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CANNABIDIOL [CBD] -- Updated 2-21-19

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Re-post 2-21-19

UPDATE:

 

On 2/19/2019 12:17 PM, Sally Rousseux wrote:
Hiyaaa
 
I know you’re busy so I’ll get right to it.
 
Your blog posts rock - but I found the resource by Wikipedia in your article to be a wee-bit outdated:
 
 
I know because I just spent an entire week researching the topic, curating the very best information and I wanted you to be the first to read it.
 
Here’s my new and improved CBD guide for 2019: https://www.stock-cannabis.com/blog/the-complete-guide-to-cbd
 
Please take a look and feel free to add it to your article :) Maybe you could mention it on your website?
 
I’d love to get you a relevant link back if you do link to it.
 
Thanks for everything you do.
 
Sally Rousseux <admin@stock-cannabis.com>
 
**************************************************************************

Cannabidiol

From Wikipedia, the free encyclopedia

Not to be confused with Cannabinol.

Cannabidiol

Cannabidiol.svg

CBD-3D-balls.png

Systematic (IUPAC) name

2-[(1R,6R)-6-isopropenyl-3-methylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol

Clinical data

Trade names

Epidiolex

AHFS/Drugs.com

International Drug Names

Legal status

Pharmacokinetic data

Bioavailability

13-19% (oral),[1] 11-45% (mean 31%; inhaled)[2]

Biological half-life

9 h[1]

Identifiers

CAS Registry Number

13956-29-1 Yes

ATC code

None

PubChem

CID: 644019

IUPHAR/BPS

4150

ChemSpider

24593618 

UNII

19GBJ60SN5 

Chemical data

Formula

C21H30O2

Molecular mass

314.4636

SMILES[show]

InChI[show]

Physical data

Melting point

66 °C (151 °F)

Boiling point

180 °C (356 °F)

(range: 160–180 °C)[3]

 Yes (what is this?)  (verify)

 

Cannabidiol(CBD) is one of at least 85 active cannabinoids identified in cannabis.[4] It is a major phytocannabinoid, accounting for up to 40% of the plant's extract.[5] CBD is considered to have a wider scope of medical applications than tetrahydrocannabinol (THC).[5] Unlike THC, CBD is generally considered to be non-psychoactive.[6] An orally-administered liquid containing CBD has received orphan drug status in the US, for use as a treatment for Dravet syndrome, under the brand name Epidiolex.[7]

Contents

Clinical applications

https://upload.wikimedia.org/wikipedia/commons/thumb/6/65/Kolkata-Kut.jpg/220px-Kolkata-Kut.jpg

The bud of a Cannabis sativa flower coated with trichomes bearing cannabidiol and other cannabinoids

Antimicrobial actions

CBD absorbed transcutaneously may reduce the excessive sebum production that is at the root of acne, according to an untested hypothesis.[8]

Neurological effects

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. The researchers attributed this attenuation of memory effects to CBD's role as a CB1 antagonist.[9] Transdermal CBD is neuroprotective in animals.[10]

Cannabidiol's strong antioxidant properties have been shown to play a role in the compound's neuroprotective and anti-ischemic effects.[11]

Psychotropic effect

CBD has anti-psychotic effects and may counteract the potential psychotomimetic effects of THC on individuals with latent schizophrenia;[5] some reports show it to be an alternative treatment for schizophrenia that is safe and well-tolerated.[12] 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.[12][13] 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.[14]

Studies have shown cannabidiol decreases activity of the limbic system [15] and decreases social isolation induced by THC.[16] Cannabidiol has also been shown to reduce anxiety in social anxiety disorder.[17][18]

Chronic cannabidiol administration in rats was found to produce reactions suggesting anxiety, indicating that prolonged treatment with cannabidiol might lead to anxiety.[19] Those results have been contested by Gururajan,[20] and contradict Réus,[21] whose experimentation cover the same duration.

Cannabidiol has demonstrated antidepressant-like effects in animal models of depression.[22][23][24]

Dravet syndrome

See also: Charlotte's Web (cannabis)

Dravet syndrome is a rare form of epilepsy that is difficult to treat. Dravet syndrome, also known as severe myoclonic epilepsy of infancy (SMEI), is a rare and catastrophic form of intractable epilepsy that begins in infancy. Initial seizures are most often prolonged events and in the second year of life other seizure types begin to emerge.[25] While high profile and anecdotal reports of results from high-CBD/low-THC preparations have sparked interest in treatment with cannabinoids,[26] there is insufficient medical evidence to draw conclusions about their safety or efficacy.[26][27]

CBD-enhanced cannabis

Decades ago, selective breeding by growers in the USA dramatically lowered the CBD content of cannabis; their customers preferred varietals that were more mind-altering due to a higher THC, lower CBD content.[28] To meet the demands of medical cannabis patients, growers are currently developing more CBD-rich strains.[29]

In November 2012, Tikun Olam, 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.[30][31] 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, a cannabinoid researcher, said "...Avidekel is thought to be the first CBD-enriched cannabis plant with no THC to have been developed in Israel".[32] In February 2014, a patent application was filed for a cannabis plant named 'avidekel'.[33]

Industrial hemp

Several industrial hemp varieties can be legally cultivated in western Europe. A variety such as "Fedora 17" has a cannabinoid profile consistently around 1% cannabidiol (CBD) with THC less than 0.1%.[34]

Extraction can be done with olive oil, ethanol, or CO2, and other nonpolar to semipolar solvents.[citation needed]

Worldwide hemp production is around 30,000 tonnes per year.

Pharmacology

Pharmacodynamics

Cannabidiol has a very low affinity for CB1 and CB2 receptors but acts as an indirect antagonist of their agonists.[11] 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.[35] It may also extend the duration of the effects of THC via inhibition of the cytochrome P-450-3A and 2C enzymes.[36] It is also an inverse agonist of CB2 receptors.[11][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.[38] Cannabidiol has also been shown to act as a 5-HT1A receptor agonist,[39] an action which is involved in its antidepressant,[22][40] anxiolytic,[40][41] and neuroprotective[42][43] effects. Cannabidiol is an allosteric modulator of μ and δ-opioid receptors.[44] Cannabidiol's pharmacological effects have also been attributed to PPAR-γ receptor agonism and intracellular calcium release.[5]

Pharmacokinetic interactions

There is some preclinical evidence to suggest that cannabidiol may reduce THC clearance, modestly increasing THC's plasma concentrations resulting in a greater amount of THC available to receptors, increasing the effect of THC in a dose-dependent manner.[45][46] Despite this the available evidence in humans suggests no significant effect of CBD on THC plasma levels.[47]

Pharmaceutical preparations

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.[48][49][50]

Isomerism

7 double bond isomers and their 30 stereoisomers

Formal numbering

Terpenoid numbering

Number of stereoisomers

Natural occurrence

Convention on Psychotropic Substances Schedule

Structure

Short name

Chiral centers

Full name

Short name

Chiral centers

Δ5-cannabidiol

1 and 3

2-(6-isopropenyl-3-methyl-5-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol

Δ4-cannabidiol

1 and 3

4

No

unscheduled

2-(6-Isopropenyl-3-methyl-5-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol.png

Δ4-cannabidiol

1, 3 and 6

2-(6-isopropenyl-3-methyl-4-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol

Δ5-cannabidiol

1, 3 and 4

8

No

unscheduled

2-(6-Isopropenyl-3-methyl-4-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol.png

Δ3-cannabidiol

1 and 6

2-(6-isopropenyl-3-methyl-3-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol

Δ6-cannabidiol

3 and 4

4

 ?

unscheduled

2-(6-Isopropenyl-3-methyl-3-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol.png

Δ3,7-cannabidiol

1 and 6

2-(6-isopropenyl-3-methylenecyclohex-1-yl)-5-pentyl-1,3-benzenediol

Δ1,7-cannabidiol

3 and 4

4

No

unscheduled

2-(6-Isopropenyl-3-methylenecyclohex-1-yl)-5-pentyl-1,3-benzenediol.png

Δ2-cannabidiol

1 and 6

2-(6-isopropenyl-3-methyl-2-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol

Δ1-cannabidiol

3 and 4

4

Yes

unscheduled

2-(6-Isopropenyl-3-methyl-2-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol.png

Δ1-cannabidiol

3 and 6

2-(6-isopropenyl-3-methyl-1-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol

Δ2-cannabidiol

1 and 4

4

No

unscheduled

2-(6-Isopropenyl-3-methyl-1-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol.png

Δ6-cannabidiol

3

2-(6-isopropenyl-3-methyl-6-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol

Δ3-cannabidiol

1

2

No

unscheduled

2-(6-Isopropenyl-3-methyl-6-cyclohexen-1-yl)-5-pentyl-1,3-benzenediol.png

Based on: Nagaraja, Kodihalli Nanjappa, Synthesis of delta-3-cannabidiol and the derived rigid analogs, Arizona University 1987.

See also: Tetrahydrocannabinol#Isomerism, Abnormal cannabidiol.

Chemistry

Cannabidiol is insoluble in water but soluble in organic solvents such as pentane. At room temperature, it is a colorless crystalline solid.[51] In strongly basic media and the presence of air, it is oxidized to a quinone.[52] Under acidic conditions it cyclizes to THC.[53] The synthesis of cannabidiol has been accomplished by several research groups.[54][55][56]

Biosynthesis

Cannabisproduces CBD-carboxylic acid through the same metabolic pathway as THC, until the last step, where CBDA synthase performs catalysis instead of THCA synthase.[57]

Legal status

Cannabidiol is not scheduled by the Convention on Psychotropic Substances.

Legal Status in Canada

Cannabidiol is a Schedule II drug in Canada.[58]

Legal Status in the United States

The legal status of Cannabidiol in the United States at the federal level is not immediately clear. The Controlled Substances Act (CSA) does not specifically list cannabidiol in Schedule I[59] nor in any of the other schedules,[60] however it appears that the Drug Enforcement Administration (DEA) presumes to assert authority to regulate cannabidiol as a Schedule I controlled substance.[61][62] The legal basis for that presumed authority is unclear.

The drug Schedules list "Tetrahydrocannabinols" and "marihuana" both as Schedule I drugs under the Controlled Substances Act,[59] however cannabidiol is unlikely to be considered as a Schedule I drug on the basis of being covered by the listing of "Marihuana" or by the listing of "Tetrahydrocannabinols" under Schedule I of the CSA.

  • "Marijuana" has a DEA Drug Code of 7360 (distinct from cannabidiol's Drug Code of 7372) and is defined by the CSA as "all parts of the plant Cannabis sativa L., whether growing or not; the seeds thereof; the resin extracted from any part of such plant; and every compound, manufacture, salt, derivative, mixture, or preparation of such plant, its seeds or resin." Exempted from regulation under the definition are "the mature stalks of such plant, fiber produced from such stalks, oil or cake made from the seeds of such plant, any other compound, manufacture, salt, derivative, mixture, or preparation of such mature stalks (except the resin extracted therefrom), fiber, oil, or cake, or the sterilized seed of such plant which is incapable of germination."[63] A DEA Interpretive Rule published in 2001 states that the "definition of marijuana was intended to include those parts of marijuana which contain THC and to exclude those parts which do not. ... The legislative history is absolutely clear that Congress meant to outlaw all plants popularly known as marijuana to the extent those plants possessed THC."[64] Cannabidiol isolated by extraction from marijuana sources does not contain THC, and synthetically produced cannabidiol does not contain THC either. It therefore stands to reason that cannabidiol is not covered under the prohibition on marijuana.
  • "Tetrahydrocannabinols" listed under Schedule I of the CSA are unlikely to include cannabidiol. Tetrahydrocannabinols are defined as follows:

Since cannabidiol is chemically not a tetrahydrocannabinol (nor indeed a "cannabinol" of any kind) and cannabidiol has a DEA Drug Code of 7372 (distinct from Tetrahydrocannabinols' designated Drug Code of 7370),[61] it stands to reason that cannabidiol is not considered one of the drugs placed into Schedule I under the listing of "Tetrahydrocannabinols" in the CSA.

Furthermore, cannabidiol was not placed into Schedule I when The Controlled Substances Act was amended in July 2012 with the US Congress' passing of the Synthetic Drug Abuse Prevention Act of 2012 (SDAPA) (which came into effect on January 4, 2013[65])[66] to ban various cannabinoids, cathinones, and phenethylamines.[59] The part adding to Schedule I various "cannabimimetic agents" which include molecules more closely resembling so-called "classically" structured cannabinoids reads as follows:

 

Since cannabidiol is chemically not a tetrahydrocannabinol (nor indeed a "cannabinol" of any kind) and cannabidiol has a DEA Drug Code of 7372 (distinct from Tetrahydrocannabinols' designated Drug Code of 7370),[61] it stands to reason that cannabidiol is not considered one of the drugs placed into Schedule I under the listing of "Tetrahydrocannabinols" in the CSA.

Furthermore, cannabidiol was not placed into Schedule I when The Controlled Substances Act was amended in July 2012 with the US Congress' passing of the Synthetic Drug Abuse Prevention Act of 2012 (SDAPA) (which came into effect on January 4, 2013[65])[66] to ban various cannabinoids, cathinones, and phenethylamines.[59] The part adding to Schedule I various "cannabimimetic agents" which include molecules more closely resembling so-called "classically" structured cannabinoids reads as follows:

Cannabidiol, while being a more "classically structured" cannabinoid (not like the much more recently discovered cannabinoid receport agonists with indole rings such as many of the JWH- and AM- named series), was not on the list of specifically newly banned cannabinoids (even among those with a more so-called "classic structure"),[65][59] and it does not fall into the category of unlisted cannabinoids which are caught by the definition above for several reasons. Primarily, CBD is not a CB1 agonist; it is a CB1 antagonist.[8][9] Also, unlike CP 47,497's homologues and similar synthetic "classical structured cannabinoids" which the above definition was written carefully to include, the cannabidiol molecule has a cyclohexene ring where the amended law requires a cyclohexane ring, and further cannabidiol does not have the required 3-hydroxyl moiety bonded to its cyclohexenyl functional group where the law requires a hydroxyl moiety bonded to the 3- position of a cyclohexyl functional group.

Extracts and concentrates of hemp products which are high in cannabidiol content are very likely legal under US federal law as long as they meet certain requirements. Marihuana is defined by 21 U.S.C. §802(16), which is part of the Controlled Substances Act, and it has a DEA Number / Drug Code of 7360. Exempted from regulation under the definition of marihana is "the mature stalks of such plant, fiber produced from such stalks, oil or cake made from the seeds of such plant, any other compound, manufacture, salt, derivative, mixture, or preparation of such mature stalks (except the resin extracted therefrom), fiber, oil, or cake, or the sterilized seed of such plant which is incapable of germination."[63][67][68] Under this exception, what are known as industrial hemp-finished products are legally imported into the United States each year.[69] Hemp finished products, including hemp oil and extracts of hemp products which are high in cannabidiol, are legal in the United States for this reason.

US 507 Patent

In October 2003, U.S. patent U.S. Patent 6,630,507 entitled "Cannabinoids as antioxidants and neuroprotectants" was assigned to "The United States Of America As Represented By The Department Of Health And Human Services." The patent was filed in April 1999 and listed as the inventors: Aidan J. Hampson, Julius Axelrod, and Maurizio Grimaldi, who all held positions at the National Institute of Mental Health (NIMH) in Bethesda, MD, which is part of the National Institutes of Health (NIH), an agency of the United States Department of Health and Human Services (HHS). The patent mentions cannabidiol's ability as an antiepileptic, to lower intraocular pressure in the treatment of glaucoma, lack of toxicity or serious side effects in large acute doses, its neuroprotectant properties, its ability to prevent neurotoxicity mediated by NMDA, AMPA, or kainate receptors; its ability to attenuate glutamate toxicity, its ability to protect against cellular damage, its ability to protect brains from ischemic damage, its anxiolytic effect, and its superior antioxidant activity which can be used in the prophylaxis and treatment of oxidation associated diseases.[70]

"Oxidative associated diseases include, without limitation, free radical associated diseases, such as ischemia, ischemic reperfusion injury, inflammatory diseases, systemic lupus erythematosus, myocardial ischemia or infarction, cerebrovascular accidents (such as a thromboembolic or hemorrhagic stroke) that can lead to ischemia or an infarct in the brain, operative ischemia, traumatic hemorrhage (for example a hypovolemic stroke that can lead to CNS hypoxia or anoxia), spinal cord trauma, Down's syndrome, Crohn's disease, autoimmune diseases (e.g. rheumatoid arthritis or diabetes), cataract formation, uveitis, emphysema, gastric ulcers, oxygen toxicity, neoplasia, undesired cellular apoptosis, radiation sickness, and others. The present invention is believed to be particularly beneficial in the treatment of oxidative associated diseases of the CNS, because of the ability of the cannabinoids to cross the blood brain barrier and exert their antioxidant effects in the brain. In particular embodiments, the pharmaceutical composition of the present invention is used for preventing, arresting, or treating neurological damage in Parkinson's disease, Alzheimer's disease and HIV dementia; autoimmune neurodegeneration of the type that can occur in encephalitis, and hypoxic or anoxic neuronal damage that can result from apnea, respiratory arrest or cardiac arrest, and anoxia caused by drowning, brain surgery or trauma (such as concussion or spinal cord shock)."[70]

     

 

Kannalife Sciences, Inc.

On November 17, 2011, the Federal Register published that the National Institutes of Health of the United States Department of Health and Human Services was "contemplating the grant of an exclusive patent license to practice the invention embodied in U.S. Patent 6,630,507" to the company KannaLife based in New York, for the development and sale of cannabinoid and cannabidiol based therapeutics for the treatment of hepatic encephalopathy in humans.[71][72][73]

On July 9, 2012 — KannaLife Sciences, Inc. (“KannaLife”) Signed an Exclusive License Agreement With National Institutes of Health – Office of Technology Transfer (“NIH-OTT”) aka the United States Federal Government for the Commercialization of U.S. Patent 6,630,507, “Cannabinoids as Antioxidants and Neuroprotectants” (the “’507 Patent”).[70]

References

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·  ·  Scuderi C, Filippis DD, Iuvone T, Blasio A, Steardo A, Esposito G (May 2009). "Cannabidiol in medicine: a review of its therapeutic potential in CNS disorders". Phytother Res (Review) 23 (5): 597–602. doi:10.1002/ptr.2625. PMID 18844286.

·  ·  [unreliable medical source?] McPartland JM, Russo EB (2001). "Cannabis and cannabis extracts: greater than the sum of their parts?" (PDF). Journal of Cannabis Therapeutics 1 (3/4): 103–132. doi:10.1300/J175v01n03_08.

·  ·  Borgelt LM, Franson KL, Nussbaum AM, Wang GS (February 2013). "The pharmacologic and clinical effects of medical cannabis". Pharmacotherapy (Review) 33 (2): 195–209. doi:10.1002/phar.1187. PMID 23386598.

·  ·  Campos AC, Moreira FA, Gomes FV, Del Bel EA, Guimarães FS (December 2012). "Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders". Philos. Trans. R. Soc. Lond., B, Biol. Sci. (Review) 367 (1607): 3364–78. doi:10.1098/rstb.2011.0389. PMC 3481531. PMID 23108553.

·  ·  Kozela E (March 2015). "Cannabidiol, a non-psychoactive cannabinoid, leads to EGR2-dependent anergy in activated encephalitogenic T cells". Journal of Neuroinflammation 12 (52). doi:10.1186/s12974-015-0273-0. PMC 4363052. PMID 25880134.

·  ·  Wilner, AN (25 March 2014). "Marijuana for Epilepsy: Weighing the Evidence". Medscape Neurology. WebMD. Retrieved 2 April 2014.

·  ·  Russo EB (August 2011). "Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects". Br. J. Pharmacol. (Review) 163 (7): 1344–64. doi:10.1111/j.1476-5381.2011.01238.x. PMC 3165946. PMID 21749363.

·  ·  Morgan, C. J. (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.

·  ·  Liput DJ, Hammell DC, Stinchcomb AL, Nixon K (2013). "Transdermal delivery of cannabidiol attenuates binge alcohol-induced neurodegeneration in a rodent model of an alcohol use disorder". Pharmacology Biochemistry and Behavior 111: 120–7. doi:10.1016/j.pbb.2013.08.013. PMID 24012796.

·  ·  Mechoulam R, Peters M, Murillo-Rodriguez E, Hanus LO (August 2007). "Cannabidiol--recent advances". Chem. Biodivers. (Review) 4 (8): 1678–92. doi:10.1002/cbdv.200790147. PMID 17712814.

·  ·  Zuardi AW, Crippa JA, Hallak JE, Moreira FA, Guimarães FS (April 2006). "Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug". Braz. J. Med. Biol. Res. (Review) 39 (4): 421–9. doi:10.1590/S0100-879X2006000400001. PMID 16612464.

·  ·  Long LE, Malone DT, Taylor DA (2005). "Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice". Neuropsychopharmacology 31 (4): 795–803. doi:10.1038/sj.npp.1300838. PMID 16052245.

·  ·  Leweke FM, Piomelli D, Pahlisch F, Muhl D, Gerth CW, Hoyer C, Klosterkötter J, Hellmich M, Koethe D (2012). "Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia". Translational Psychiatry 2 (3): e94–. doi:10.1038/tp.2012.15. PMC 3316151. PMID 22832859.

·  ·  Crippa JA, Zuardi AW, Garrido GE, Wichert-Ana L, Guarnieri R, Ferrari L, Azevedo-Marques PM, Hallak JE, McGuire PK, Filho Busatto G (October 2003). "Effects of Cannabidiol (CBD) on Regional Cerebral Blood Flow". Neuropsychopharmacology 29 (2): 417–426. doi:10.1038/sj.npp.1300340. PMID 14583744.

·  ·  Malone DT, Jongejan D, Taylor DA (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.

·  ·  Bergamaschi MM, Queiroz RH, Chagas MH, de Oliveira DC, De Martinis BS, Kapczinski F, Quevedo J, Roesler R, Schröder N, Nardi AE, Martín-Santos R, Hallak JE, Zuardi AW, Crippa JA (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.

·  ·  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.

·  ·  ElBatsh MM, Assareh N, Marsden CA, Kendall DA (May 2012). "Anxiogenic-like effects of chronic cannabidiol administration in rats". Psychopharmacology 221 (2): 239–247. doi:10.1007/s00213-011-2566-z. PMID 22083592.

·  ·  Gururajan A (2012). "Comment on: "Anxiogenic-like effects of chronic cannabidiol administration in rats" (Elbatsh MM, Assareh N, Marsden CA, Kendall DA, Psychopharmacology 2012)". Psychopharmacology 222 (4): 725–6; author reply 727. doi:10.1007/s00213-012-2780-3. PMID 22760485.

·  ·  Réus GZ, Stringari RB, Ribeiro KF, Luft T, Abelaira HM, Fries GR, Aguiar BW, Kapczinski F, Hallak JE, Zuardi AW, Crippa JA, Quevedo J (2011). "Administration of cannabidiol and imipramine induces antidepressant-like effects in the forced swimming test and increases brain-derived neurotrophic factor levels in the rat amygdala". Acta Neuropsychiatrica 23 (5): 241–248. doi:10.1111/j.1601-5215.2011.00579.x. PMID 25379896.

·  ·  Zanelati TV, Biojone C, Moreira FA, Guimarães FS, Joca SR (January 2010). "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.

·  ·  Réus, GZ; Stringari, RB; Ribeiro, KF; Luft, T; Abelaira, HM; Fries, GR; Aguiar, BW; Kapczinski, F; Hallak, JE; Zuardi, AW; Crippa JA; Quevedo, J (October 2011). "Administration of cannabidiol and imipramine induces antidepressant-like effects in the forced swimming test and increases brain-derived neurotrophic factor levels in the rat amygdala". Acta Neuropsychiatrica 23 (5): 241–248. doi:10.1111/j.1601-5215.2011.00579.x. PMID 25379896.

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·  ·  http://www.dravetfoundation.org/dravet-syndrome/what-is-dravet-syndrome#sthash.jAC0bZ89.dpuf What is Dravet Syndrome?

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·  ·  Controlled Drugs and Substances Act - Schedule II

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·  ·  [1], SCHEDULE AND DRUG CODES

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External links

  • Project CBD Non-profit educational service dedicated to promoting and publicizing research into the medical utility of cannabidiol.

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Analgesics (N02A, N02B)

 

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Cannabinoids

 

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Cannabisplant, Cannabis marijuana

 

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Cannabinoidergics

 

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https://en.wikipedia.org/wiki/Cannabidiol