Preparing Delta-9-Tetrahydrocannabinol

Delta -Tetrahydrocannabinol (delta -THC) is considered to be the predominant compound in preparations of Cannabis saliva (marijuana, hashish, bhang) responsible for CNS effects in humans. The recognized CNS responses to these preparations include alterations in cognition and memory, euphoria, and sedation. Potential therapeutic applications of cannabis preparations include analgesia, attenuation of the nausea and vomiting of cancer chemotherapy, appetite stimulation, decreased intestinal motility of diarrhea, decreased bronchial constriction of asthma, decreased lOP of glaucoma, antirheumatic and antipyretic actions, and treatment of convulsant disorders. 

Cannabis preparations are smoked in order to deliver their psychoactive substances, cannabinoids, especially THC delta-9-tetrahydrocannabinol (THC) (Fig. 13—14). 

The main active ingredients of cannabis are cannabinol, cannabidiol and several isomers of tetrahydrocannabinol, of which delta-9-tetrahydro-cannabinol (THC) is probably responsible for most of the psychoactive effects of the various preparations. It is of interest to note that THC does not contain nitrogen in its three-membered ring system. The structure of THC is shown in Figure 15.8. 

Delta-9-Tetrahydrocannabinol (Delta-9-THC) and, to a small extent, also Delta-8-THC are the biologically active constituents in extracts of the plant Cannabis sativa (marihuana, hashish) and are responsible for the effects on the human central nervous system (CNS). Potential historical and contemporary therapeutic uses of cannahis preparations include, interalia, analgesia, emesis, anorexia, glaucoma and motor disorders. 

Results from previous experiments, in which we compared the inhibitory effects of the 1,1-dimethylheptyl homologs of (+) and (-)-ll-hydroxy-delta-8-tetrahydrocannabinol on the electrically-evoked twitch response of the mouse vas deferens, indicate that this preparation is suitable as a model for investigating the mode(s) of action of psychotropic cannabinoids. R. G. Pertwee, L. A. Stevenson, D. B. Elrick, R. Mechoulam, A. D. Corbett, Brit. J. Pharmacol. 105, 980 (1992). Anandamide produced a concentration-dependent inhibition of the twitch response (FIG. 2). The inhibition was not reversed by naloxone (300 nM). The levels of inhibition are comparable to those of binding to the receptor. 

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