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07-SEPTEMBER-2008 03:17:44 - Tetrahydrocannabinol Redirected from Dronabinol THC redirects here. For other uses, see THC disambiguation. Δ9-tetrahydrocannabinol Systematic IUPAC name --6aR,10aR-6,6,9-trimethyl- 3-pentyl-6a,7,8,10a-tetrahydro- 6H-benzocchromen-1-ol Identifiers CAS number 1972-08-3 ATC code A04AD10 PubChem 16078 DrugBank APRD00571 Chemical data Formula C21H30O2 Mol. mass 314.45 SMILES eMolecules PubChem Synonyms Dronabinol Physical data Boiling point 200 °C 392 °F 0.02mmHg Solubility in water 2.8 mg/L1 23 °C mg/mL 20 °C Spec. rot -152° ethanol Pharmacokinetic data Bioavailability 10-35% inhalation, 6-20% oral2 Protein binding 95-99%2 Metabolism mostly hepatic by CYP2C2 Half life 1.6-59 hours 2, 25-36 hours orally administered Dronabinol Excretion 65-80% feces, 20-35% urine as acid metabolites2 Therapeutic considerations Pregnancy cat. C Legal status Schedule IIIUS Routes ? 3D rendering of the THC molecule. 3D rendering of the THC molecule. Tetrahydrocannabinol, also known as THC, Δ9-THC, Δ9-tetrahydrocannabinol delta-9-tetrahydrocannabinol, Δ1-tetrahydrocannabinol using an older numbering scheme, or dronabinol, is the main psychoactive substance found in the Cannabis plant. It was isolated by Raphael Mechoulam, Yechiel Gaoni, and Habib Edery from the Weizmann Institute of Science in Rehovot, Israel in 1964.3 4 5 In pure form, it is a glassy solid when cold, and becomes viscous and sticky if warmed. An aromatic terpenoid, THC has a very low solubility in water, but good solubility in most organic solvents such as butane or hexane. As is the case with nicotine and caffeine, the role of THC in Cannabis, it seems, is to protect the plant from herbivores. THC also possesses high UV-B 280-315 nm absorption properties and it seems likely that this protects the seed buds from potentially harmful radiation. THC is also a neuroprotective antioxidant.6 Dronabinol is the International Nonproprietary Name INN of THC. It is sold as Marinol® a registered trademark of Solvay Pharmaceuticals. Contents 1 Pharmacology 1.1 Toxicity 2 Research 3 Biosynthesis 4 Metabolism 5 Dronabinol 5.1 Comparisons to medical marijuana 5.2 Regulatory history 6 See also 7 References 8 External links Pharmacology The pharmacological actions of THC result from its binding to the cannabinoid receptor CB1, located in the central nervous system. The presence of these specialized receptors in the brain implied to researchers that endogenous cannabinoids are manufactured by the body, so the search began for a substance normally manufactured in the brain that binds to these receptors, the so-called natural ligand or agonist, leading to the eventual discovery of anandamide, 2-arachidonyl glyceride 2-AG, and other related compounds known as endocannabinoids. This story resembles the discovery of the endogenous opiates endorphins, enkephalins, and dynorphin, after the realization that morphine and other opiates bind to specific receptors in the brain. In addition, it has been shown that cannabinoids, through an unknown mechanism, activate endogenous opioid pathways via the μ1 opioid receptor, precipitating a dopamine release in the nucleus accumbens. The effects of the drug can be suppressed by the CB1 cannabinoid receptor antagonist rimonabant SR141716A as well as opioid receptor antagonists opioid blockers naloxone and naloxonazine.7 The mechanism of endocannabinoid synaptic transmission is believed to occur as follows: first, transmission of the excitatory neurotransmitter glutamate causes an influx of calcium ions into the post-synaptic neuron. Through a mechanism not yet fully understood, the presence of calcium post-synaptically induces the production of endocannabinoids in the post-synaptic neuron. These endocannabinoids such as anandamide are released into the synaptic cleft, where binding occurs at cannabinoid receptors present on pre-synaptic neurons, where they modulate neurotransmission. Thus, this form of neurotransmission is termed retrograde transmission, as the signal is carried in the opposite direction of orthodox propagation, which previously was thought to be exclusively one way. THC has mild to moderate analgesic effects, and medical cannabis can be used to treat pain. The mechanism for analgesic effects caused directly by THC or other cannabinoid agonists is not fully elucidated. Other effects include relaxation; euphoria; altered space-time perception; alteration of visual, auditory, and olfactory senses; disorientation; fatigue; and appetite stimulation. The mechanism for appetite stimulation in subjects is believed to result from activity in the gastro-hypothalamic axis. CB1 activity in the hunger centers in the hypothalamus increases the palatability of food when levels of a hunger hormone, ghrelin, increase as food enters the stomach. After chyme is passed into the duodenum, signaling hormones such as cholecystokinin and leptin are released, causing reduction in gastric emptying and transmission of satiety signals to the hypothalamus, respectively. Cannabinoid activity is reduced through the satiety signals induced by leptin release. It also has anti-emetic properties, and also may reduce aggression in certain subjects. THC has an active metabolite, 11-Hydroxy-THC, which may also play a role in the analgesic and recreational effects of cannabis. Toxicity Main article: LD50 of THC See also: Health issues and effects of cannabis According to the Merck Index, 12th ion, THC has a LD50 value of 1270 mg/kg male rats and 730 mg/kg female rats administered orally dissolved in sesame oil.8 The LD50 value for rats by inhalation of THC is 42 mg/kg of body weight. It is important to note, however, that toxicity in animal models does not necessarily correlate to human toxicity. THC receptor distribution in the rat central nervous system is different from that of humans, meaning that there is the significant possibility that toxicity in humans varies from the published animal LD50 studies. There has never been a documented fatality from marijuana.9 Absorption is limited by serum lipids, which can become saturated with THC, thus the inherent solubility may mitigate toxicity. In order to create a lethal overdose in a human, one would have to consume 1500 pounds in under 15 minutes.10 Studies of the distribution of the cannabinoid receptors in the brain explain why THC's toxicity is so low i.e., the LD50 of the compound is so large: parts of the brain that control vital functions such as respiration do not have many receptors, so they are relatively unaffected even by doses larger than could ever be ingested under any normal conditions. Research The original discovery appeared as Isolation, structure and partial synthesis of an active constituent of hashish, published in the Journal of the American Chemical Society in 1964.11 Research was also published in the academic journal Science, with Marihuana chemistry by Raphael Mechoulam in June 1970,12 followed by Chemical basis of hashish activity in August 1970.13 In the latter, the team of researchers from Hebrew University Pharmacy School and Tel Aviv University Medical School experimented on monkeys to isolate the active compounds in hashish. Their results provided evidence that, except for tetrahydrocannabinol, no other major active compounds were present in hash. A number of studies indicate that THC may provide medical benefits for cancer and AIDS patients by increasing appetite and decreasing nausea. It has been shown to assist some glaucoma patients by reducing pressure within the eye, and is used in the form of cannabis by a number of multiple sclerosis patients, who can use it to alleviate neuropathic pain and spasticity. The National Multiple Sclerosis Society is currently supporting research into these uses.14 New scientific evidence is showing that THC can prevent Alzheimer's Disease in an animal model by preventing the inflammation caused by microglia cells which are activated by binding of amyloid protein.15 Research in rats has indicated that THC prevented hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical Fenton reaction system and neuronal cultures.6 The long-term effects of THC on humans have been disputed because its status as an illegal drug makes research difficult. Preliminary research on synthetic THC has been conducted on patients with Tourette syndrome, with results suggesting that it may help in reducing nervous tics and urges by a significant degree. Animal studies suggested that Marinol and nicotine could be used as an effective adjunct to neuroleptic drugs in treating TS. Research on twelve patients showed that Marinol reduced tics with no significant adverse effects. A six-week controlled study on 24 patients showed the patients taking Marinol had a significant reduction in tic severity without serious adverse effects. Seven patients dropped out or had to be excluded from the study, one due to adverse side-effects. More significant reduction in tic severity was reported with longer treatment. No detrimental effects on cognitive functioning and a trend towards improvement in cognitive functioning were reported during and after treatment. Marinol's usefulness as a treatment for TS cannot be determined until/unless longer controlled studies on larger samples are undertaken.161718 Recent research has shown that many adverse side-effects, generally known as the stoner stereotype, fail to hold up to the scientific method. Recent studies with synthetic cannabinoids show that activation of CB1 receptors can facilitate neurogenesis, as well as neuroprotection, and can even help prevent natural neural degradation from neurodegenerative diseases such as MS, Parkinson's, and Alzheimer's. This, along with research into the CB2 receptor throughout the immune system, has given the case for medical marijuana more support.citation needed In in-vitro experiments, THC at extremely high concentrations, which could not be reached with commonly-consumed doses, caused inhibition of plaque formation, the cause of Alzheimer's disease, better than currently-approved drugs.19 THC may also be an effective anti-cancer treatment, with studies showing tumor size reduction in mice conducted in 197520 and 200721, as well as in a pilot study in humans with glioblastoma multiforme a type of brain cancer.22 On July 28, 2007, British medical journal The Lancet published a study that indicates that cannabis users have, on average, a 41% greater risk of developing psychosis than non-users. The risk was most pronounced in cases with an existing risk of psychotic disorder, and was said to grow up to 200% for the most-frequent users.23 Other studies have revealed similar associations, especially in individuals predisposed to psychosis prior to cannabis use.24 Recent research has also shown a correlation between cannabis use and increased cognitive function in schizophrenic patients.25 A two-year study in which rats and mice were force-fed tetrahydrocannabinol dissolved in corn oil showed reduced body mass, enhanced survival rates, and decreased tumor incidences in several sites, mainly organs under hormonal control. It also caused testicular atrophy and uterine and ovarian hypoplasia, as well as hyperactivity and convulsions immediately after administration.26 A 2008 study by the National Institutes of Health suggested that chronic heavy marijuana use might increase risk of heart attack or stroke, as these users showed elevated levels of apolipoprotein C-III, a risk factor for cardiovascular disease.27 The marijuana users in the study averaged smoking 78 to 350 marijuana cigarettes per week, i.e. between 2 and 9 ounces of marijauana or between $600 and $2700 a week. The study also only measured 18 long term smokers along with 24 others who do not use the drug. 2829 A 2008 study by the University of Melbourne found that daily, long-term marijuana use may be linked to abnormalities in parts of the brain.30 The daily long-term users consumed at least 5 marijuana cigarettes daily for on average 20 years. Among the 15 heavy marijuana users in the study, the hippocampus volume was 12 percent less and the amygdala volume was 7 percent less than in 16 men who were not marijuana users, the researchers said.31 In mice low doses of Δ9-THC reduce the progression of atherosclerosis.32 Biosynthesis Biosynthesis of THC Biosynthesis of THC In the cannabis plant THC occurs mainly as tetrahydrocannabinol carboxylic acid THC-COOH. The enzymatic condensation of geranyl pyrophosphate and olivetolic acid gives cannabigerolic acid which is cyclized by the enzyme THC acid synthase to give THC-COOH. Heating decarboxylates the acid to THC. Metabolism THC is mainly metabolized to 11-OH-THC 11-hydroxy-THC by the human body. This metabolite is still psychoactive and is further oxidized to 11-Nor-9-carboxy-THC THC-COOH. In humans and animals more than 100 metabolites could be identified but 11-OH-THC and THC-COOH are the dominating metabolites. Metabolism mainly occurs in the liver by cytochrome P450 enzymes CYP2C9, CYP2C19, and CYP3A4. More than 55% of THC are excreted in the feces and ~20% in the urine. The main metabolite in urine is the ester of glucuronic acid and THC-COOH and free THC-COOH. In the feces mainly 11-OH-THC was detected.33 Dronabinol Synthetic THC is known as dronabinol. It is available as a prescription drug under the trade name Marinol in several countries including the United States and Germany. In the United States, Marinol is a Schedule III drug, available by prescription, considered to be non-narcotic and to have a low risk of physical or mental dependence. Efforts to get cannabis rescheduled as analogous to Marinol have not succeeded thus far, though a 2002 petition has been accepted by the DEA. As a result of the rescheduling of Marinol from Schedule II to Schedule III, refills are now permitted for this substance. Marinol has been approved by the FDA in the treatment of anorexia in AIDS patients, as well as for refractory nausea and vomiting of patients undergoing chemotherapy, which has raised much controversy as to why natural THC is still a schedule I drug. An analog of dronabinol, nabilone, is available commercially in Canada under the trade name Cesamet, manufactured by Valeant. Cesamet has also received FDA approval and has began marketing in the U.S. as of 2006 and is a Schedule II drug. In April 2005, Canadian authorities approved the marketing of Sativex, a mouth spray for multiple sclerosis patients, who can use it to alleviate neuropathic pain and spasticity. Sativex contains tetrahydrocannabinol together with cannabidiol. It is marketed in Canada by GW Pharmaceuticals, being the first cannabis-based prescription drug in the world. Comparisons to medical marijuana Main article: Medical marijuana Picture of Marinol capsule Picture of Marinol capsule Isolated tetrahydrocannabinol is very expensive, costing for example $723.16 U.S. for 30 doses at 10 mg online, as of May, 2008.34 This is economically out of reach for most of the world's population, half of which lives on less than $2 U.S. per day.35363738 Medical marijuana, in comparison, can be grown from seed for little or no cost. Dronabinol is known to produce mild side-effects similar to cannabis. Some have posited that dronabinol lacks beneficial properties of cannabis, which contains more than 60 cannabinoids, including cannabidiol CBD, thought to be the major anti-convulsant that helps multiple sclerosis patients, and cannabichromene CBC, an anti-inflammatory which may contribute to the pain-killing effect of cannabis. Others have countered that the effects of all of cannabis's cannabinoids have not been completely studied and are not fully understood to be beneficial. It takes over one hour for Marinol to reach full systemic effect, compared to minutes for smoked or vaporized cannabis. Some patients accustomed to inhaling just enough cannabis smoke to manage symptoms have complained of too-intense intoxication via Marinol's predetermined dosages. This powerful psychoactive effect, however, has led to recreational use of Marinol.39 Many have said that Marinol produces a more acute psychedelic effect than cannabis and it has been speculated that this disparity can be explained by the moderating effect of the many non-THC cannibinoids present in cannabis, Marinol does not, however, contain the psychoactive effect found in the cannabis plant. Mark Kleiman, director of the Drug Policy Analysis Program at UCLA's School of Public Affairs had this to say about Marinol-- It wasn't any fun and made the user feel bad, Kleiman says, so it could be approved without any fear that it would penetrate the recreational market, and then used as a club with which to beat back the advocates of whole cannabis as a medicine.40 United States federal law currently registers Dronabinol as a Schedule III controlled substance, but all other Cannabis remains Schedule I, except Nabilone. Taking a Marinol pill to manage nausea can be ineffective because nausea can cause the pill to be ejected before it is absorbed by the body. Regulatory history Since at least 1986, the trend has been for THC in general, and especially the Marinol preparation, to be downgraded to less and less stringently-controlled schedules of controlled substances, in the U.S. and internationally. On July 13, 1986, the Drug Enforcement Administration DEA issued a Final Rule and Statement of Policy authorizing the Rescheduling of Synthetic Dronabinol in Sesame Oil and Encapsulated in Soft Gelatin Capsules From Schedule I to Schedule II DEA 51 FR 17476-78. This permitted medical use of Marinol, albeit with the severe restrictions associated with Schedule II status. For instance, refills of Marinol prescriptions were not permitted. At its 1045th meeting, on April 29, 1991, the Commission on Narcotic Drugs, in accordance with article 2, paragraphs 5 and 6, of the Convention on Psychotropic Substances, decided that Δ9-tetrahydrocannabinol also referred to as Δ9-THC and its stereochemical variants should be transferred from Schedule I to Schedule II of that Convention. This released Marinol from the restrictions imposed by Article 7 of the Convention5. An abstract published in the April-June 1998 issue of the Journal of Psychoactive Drugs found that Healthcare professionals have detected no indication of scrip-chasing or doctor-shopping among the patients for whom they have prescribed dronabinol6. The authors suggested that Marinol had a low potential for abuse. In 1999, Marinol was rescheduled from Schedule II to III of the Controlled Substances Act, reflecting a finding that THC had a potential for abuse less than that of cocaine, and heroin. This rescheduling comprised part of the argument for a 2002 petition for removal of cannabis from Schedule I of the Controlled Substances Act, in which petitioner Jon Gettman noted, Cannabis is a natural source of dronabinol THC, the ingredient of Marinol, a Schedule III drug. There are no grounds to schedule cannabis in a more restrictive schedule than Marinol41. At its 33rd meeting, the World Health Organization Expert Committee on Drug Dependence recommended transferring THC to Schedule IV of the Convention, citing its medical uses and low abuse potential. This would put THC in the Convention's least stringently-controlled Schedule. See also Cannabis drug Psychoactive drug Cannabinoids HU-210 WIN 55,212-2 Medical cannabis War on Drugs THC Ministry Cannabis rescheduling in the United States Cannabidiol, an isomer of THC Health issues and the effects of cannabis References ^ ChemIDplus Lite. chem.sis.nlm.nih.gov. Retrieved on 2008-08-08. ^ a b c d e Grotenhermen F 2003. Pharmacokinetics and pharmacodynamics of cannabinoids. Clin Pharmacokinet 42 4: 327-60. doi:10.2165/00003088-200342040-00003. PMID 12648025. ^ Gaoni, Yechiel; Raphael Mechoulam 1964. Isolation, structure and partial synthesis of an active constituent of hashish. Journal of the American Chemical Society 86 8: 1646-1647. doi:10.1021/ja01062a046. Retrieved on 2008-05-31. ^ Interview with the winner of the first ECNP Lifetime Achievement Award: Raphael Mechoulam, Israel February 2007 ^ Cannabinoids: A Secret History by Tom Geller, Chemical Heritage Newsmagazine, 25 2, Summer 2007. ^ a b Cannabidiol and -Δ9-tetrahydrocannabinol are neuroprotective antioxidants, A. J. Hampson, M. Grimaldi, J. Axelrod, and D. Wink, Proc Natl Acad Sci U S A. 1998 July 7; 9514: 8268-8273. ^ Lupica CR, Riegel AC, Hoffman AF. Marijuana and cannabinoid regulation of brain reward circuits. British Journal of Pharmacology. 2004 Sep;1432:227-34. PMID 15313883. doi:10.1038/sj.bjp.0705931 ^ Erowid. Cannabis Chemistry. Retrieved on 2006-03-20. ^ Walker JM, Huang SM. Cannabinoid analgesia. Pharmacology and Therapeutics. 2002 Aug;952:127-35. PMID 12182960 - ...to date, there are no deaths known to have resulted from overdose of cannabis. p. 128 ^ 1 What is the lethal dose of marijuana? ^ Gaoni, Yechiel; Raphael Mechoulam 1964. Isolation, structure and partial synthesis of an active constituent of hashish. Journal of the American Chemical Society 86 8: 1646-1647. doi:10.1021/ja01062a046. Retrieved on 2008-05-31. ^ Mechoulam, Raphael 5 June 1970. Marihuana Chemistry. Science 168 3936: 1159-1165. doi:10.1126/science.168.3936.1159. PMID 4910003. Retrieved on 2008-05-31. ^ Mechoulam, Raphael; Arnon Shani, Habib Edery, and Yona Grunfeld 7 August 1970. Chemical Basis of Hashish Activity. Science 169 3945: 611-612. doi:10.1126/science.169.3945.611. PMID 4987683. Retrieved on 2008-05-31. ^ 2 ^ RamÃrez BG, Blázquez C, Gómez del Pulgar T, Guzmán M, de Ceballos ML 2005. Prevention of Alzheimer's disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation. J. Neurosci. 25 8: 1904-13. doi:10.1523/JNEUROSCI.4540-04.2005. PMID 15728830. ^ Müller-Vahl,K.R. Schneider,U. Koblenz,A. Jöbges,M. Kolbe,H. Daldrup,T. Emrich,H.M. 2002. Treatment of Tourette's Syndrome with Δ9-Tetrahydrocannabinol THC: A Randomized Crossover Trial. Pharmacopsychiatry 35 2: 57-61. doi:10.1055/s-2002-25028. PMID 11951146. ^ Müller-Vahl KR, Schneider U, Prevedel H, Theloe K, Kolbe H, Daldrup T, Emrich HM. April 2003. Delta 9-tetrahydrocannabinol THC is effective in the treatment of tics in Tourette syndrome: a 6-week randomized trial. J Clin Psychiatry 64 4: 459-65. PMID 12716250. ^ Muller-Vahl KR, Prevedel H, Theloe K, Kolbe H, Emrich HM, Schneider U. February 2003. Treatment of Tourette syndrome with delta-9-tetrahydrocannabinol delta 9-THC: no influence on neuropsychological performance. Neuropsychopharmacology 28 2: 384-388. doi:10.1038/sj.npp.1300047. PMID 12589392. ^ Eubanks LM, Rogers CJ, Beuscher AE, et al 2006. A molecular link between the active component of marijuana and Alzheimer's disease pathology. Mol. Pharm. 3 6: 773-7. doi:10.1021/mp060066m. PMID 17140265. ^ Munson AE, Harris LS, Friedman MA, Dewey WL, Carchman RA. Anticancer activity of cannabinoids. Journal of the National Cancer Institute. September 1975;553:597-602. Accessed 2007-10-27. ^ Preet A, Ganju RK, Groopman JE. Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene. 2008 Jan 10;273:339-46. PMID 17621270. doi:10.1038/sj.onc.1210641 ^ Guzmán M, Duarte MJ, Blázquez C, Ravina J, Rosa MC, Galve-Roperh I et al. A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer. 2006 Jul 17;952:197-203. PMID 16804518. doi:10.1038/sj.bjc.6603236 ^ Moore TH, Zammit S, Lingford-Hughes A, Barnes TR, Jones PB, Burke M, Lewis G. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007 Jul 28;3709584:319-28. PMID 17662880. doi:10.1016/S0140-67360761162-3 ^ Henquet C, Krabbendam L, Spauwen J, Kaplan C, Lieb R, Wittchen HU, van Os J. Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ. 2005 Jan 1;3307481:11. PMID 15574485. doi:10.1136/bmj.38267.664086.63 ^ Coulston CM, Perdices M, Tennant CC. The neuropsychological correlates of cannabis use in schizophrenia: Lifetime abuse/dependence, frequency of use, and recency of use. Schizophrenia Research 2007; 961-3:169-184. ^ Chan PC, Sills RC, Braun AG, Haseman JK, Bucher JR 1996. Toxicity and carcinogenicity of delta 9-tetrahydrocannabinol in Fischer rats and B6C3F1 mice. Fundamental and applied toxicology : official journal of the Society of Toxicology 30 1: 109-17. PMID 8812248. ^ Jayanthi S, Buie S, Moore S, Herning RI, Better W, Wilson NM, et al. Heavy marijuana users show increased serum apolipoprotein C-III levels: evidence from proteomic analyses. Molecular Psychiatry. 2008 May 13. Epub ahead of print PMID 18475272. doi:10.1038/mp.2008.50 ^ Marijuana may up heart attack, stroke risk: study, Reuters. ^ Marijuana may up heart attack, stroke risk-if you smoke 2-9 Oz. a week, NORML.org. ^ Long-term marijuana use linked to brain abnormalities, CBC. ^ Heavy marijuana use shrinks brain parts - study, Reuters. ^ Steffens S, Veillard NR, Arnaud C, et al 2005. Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. Nature 434 7034: 782-6. doi:10.1038/nature03389. PMID 15815632. ^ Huestis MA 2005. Pharmacokinetics and metabolism of the plant cannabinoids, Δ9-tetrahydrocannabinol, cannabidiol and cannabinol. Handb Exp Pharmacol 168: 657-90. PMID 16596792. ^ Compare Marinol Prices on PharmacyChecker.com. www.pharmacychecker.com. Retrieved on 2008-05-31. ^ More Than Half the World Lives on Less Than $2 a Day - Population Reference Bureau. www.prb.org. Retrieved on 2008-08-08. ^ Poverty Facts and Stats - Global Issues. www.globalissues.org. Retrieved on 2008-08-08. ^ HDR 2007/2008 - Human Development Reports UNDP. hdr.undp.org. Retrieved on 2008-08-08. ^ Nations Online, World Population by continents and countries. www.nationsonline.org. Retrieved on 2008-08-08. ^ 3 ^ Greenberg, Gary 2005-11-01. Respectable Reefer, Mother Jones. Retrieved on 2007-04-03. ^ 4 Calhoun, S. R., Galloway, G. P., and Smith, D. E. 1998. Abuse potential of dronabinol Marinol. Journal of Psychoactive Drugs, 30, 187-196. DEA Moves Marinol To Schedule Three, But Leaves Marijuana in Schedule One. The Magic of Sesame Oil, Richard Cowan, MarijuanaNews.Com. Petition to Reschedule Cannabis Marijuana per 21 CFR §1308.44b, Filed October 9, 2002 with the DEA by the Coalition for Rescheduling Cannabis. External links Marijuana research: Current restrictions on marijuana research are absurd, by the ors of Scientific American, November 2004 Compounds found in Cannabis Sativa, Erowid Cannabis Vault Cannabinoid Chemistry in Cannabinoids: A Secret History by Tom Geller, Chemical Heritage Newsmagazine, 25 2, Summer 2007. Machinery of the marijuana munchies Resurrection of the Higher Self by Matthew Webb http://www.marinol.com/ Is Marinol better medicine than marijuana? Debate on Marinol in a pro-con format v d e Cannabinoids Plant cannabinoids CBD CBDV CBN CBG CBV CBL THC THC-C4 THCV Cannabinoid metabolites 11-Hydroxy-THC 11-nor-9-Carboxy-THC Endogenous cannabinoids Arachidonoyl ethanolamide Anandamide or AEA 2-Arachidonoylglycerol 2-AG 2-Arachidonyl glyceryl ether noladin ether Virodhamine N-arachidonoyl-dopamine NADA; Oleamide Synthetic cannabinoid agonists Classical cannabinoids Dibenzopyrans A-41988 Ajulemic acid AM-087 AM-411 AM-855 AM-905 AM-906 AM-919 AM-938 AM-4030 AMG-1 AMG-3 AMG-36 AMG-41 Dexanabinol HU-211 DMHP Dronabinol HU-210 JWH-051 JWH-133 JWH-139 L-759,633 L-759,656 Levonantradol Nabilone Nabitan O-806 O-823 O-1057 O-1125 O-1238 O-2545 O-2694 Parahexyl THC-O-acetate THC-O-phosphate Nonclassical cannabinoids CP 47,497 CP 55,244 CP 55,940 HU-308 2-Isopropyl-5-methyl-1-2,6-dihydroxy-4-nonylphenylcyclohex-1-ene Aminoalkylindoles AM-630 AM-1241 JWH-015 JWH-018 JWH-073 JWH-081 JWH-200 L-768,242 Pravadoline WIN 55,212-2 Aminoalkylpyrroles JWH-030 JWH-147 JWH-307 Eicosanoids AM-883 Arachidonyl-2'-chloroethylamide Arachidonylcyclopropylamide Methanandamide O-585 O-689 O-1812 O-1860 O-1861 Others BAY 38-7271 BAY 59-3074 GW 842,166X JWH-171 O-2220 Endocannabinoid activity enhancers AM-404 CAY-10401 CAY-10402 N-arachidonoyl-serotonin O-1624 PF-622 PF-750 URB-597 URB-602 URB-754 Cannabinoid antagonists and inverse agonists AM-251 AM-281 AM-630 AVE-1625 BML-190 CAY-10508 CB-25 CB-52 JTE-907 LY-320,135 MK-9470 NESS-0327 O-1184 O-2050 O-2654 Rimonabant SLV-319 SR-144,528 Surinabant Taranabant VCHSR v d e Antiemetics and antinauseants A04 Serotonin 5-HT3 antagonists Azasetron Dolasetron Ondansetron Granisetron Palonosetron Ramosetron Tropisetron Dopamine antagonists Alizapride Domperidone Metoclopramide Metopimazine Prochlorperazine Antihistamines Cyclizine Meclizine Promethazine NK1 receptor antagonists Aprepitant Casopitant Fosaprepitant Cannabinoids Dronabinol Nabilone Benzodiazepines Lorazepam Midazolam Anticholinergics Scopolamine Corticosteroids Dexamethasone Other Cerium oxalate Chlorobutanol Propofol Trimethobenzamide v d e Anesthetic: Ancient anaesthesia Plants/animals Aconite Argyreia speciosa Castoreum Cannabis Coca Deadly nightshade Henbane Lactucarium Mandrake Metel nut Opium Poison hemlock Saussurea Toloatzin Willow People Abulcasis Avicenna Celsus Dioscorides Galen Hippocrates Rhazes SabuncuoÄŸlu Susrutha Theophrastus Zhang Molecules Aconitine Δ9-THC Atropine Cocaine Coniine Hyoscyamine Morphine Salicylate Scopolamine Retrieved from http://en..org/wiki/Tetrahydrocannabinol Categories: Cannabinoids | Amorphous solids | AntiemeticsHidden categories: All articles with statements | Articles with statements since February 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Bosanski БългарÑ?ки Català Česky Cymraeg Dansk Deutsch Español Français Galego Hrvatski Italiano עברית Lietuvių Magyar Nederlands 日本語 ‪Norsk bokmÃ¥l‬ Polski Português Română РуÑ?Ñ?кий SlovenÄ?ina SlovenÅ¡Ä?ina СрпÑ?ки / Srpski Suomi Svenska ไทย Türkçe УкраїнÑ?ька This page was last modified on 26 August 2008, at 13:4
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