2 more than weed.
 
BilZ0r said:
You know what shits me? There are still no commercially available water soluble CB1 agonists! What a fucking joke.
Click to expand...

THC phosphate ester is water soluble, and can be made pretty easily from THC.
 
Here's a change of pace, cannabimimetic indole derivitives, a few which are supposedly very potent at both cb1 and cb2, but primarily cb1.:)
Patent # US 6,900,236 B1
(May 31st 2005)
1.2 mb
http://www.freepatentsonline.com/6900236.pdf

Check out AM694 and AM1295. I wonder if a 2-iodophenyl AM1295 would be even more active than the first two.


http://rapidshare.de/files/23269912/cannabinoid_ligands_2.pdf.html
Also, this^ pdf is pretty interesting, including tables that compare THC to synthetic market ligands like WIN55,212-2.

sorry about the rapidshare, the file is 800 kb so I can't attach it.
 
mad_scientist said:
THC phosphate ester is water soluble, and can be made pretty easily from THC.
Click to expand...

Always thought that it would be possible to make a variation of the acetate ester of THC, but instead of using acetic acid, using something like N,N-dimethylglycine to form the ester. The tertiary amine group would be an ideal proton acceptor to form an ammonium salt such as the hydrochloride salt. The only problem I could forsee would be that the ionic group could interfere with binding to the CB1 receptor, but if the phosphate ester sodium salt doesn't 'get in the road', I cant imagine a dimethylammonium salt would either...
 
nitrogenous cannabinoids

I think a lot of work was done in the 70's and 80's on nitrogen analogs of cannabinoids by raphael mechoulam. If i remember correctly there is a reference in RE schultes botany and chemistry of hallucinogens. I don't have the ref myself. but that molecule looks familiar
v
 
If the agonist binding site of the CB1 receptor is in the membrane as many people seem to think, this would helpe explain why there are not any water-soluble CB1 agonists available: they wouldn't be able to get to the binding site (unless it was an enzymatically hydrolyzable ester).

Also, the reports of people who have tried commercially available CB1 agonists are interesting. Some researchers who work on cannabinoids claim that THC "withdrawals" would be extremely severe if THC wasn't stored in adipose tissue and flushed from the body relatively slowly. They people have given rimbonabant to rodents chronically treated with THC and claim to see a "heroin-like" withdrawal syndrome similar to that precipitated by naloxone or naltrexone in opiate-dependent animals. Thus, they predicted that the synthetic CB1 agonists, which are supposedly metabolized and excreted more efficiently than THC, could have a bad comedown and be extremely addictive. These experience reports don't seem to support those speculations.
 
It will be interesting to see whether rimonabant precipitates acute cannabis withdrawal in human heavy cannabis users. Will they warn obese people of this possibility when they get prescribed rimonabant I wonder, or just ignore recreational use of illegal drugs because they are illegal and therefore don't count...

I would imagine enough people smoke weed that this effect would start to appear even in the Phase 3 trials currently underway, unless they specifically excluded heavy cannabis smokers from the trial.
 
Cool, i hadn't noticed that one, or maybe i forgot because it doesn't look too interesting from that. How potent is it? Looks like a bitch of a synth.

Maybe not, just a bit fiddly from 2,6-dimethoxyphenol.
 
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