Cannabidiol

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Not to be confused with Cannabinol.
Cannabidiol
Systematic (IUPAC) name
2-[(1R,6R)-6-isopropenyl-3-methylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
Clinical data
AHFS/Drugs.com International Drug Names
Pregnancy cat.  ?
Legal status Schedule I (US) Schedule II (Can)
Identifiers
CAS number 13956-29-1 YesY
ATC code None
PubChem CID 644019
ChemSpider 24593618 YesY
UNII 19GBJ60SN5 YesY
Chemical data
Formula C21H30O2 
Mol. mass 314.4636
Physical data
Melt. point 66 °C (151 °F)
Boiling point 180 °C (356 °F)
(Range: 160°C-180°C) [1]
 N (what is this?)  (verify)

Cannabidiol (CBD) is one of at least 85 cannabinoids found in cannabis.[2] It is a major constituent of the plant, second to THC, and represents up to 40% in its extracts.[3] Compared with THC, cannabidiol is non-psychoactive, and is considered to have a wider scope of medical applications than THC,[citation needed] including to epilepsy,[4] multiple sclerosis spasms,[5] anxiety disorders, schizophrenia,[6] nausea, convulsion and inflammation, as well as inhibiting cancer cell growth.[7] CBD may decrease the rate of THC clearance from the body, perhaps by interfering with the metabolism of THC in the liver. Cannabidiol has displayed sedative effects in animal tests.[8] Other research indicates that CBD increases alertness.[9] CBD has been shown to reduce growth of aggressive human breast cancer cells in vitro, and to reduce their invasiveness.[10]

Contents

Clinical applications and use [edit]

The bud of a Cannabis sativa flower coated with trichomes, which contain more CBD than any other part of the plant.[citation needed]

Cannabidiol's strong antioxidant properties have been shown to play a role in the compound's neuroprotective and anti-ischemic effects.[7]

Studies have shown cannabidiol decreases activity of the limbic system[11] and decreases social isolation induced by THC.[12] Cannabidiol has also been shown to reduce anxiety in social anxiety disorder.[13][14]

Cannabidiol has proven effective in treating an often drug-induced set of neurological movement disorders known as dystonia.[15] In one study, five out of five participants showed noted improvement in their dystonic symptoms by 20-50%.[16][16][15]

In 1985 a single case study suggested that CBD may be effective in the management of levodopa-induced dyskinesia in a Parkinson's Disease patient.[17]

Effects on the brain [edit]

A 2010 study found that strains of cannabis containing higher concentrations of cannabidiol did not produce short-term memory impairment vs. strains with similar concentrations of THC, but lower concentrations of CBD.[18] The researchers attributed this attenuation of memory effects to CBD's role as a CB1 antagonist.[19] CBD also appears to protect against 'binge' alcohol induced neurodegeneration.[20][21]

Recent studies have shown cannabidiol to be as effective as atypical antipsychotics in treating schizophrenia.[22] Studies have shown CBD may reduce schizophrenic symptoms due to its apparent ability to stabilize disrupted or disabled NMDA receptor pathways in the brain, which are shared and sometimes contested by norepinephrine and GABA.[22][23] Leweke et al. performed a double blind, 4 week, explorative controlled clinical trial to compare the effects of purified cannabidiol and the atypical antipsychotic amisulpride on improving the symptoms of schizophrenia in 42 patients with acute paranoid schizophrenia. Both treatments were associated with a significant decrease of psychotic symptoms after 2 and 4 weeks as assessed by Brief Psychiatric Rating Scale and Positive and Negative Syndrome Scale. While there was no statistical difference between the two treatment groups, cannabidiol induced significantly fewer side effects (extrapyramidal symptoms, increase in prolactin, weight gain) when compared to amisulpride.[24]

A 2008 study published in the British Journal of Psychiatry showed significant differences in the Oxford-Liverpool Inventory of Feelings and Experiences scores between three groups: the first consisted of non-cannabis users, the second consisted of users with THC detected, and the third consisted of users with both THC and CBD detected. The THC-only group scored significantly higher for unusual experiences than the THC-and-CBD group, whereas the THC-and-CBD group had significantly lower introvertive anhedonia scores than the THC-only group and the non-cannabis user group. This research indicates that CBD acts as an anti-psychotic and may counteract the potential psychotomimetic effects of THC on individuals with latent schizophrenia.[25]

Cancer research [edit]

In November 2007, researchers at the California Pacific Medical Center reported that CBD shows promise for controlling the spread of metastatic breast cancer. In vitro CBD down-regulates, or "turns off", the activity of ID1, the gene responsible for tumor metastasis[10] in breast and other types of cancers, including the particularly aggressive triple negative breast cancer.[26][27][28] The researchers in September 2012 said they hope to start human trials soon.[29]

Cannabidiol has been shown to inhibit cancer cell growth with low potency in non-cancer cells. Although the inhibitory mechanism is not yet fully understood, Ligresti et al. suggest that "cannabidiol exerts its effects on these cells through a combination of mechanisms that include either direct or indirect activation of CB2 and TRPV1 receptors, and induction of oxidative stress, all contributing to induce apoptosis."[30]

Non-psychoactive cannabinoids, including cannabidiol (CBD) and other more pronounced CB2 agonists such as cannabinol (CBN, an immunosuppressant), are now seen as promising targets for anti-tumor drugs since they experimentally reduce the size of in-vivo xenografts, for example gliomas. Combinations of submaximal THC doses and CBD have both been successfully applied to greatly increase in-vitro efficacy of temozolomide in glioblastoma multiforme cell lines. CBD likely exerts its effects through the induction of apoptosis by Reactive oxygen species.[31] Non-psychoactive cannabinoids can be administered at much higher doses without the well-known side effects that are sometimes associated with the drop-out rate in trials involving psychoactive cannabinoids.

A team of researchers from the University of California at Irvine proposed in February 2013 that CBD's anti-malignant effect by way of apoptosis may be due to its potential action on "mutant p53 proteins in cancer cells," due to cannabidiol's chemo-physical similarity to stictic acid, a promising anti-cancer compound found in some species of lichens that acts on the aforementioned proteins. The University biologists, chemists and computer scientists "identified an elusive pocket on the surface of the p53 protein that can be targeted by cancer-fighting drugs".[32][33]

CBD enhanced cannabis [edit]

In November 2012, an Israeli medical cannabis facility announced a new strain of the plant which has only cannabidiol as an active ingredient, and virtually no THC, providing some of the medicinal benefits of cannabis without the euphoria.[34][35] The researchers said the cannabis plant, enriched with CBD, "can be used for treating diseases like rheumatoid arthritis, colitis, liver inflammation, heart disease and diabetes". Research on CBD enhanced cannabis began in 2009, resulting in Avidekel, a cannabis strain that contains 15.8% CBD and less than 1% THC. Raphael Mechoulam, leading cannabinoid researcher, noted "It is possible that (Avidekel's) CBD to THC ratio is the highest among medical marijuana companies in the world, but the industry is not very organised, so one cannot keep exact track of what each company is doing".[36]

Pharmacology [edit]

Cannabidiol has a very low affinity for CB1 and CB2 receptors but acts as an indirect antagonist of their agonists.[7][37] While one would assume that this would cause cannabidiol to reduce the effects of THC, it may potentiate THC's effects by increasing CB1 receptor density or through another CB1-related mechanism.[38] It is also an inverse agonist of CB2 receptors.[7][37] Recently, it was found to be an antagonist at the putative new cannabinoid receptor, GPR55, a GPCR expressed in the caudate nucleus and putamen.[39] Cannabidiol has also been shown to act as a 5-HT1A receptor agonist,[40] an action which is involved in its antidepressant,[41][42] anxiolytic,[42][43] and neuroprotective[44][45] effects. Cannabidiol is an allosteric modulator of μ and δ-opioid receptors.[46] Cannabidiol's pharmacologial effects have also been attributed to PPAR-γ receptor agonism and intracellular calcium release.[47]

Pharmaceutical preparations [edit]

A CBD extract made from industrial hemp was introduced to the US market in 2012. Because the FDA considers cannabinoids derived from hemp to be "food-based" products, no legal restrictions exist.[48]

Nabiximols (USAN, trade name Sativex) is an aerosolized mist for oral administration containing a near 1:1 ratio of CBD and THC. The drug was approved by Canadian authorities in 2005 to alleviate pain associated with multiple sclerosis.[49][50][51]

Chemistry [edit]

Cannabidiol is insoluble in water but soluble in organic solvents, such as pentane. At room temperature it is a colorless crystalline solid.[52] In strongly basic medium and the presence of air it is oxidized to a quinone.[53] Under acidic conditions it cyclizes to THC.[54] The synthesis of cannabidiol has been accomplished by several research groups.[55][56][57]

Biosynthesis [edit]

Cannabis produces CBD-carboxylic acid through the same metabolic pathway as THC, until the last step, where CBDA synthase performs catalysis instead of THCA synthase.[58]

Natural occurrence [edit]

Main article: Medical cannabis#Difference between C. indica and C. sativa

Cannabis indica may have a CBD:THC ratio 3–5 times that of Cannabis sativa.

Legal Status [edit]

CBD is in Schedule I in the United States. It is included in the DEA material under "Tetrahydrocannabinols," which is a broad category that encompasses all the phytocannabinoids as analogs of THC. Its DEA # is 7372, and it remains illegal.[59]

Tetrahydrocannabinols, both naturally and synthetically occurring, are currently classified under Schedule I of the US Controlled Substances Act.[60]

Cannabidiol is a Schedule 2 Drug in Canada.[61]

See also [edit]

References [edit]

  1. ^ McPartland, JM; Russo, EB (2001). "Cannabis and Cannabis Extracts: Greater Than the Sum of Their Parts?". Journal of Cannabis Therapeutics (PDF) 1 (3/4): 103–132. doi:10.1300/J175v01n03_08. 
  2. ^ El-Alfy, Abir T, et al. (Jun 2010). "Antidepressant-like effect of delta-9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L". Pharmacology Biochemistry and Behavior 95 (4): 434–42. doi:10.1016/j.pbb.2010.03.004. PMC 2866040. PMID 20332000 
  3. ^ Grlić, Ljubiša (1962). "A comparative study on some chemical and biological characteristics of various samples of cannabis resin". Bulletin on Narcotics (UNODC) (3): 37–46. 
  4. ^ http://www.advancedholistichealth.org/PDF_Files/The%20anti-convulsant%20activity%20of%20CBD.pdf
  5. ^ Cannabidiol inhibits pathogenic T cells, decr... [Br J Pharmacol. 2011] - PubMed - NCBI
  6. ^ Brazilian Journal of Medical and Biological Research - Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug
  7. ^ a b c d Mechoulam, R.; M. Peters, Murillo-Rodriguez (21 Aug 2007). "Cannabidiol - recent advances". Chemistry & Biodiversity 4 (8): 1678–1692. doi:10.1002/cbdv.200790147. PMID 17712814. 
  8. ^ Pickens JT (1981). "Sedative activity of cannabis in relation to its delta'-trans-tetrahydrocannabinol and cannabidiol content". Br. J. Pharmacol. 72 (4): 649–56. doi:10.1111/j.1476-5381.1981.tb09145.x. PMC 2071638. PMID 6269680. 
  9. ^ Nicholson, AN; C Turner, BM Stone, and PJ Robson (June 2004). "Effect of Delta-9-tetrahydrocannabinol and cannabidiol on nocturnal sleep and early-morning behavior in young adults" (fee required). J Clin Psychopharmacol 24 (3): 305–13. doi:10.1097/01.jcp.0000125688.05091.8f. ISSN 0271-0749. PMID 15118485. Retrieved 2007-05-03. 
  10. ^ a b McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY (2007). "Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells". Mol. Cancer Ther. 6 (11): 2921–7. doi:10.1158/1535-7163.MCT-07-0371. PMID 18025276. 
  11. ^ José Alexandre de Souza Crippa, Antonio Waldo Zuardi, Griselda E J Garrido, Lauro Wichert-Ana, Ricardo Guarnieri, Lucas Ferrari, Paulo M Azevedo-Marques, Jaime Eduardo Cecílio Hallak, Philip K McGuire and Geraldo Filho Busatto (October 2003). "Effects of Cannabidiol (CBD) on Regional Cerebral Blood Flow". Neuropsychopharmacology 29 (2): 417–426. doi:10.1038/sj.npp.1300340. PMID 14583744. 
  12. ^ Daniel Thomas Malone, Dennis Jongejana and David Alan Taylora (August 2009). "Cannabidiol reverses the reduction in social interaction produced by low dose Δ9-tetrahydrocannabinol in rats". Pharmacology Biochemistry and Behavior 93 (2): 91–96. doi:10.1016/j.pbb.2009.04.010. PMID 19393686. 
  13. ^ Mateus M Bergamaschi, Regina Helena Costa Queiroz, Marcos Hortes Nisihara Chagas, Danielle Chaves Gomes de Oliveira, Bruno Spinosa De Martinis, Flávio Kapczinski, João Quevedo, Rafael Roesler, Nadja Schröder, Antonio E Nardi, Rocio Martín-Santos, Jaime Eduardo Cecílio (may 2011). "Cannabidiol Reduces the Anxiety Induced by Simulated Public Speaking in Treatment-Naïve Social Phobia Patients". Neuropsychopharmacology 36 (6): 1219–1226. doi:10.1038/npp.2011.6. PMC 3079847. PMID 21307846. 
  14. ^ Crippa JA, Derenusson GN, Ferrari TB, Wichert-Ana L, Duran FL, Martin-Santos R, Simões MV, Bhattacharyya S, Fusar-Poli P, Atakan Z, Santos Filho A, Freitas-Ferrari MC, McGuire PK, Zuardi AW, Busatto GF, Hallak JE. (January 2011). "Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder: a preliminary report". J Psychopharmacol. 25 (1): 121–130. doi:10.1177/0269881110379283. PMID 20829306. 
  15. ^ a b Snider, Stuart R.; Consroe, Paul (1985). "Beneficial and Adverse Effects of Cannabidiol in a Parkinson Patient with Sinemet-Induced Dystonic Dyskinesia". Neurology (Suppl 1): 201. 
  16. ^ a b Consroe, P.; Sandyk, R.; Snider, S. R. (1986). "Open label evaluation of cannabidiol in dystonic movement disorders". The International journal of neuroscience 30 (4): 277–282. doi:10.3109/00207458608985678. PMID 3793381.  edit
  17. ^ Snider, SR; Consroe P (1985). "Beneficial and adverse effects of cannabidiol in a Parkinson patient with sinemet-induced dystonic dyskinesia". Neurology 35: 201. 
  18. ^ Frood, A. (2010). "Key ingredient staves off marijuana memory loss". Nature. doi:10.1038/news.2010.508.  edit
  19. ^ Morgan, C. J.; Schafer, G.; Freeman, T. P.; Curran, H. V. (October 2010). "Impact of cannabidiol on the acute memory and psychotomimetic effects of smoked cannabis: naturalistic study: naturalistic study [corrected]". British Journal of Psychiatry 197 (4): 285–90. doi:10.1192/bjp.bp.110.077503. PMID 20884951. 
  20. ^ http://dx.doi.org/10.1124/jpet.105.085779 Comparison of Cannabidiol, Antioxidants, and Diuretics in Reversing Binge Ethanol-Induced Neurotoxicity
  21. ^ http://www.ncbi.nlm.nih.gov/pubmed/19631736 White matter integrity in adolescents with histories of marijuana use and binge drinking.
  22. ^ a b Zuardi, A.W; J.A.S. Crippa, J.E.C. Hallak, F.A. Moreira, F.S. Guimarães (2006). "Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug" (PDF). Braz. J. Med. Biol. Res. 39 (4): 421–429. doi:10.1590/S0100-879X2006000400001. PMID 16612464. 
  23. ^ Neuropsychopharmacology - Abstract of article: Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice
  24. ^ Leweke, FM; Piomelli D, Pahlisch F, Muhl D, Gerth CW, Hoyer C, Klosterkötter J, Hellmich M and Koethe D. (2012). "Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia" (PDF). Translational Psychiatry 2 (3): e94. doi:10.1038/tp.2012.15. 
  25. ^ Morgan, Celia J. A.; Curran, H. Valerie (2008). "Effects of cannabidiol on schizophrenia-like symptoms in people who use cannabis". British Journal of Psychiatry 192 (4): 306–307. doi:10.1192/bjp.bp.107.046649. PMID 18378995.  edit
  26. ^ Pot compound seen as tool against cancer - SFGate
  27. ^ Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells
  28. ^ Antitumor activity of plant cannabinoid... [J Pharmacol Exp Ther. 2006] - PubMed - NCBI
  29. ^ Marijuana Compound Fights Cancer; Human Trials Next | NBC Bay Area
  30. ^ Ligresti A, Moriello AS, Starowicz K, et al. (2006). "Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma". J. Pharmacol. Exp. Ther. 318 (3): 1375–87. doi:10.1124/jpet.106.105247. PMID 16728591. 
  31. ^ Velasco G et al. (January 2011). "A Combined Preclinical Therapy of Cannabinoids and Temozolomide against Glioma." Mol Cancer Ther 10:90-103 doi: 10.1371/journal.pone.0054795
  32. ^ UCI team finds new target for treating wide spectrum of cancers | UCIrvine News
  33. ^ Computational identification of a transiently open L1/S3 pocket for reactivation of mutant p53 : Nature Communications : Nature Publishing Group
  34. ^ CNN Video - Breaking News Videos from CNN.com
  35. ^ http://www.wired.com/wiredscience/2012/07/marijuana-high-arthritis/
  36. ^ http://www.reuters.com/article/2012/07/03/uk-israel-marijuana-idUSLNE86201S20120703
  37. ^ a b Pertwee, R. G. (2008). "The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: Δ9-tetrahydrocannabinol, cannabidiol and Δ9-tetrahydrocannabivarin". British Journal of Pharmacology 153 (2): 199–215. doi:10.1038/sj.bjp.0707442. PMC 2219532. PMID 17828291.  edit
  38. ^ Hayakawa, K.; Mishima, K.; Hazekawa, M.; Sano, K.; Irie, K.; Orito, K.; Egawa, T.; Kitamura, Y. et al. (2008). "Cannabidiol potentiates pharmacological effects of Δ9-tetrahydrocannabinol via CB1 receptor-dependent mechanism". Brain Research 1188: 157–164. doi:10.1016/j.brainres.2007.09.090. PMID 18021759.  edit
  39. ^ Ryberg E, Larsson N, Sjögren S, et al. (2007). "The orphan receptor GPR55 is a novel cannabinoid receptor". British Journal of Pharmacology 152 (7): 1092–101. doi:10.1038/sj.bjp.0707460. PMC 2095107. PMID 17876302. 
  40. ^ Russo EB, Burnett A, Hall B, Parker KK (August 2005). "Agonistic properties of cannabidiol at 5-HT1a receptors". Neurochemical Research 30 (8): 1037–43. doi:10.1007/s11064-005-6978-1. PMID 16258853. 
  41. ^ Zanelati T, Biojone C, Moreira F, Guimarães F, Joca S (December 2009). "Antidepressant-like effects of cannabidiol in mice: possible involvement of 5-HT1A receptors". British Journal of Pharmacology 159 (1): 122–8. doi:10.1111/j.1476-5381.2009.00521.x. PMC 2823358. PMID 20002102. 
  42. ^ a b Resstel LB, Tavares RF, Lisboa SF, Joca SR, Corrêa FM, Guimarães FS (January 2009). "5-HT1A receptors are involved in the cannabidiol-induced attenuation of behavioural and cardiovascular responses to acute restraint stress in rats". British Journal of Pharmacology 156 (1): 181–8. doi:10.1111/j.1476-5381.2008.00046.x. PMC 2697769. PMID 19133999. 
  43. ^ Campos AC, Guimarães FS (August 2008). "Involvement of 5HT1A receptors in the anxiolytic-like effects of cannabidiol injected into the dorsolateral periaqueductal gray of rats". Psychopharmacology 199 (2): 223–30. doi:10.1007/s00213-008-1168-x. PMID 18446323. 
  44. ^ Mishima K, Hayakawa K, Abe K, et al. (May 2005). "Cannabidiol prevents cerebral infarction via a serotonergic 5-hydroxytryptamine1A receptor-dependent mechanism". Stroke; a Journal of Cerebral Circulation 36 (5): 1077–82. doi:10.1161/01.STR.0000163083.59201.34. PMID 15845890. 
  45. ^ Hayakawa K, Mishima K, Nozako M, et al. (March 2007). "Repeated treatment with cannabidiol but not Delta9-tetrahydrocannabinol has a neuroprotective effect without the development of tolerance". Neuropharmacology 52 (4): 1079–87. doi:10.1016/j.neuropharm.2006.11.005. PMID 17320118. 
  46. ^ Kathmann, Markus; Flau, Karsten; Redmer, Agnes; Tränkle, Christian; Schlicker, Eberhard (2006). "Cannabidiol is an allosteric modulator at mu- and delta-opioid receptors". Naunyn-Schmiedeberg's Archives of Pharmacology 372 (5): 354–361. doi:10.1007/s00210-006-0033-x. PMID 16489449.  edit
  47. ^ Campos, A. C.; Moreira, F. A.; Gomes, F. V.; Del Bel, E. A.; Guimaraes, F. S. (2012). "Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders". Philosophical Transactions of the Royal Society B: Biological Sciences 367 (1607): 3364–3378. doi:10.1098/rstb.2011.0389. PMC 3481531. PMID 23108553.  edit
  48. ^ Dixie Launches Cannabidiol-Based Dixie Products | Dixie Elixirs & Edibles
  49. ^ United States Adopted Names Council: Statement on a nonproprietary name
  50. ^ "Fact Sheet - Sativex". Health Canada. Retrieved 16 May 2013. 
  51. ^ GWPharma - Welcome
  52. ^ Jones PG, Falvello L, Kennard O, Sheldrick GM Mechoulam R (1977). "Cannabidiol". Acta Cryst. B33 (10): 3211–3214. doi:10.1107/S0567740877010577. 
  53. ^ Mechoulam R, Ben-Zvi Z (1968). "Hashish—XIII On the nature of the beam test". Tetrahedron 24 (16): 5615–5624. doi:10.1016/0040-4020(68)88159-1. PMID 5732891. 
  54. ^ Gaoni Y, Mechoulam R (1966). "Hashish—VII The isomerization of cannabidiol to tetrahydrocannabinols". Tetrahedron 22 (4): 1481–1488. doi:10.1016/S0040-4020(01)99446-3. 
  55. ^ Petrzilka T, Haefliger W, Sikemeier C, Ohloff G, Eschenmoser A (1967). "Synthese und Chiralität des (-)-Cannabidiols". Helv. Chim. Acta 50 (2): 719–723. doi:10.1002/hlca.19670500235. PMID 5587099. 
  56. ^ Gaoni Y, Mechoulam R (1985). "Boron trifluoride etherate on alumuna - a modified Lewis acid reagent. An improved synthesis of cannabidiol". Tetrahedron Letters 26 (8): 1083–1086. doi:10.1016/S0040-4039(00)98518-6. 
  57. ^ Kobayashi Y, Takeuchi A, Wang YG (2006). "Synthesis of cannabidiols via alkenylation of cyclohexenyl monoacetate". Org. Lett. 8 (13): 2699–2702. doi:10.1021/ol060692h. PMID 16774235. 
  58. ^ Marks, M.; Tian, L.; Wenger, J.; Omburo, S.; Soto-Fuentes, W.; He, J.; Gang, D.; Weiblen, G. et al. (2009). "Identification of candidate genes affecting Δ9-tetrahydrocannabinol biosynthesis in Cannabis sativa". Journal of Experimental Botany 60 (13): 3715–3726. doi:10.1093/jxb/erp210. PMC 2736886. PMID 19581347.  edit
  59. ^ DEA Form 225 - Application for Registration - Manufacturer, Distributor, Researcher, Analytical Laboratory, Importer, Exporter
  60. ^ Section 1308.11 Schedule I
  61. ^ http://laws.justice.gc.ca/en/showdoc/cs/C-38.8//20090606/en?command=search&caller=SI&fragment=schedule%201&search_type=all&day=6&month=6&year=2009&search_domain=cs&showall=L&statuteyear=all&lengthannual=50&length=50&offset=2

External links [edit]

  • Erowid Compounds found in Cannabis sativa
  • Project CBD Non-profit educational service dedicated to promoting and publicizing research into the medical utility of cannabidiol.
General
Cannabis strains
with subset strains
Pure indica
Indica-dominant
Pure sativa
Sativa-dominant
Usage
General
Preparations
Consumption
Phytocannabinoids
Effects
Culture
Pro-Cannabis
organizations
Use demographics
Politics
General
Politicians
and parties
GABAA
PAMs
non-N05B
α2δ VDCC Blockers
5-HT1A Agonists
H1 Antagonists
CRH1 Antagonists
NK2 Antagonists
MCH1 antagonists
mGluR2/3 Agonists
mGluR5 NAMs
TSPO agonists
σ1 agonists
Others

M: PSO/PSI

dsrd (o, p, m, p, a, d, s), sysi/epon, spvo

proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D)
Antipsychotics (neuroleptics) (N05A)
Typical
Benzamides
Levosulpiride
Nemonapride
Sulpiride
Sultopride
Tiapride
Veralipride
Butyrophenones
Azaperone
Benperidol
Bromperidol
Droperidol
Fluanisone
Haloperidol
Lenperone
Moperone
Pipamperone
Spiperone
Timiperone
Trifluperidol
Diphenylbutylpiperidines
Clopimozide
Fluspirilene
Penfluridol
Pimozide
Phenothiazines
Acepromazine
Acetophenazine
Butaperazine
Carphenazine
Chloracizine
Chlorproethazine
Chlorpromazine
Cyamemazine
Dixyrazine
Fluacizine
Fluphenazine
Levomepromazine/Methotrimeprazine
Mesoridazine
Perazine
Pericyazine
Perphenazine
Piperacetazine
Pipotiazine
Prochlorperazine
Promazine
Promethazine
Propiomazine
Sulforidazine
Thiethylperazine
Thiopropazate
Thioproperazine
Thioridazine
Trifluoperazine
Triflupromazine
Thioxanthenes
Chlorprothixene
Clopenthixol
Flupentixol
Thiothixene
Zuclopenthixol
Tricyclics
Amoxapine
Butaclamol
Fluotracen
Loxapine
Trimipramine
Others
Prothipendyl
Atypical
Others

M: PSO/PSI

dsrd (o, p, m, p, a, d, s), sysi/epon, spvo

proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D)
Retrieved from "http://en.wikipedia.org/w/index.php?title=Cannabidiol&oldid=555700417"