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definition - Cannabinoid

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Cannabinoid

                   

Cannabinoids are a class of diverse chemical compounds that activate cannabinoid receptors. These include the endocannabinoids (produced naturally in the body by humans and animals),[1] the phytocannabinoids (produced by various plants), and synthetic cannabinoids (produced chemically by man). The most notable cannabinoid is the phytocannabinoid ∆9-tetrahydrocannabinol (THC), the primary psychoactive compound of cannabis.[2][3] However, there are known to exist numerous other cannabinoids with varied effects.

Synthetic cannabinoids encompass a variety of distinct chemical classes: the classical cannabinoids structurally related to THC, the nonclassical cannabinoids (cannabimimetics) including the aminoalkylindoles, 1,5-diarylpyrazoles, quinolines, and arylsulphonamides, as well as eicosanoids related to the endocannabinoids.[2]

Contents

  Cannabinoid receptors

Before the 1980s, it was often speculated that cannabinoids produced their physiological and behavioral effects via nonspecific interaction with cell membranes, instead of interacting with specific membrane-bound receptors. The discovery of the first cannabinoid receptors in the 1980s helped to resolve this debate. These receptors are common in animals, and have been found in mammals, birds, fish, and reptiles. At present, there are two known types of cannabinoid receptors, termed CB1 and CB2,[1] with mounting evidence of more.[4]

  Cannabinoid receptor type 1

CB1 receptors are found primarily in the brain, to be specific in the basal ganglia and in the limbic system, including the hippocampus.[1] They are also found in the cerebellum and in both male and female reproductive systems. CB1 receptors are absent in the medulla oblongata, the part of the brain stem responsible for respiratory and cardiovascular functions. Thus, there is not the risk of respiratory or cardiovascular failure that can be produced by some drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis.

  Cannabinoid receptor type 2

CB2 receptors are predominantly found in the immune system, or immune-derived cells[5] with the greatest density in the spleen. While found only in the peripheral nervous system, a report does indicate that CB2 is expressed by a subpopulation of microglia in the human cerebellum .[6] CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.[5]

  Phytocannabinoids

Type Skeleton Cyclization
Cannabigerol-type
CBG
Chemical structure of a CBG-type cannabinoid. Chemical structure of the CBG-type cyclization of cannabinoids.
Cannabichromene-type
CBC
Chemical structure of a CBC-type cannabinoid. Chemical structure of the CBC-type cyclization of cannabinoids.
Cannabidiol-type
CBD
Chemical structure of a CBD-type cannabinoid. Chemical structure of the CBD-type cyclization of cannabinoids.
Tetrahydrocannabinol-
and
Cannabinol-type
THC, CBN
Chemical structure of a CBN-type cannabinoid. Chemical structure of the CBN-type cyclization of cannabinoids.
Cannabielsoin-type
CBE
Chemical structure of a CBE-type cannabinoid. Chemical structure of the CBE-type cyclization of cannabinoids.
iso-
Tetrahydrocannabinol-
type
iso-THC
Chemical structure of an iso-CBN-type cannabinoid. Chemical structure of the iso-CBN-type cyclization of cannabinoids.
Cannabicyclol-type
CBL
Chemical structure of a CBL-type cannabinoid. Chemical structure of the CBL-type cyclization of cannabinoids.
Cannabicitran-type
CBT
Chemical structure of a CBT-type cannabinoid. Chemical structure of the CBT-type cyclization of cannabinoids.
Main classes of natural cannabinoids

Phytocannabinoids (also called natural cannabinoids, herbal cannabinoids, and classical cannabinoids) are known to occur in several different plant species. These include Cannabis sativa, Cannabis indica, Echinacea purpurea, Echinacea angustifolia, Echinacea pallida, Acmella oleracea, Helichrysum umbraculigerum, and Radula marginata.[7] The best known herbal cannabinoids are Δ9-tetrahydrocannabinol (THC) from Cannabis and the lipophilic alkamides (alkylamides) from Echinacea species.[7]

A significant number of cannabinoids are found in both Cannabis and Echinacea plants. In Cannabis, these cannabinoids are concentrated in a viscous resin produced in structures known as glandular trichomes. In Echinacea species, cannabinoids are found throughout the plant structure, but are most concentrated in the roots and stems.[8] Tea (Camellia sinensis) catechins have an affinity for human cannabinoid receptors.[9]

  Health Effects of Cannabinoids

Phytocannabinoids are nearly insoluble in water but are soluble in lipids, alcohols, and other non-polar organic solvents. However, as phenols, they form more water-soluble phenolate salts under strongly alkaline conditions.

All-natural cannabinoids are derived from their respective 2-carboxylic acids (2-COOH) by decarboxylation (catalyzed by heat, light, or alkaline conditions).

  Types

At least 85 different cannabinoids have been isolated from the Cannabis plant.[10] At least 25 different cannabinoids have been isolated from Echinacea species.[11] To the right, the main classes of cannabinoids from Cannabis are shown. All classes derive from cannabigerol-type compounds and differ mainly in the way this precursor is cyclized.

Tetrahydrocannabinol (THC), cannabidiol (CBD), cannabinol (CBN), and Dodeca-2E,4E,8Z,10E/Z-tetraenoic-acid-isobutylamides (from Echinacea species) are the most prevalent natural cannabinoids and have received the most study. Other common cannabinoids are listed below:

  Tetrahydrocannabinol

Tetrahydrocannabinol (THC) is the primary psychoactive component of the plant. It appears to ease moderate pain (analgesic) and to be neuroprotective. THC has approximately equal affinity for the CB1 and CB2 receptors.[12]

Delta-9-Tetrahydrocannabinol9-THC, THC) and delta-8-tetrahydrocannabinol (Δ8-THC), mimic the action of anandamide, a neurotransmitter produced naturally in the body. These two THC's produce the effects associated with cannabis by binding to the CB1 cannabinoid receptors in the brain.

  Cannabidiol

Cannabidiol (CBD) is not particularly psychoactive in and of itself, and was thought not to affect the psychoactivity of THC.[13] However, recent evidence shows that smokers of cannabis with a higher CBD/THC ratio were less likely to experience schizophrenia-like symptoms.[14] This is supported by psychological tests, in which participants experience less intense psychotic-like effects when intravenous THC was co-administered with CBD (as measured with a PANSS test).[15] Cannabidiol has little affinity for CB1 and CB2 receptors but acts as an indirect antagonist of cannabinoid agonists.[16] Recently it was found to be an antagonist at the putative new cannabinoid receptor, GPR55, a GPCR expressed in the caudate nucleus and putamen.[17] Cannabidiol has also been shown to act as a 5-HT1A receptor agonist,[18] an action that is involved in its antidepressant,[19][20] anxiolytic,[20][21] and neuroprotective[22][23] effects.

It appears to relieve convulsion, inflammation, anxiety, and nausea.[24] CBD has a greater affinity for the CB2 receptor than for the CB1 receptor.[24]

CBD shares a precursor with THC and is the main cannabinoid in low-THC Cannabis strains. CBD apparently plays a role in preventing the short-term memory loss associated with THC in mammals.

  Cannabinol

Cannabinol (CBN) is the primary product of THC degradation, and there is usually little of it in a fresh plant. CBN content increases as THC degrades in storage, and with exposure to light and air. It is only mildly psychoactive. Its affinity to the CB2 receptor is higher than for the CB1 receptor.[25]

  Cannabigerol

Cannabigerol (CBG) is non-psychotomimetic but still affects the overall effects of Cannabis. It acts as an α2-adrenergic receptor agonist, 5-HT1A receptor antagonist, and CB1 receptor antagonist.[26] It also binds to the CB2 receptor.[26]

  Tetrahydrocannabivarin

Tetrahydrocannabivarin (THCV) is prevalent in certain central Asian and southern African strains of Cannabis.[27] [28] It is an antagonist of THC at CB1 receptors and attenuates the psychoactive effects of THC.[29]

  Cannabidivarin

Although cannabidivarin (CBDV) is usually a minor constituent of the cannabinoid profile, enhanced levels of CBDV have been reported in feral plants from the northwest Himalayas, and in hashish from Nepal. [30][28]

  Cannabichromene

Cannabichromene (CBC) is non-psychoactive and does not affect the psychoactivity of THC .[13]

  Double bond position

In addition, each of the compounds above may be in different forms depending on the position of the double bond in the alicyclic carbon ring. There is potential for confusion because there are different numbering systems used to describe the position of this double bond. Under the dibenzopyran numbering system widely used today, the major form of THC is called Δ9-THC, while the minor form is called Δ8-THC. Under the alternate terpene numbering system, these same compounds are called Δ1-THC and Δ6-THC, respectively.

  Length

Most herbal cannabinoid compounds are 21-carbon compounds. However, some do not follow this rule, primarily because of variation in the length of the side-chain attached to the aromatic ring. In THC, CBD, and CBN, this side-chain is a pentyl (5-carbon) chain. In the most common homologue, the pentyl chain is replaced with a propyl (3-carbon) chain. Cannabinoids with the propyl side-chain are named using the suffix varin, and are designated, for example, THCV, CBDV, or CBNV.

  Plant profile

Cannabis plants can exhibit wide variation in the quantity and type of cannabinoids they produce. The mixture of cannabinoids produced by a plant is known as the plant's cannabinoid profile. Selective breeding has been used to control the genetics of plants and modify the cannabinoid profile. For example, strains that are used as fiber (commonly called hemp) are bred such that they are low in psychoactive chemicals like THC. Strains used in medicine are often bred for high CBD content, and strains used for recreational purposes are usually bred for high THC content or for a specific chemical balance.

Quantitative analysis of a plant's cannabinoid profile is often determined by gas chromatography (GC), or more reliably by gas chromatography combined with mass spectrometry (GC/MS). Liquid chromatography (LC) techniques are also possible, and, unlike GC methods, can differentiate between the acid and neutral forms of the cannabinoids. There have been systematic attempts to monitor the cannabinoid profile of cannabis over time, but their accuracy is impeded by the illegal status of the plant in many countries.

  Pharmacology

Cannabinoids can be administered by smoking, vaporizing, oral ingestion, transdermal patch, intravenous injection, sublingual absorption, or rectal suppository. Once in the body, most cannabinoids are metabolized in the liver, especially by cytochrome P450 mixed-function oxidases, mainly CYP 2C9. Thus supplementing with CYP 2C9 inhibitors leads to extended intoxication.

Some is also stored in fat in addition to being metabolized in liver. Δ9-THC is metabolized to 11-hydroxy-Δ9-THC, which is then metabolized to 9-carboxy-THC. Some cannabis metabolites can be detected in the body several weeks after administration. These metabolites are the chemicals recognized by common antibody-based "drug tests"; in the case of THC et al., these loads do not represent intoxication (compare to ethanol breath tests that measure instantaneous blood alcohol levels) but an integration of past consumption over an approximately month-long window.

  Plant synthesis

Cannabinoid production starts when an enzyme causes geranyl pyrophosphate and olivetolic acid to combine and form CBG. Next, CBG is independently converted to either CBD or CBC by two separate synthase enzymes. CBD is then enzymatically cyclized to THC. For the propyl homologues (THCV, CBDV and CBNV), there is a similar pathway that is based on CBGV. (recent studies show that THC is not cyclized from CBD but rather directly from CBG. no experiment thus far has turned up an enzyme that converts CBD into THC although it is still hypothesized.)

  Separation

Cannabinoids can be separated from the plant by extraction with organic solvents. Hydrocarbons and alcohols are often used as solvents. However, these solvents are flammable and many are toxic. Butane may be used, which evaporates extremely quickly. Supercritical solvent extraction with carbon dioxide is an alternative technique. Although this process requires high pressures (73 atmospheres or more), there is minimal risk of fire or toxicity, solvent removal is simple and efficient, and extract quality can be well-controlled. Once extracted, cannabinoid blends can be separated into individual components using wiped film vacuum distillation or other distillation techniques. However, to produce high purity cannabinoids, chemical synthesis or semisynthesis is generally required.

  History

Cannabinoids were first discovered in the 1940s, when CBD and CBN were identified. The structure of THC was first determined in 1964.

Due to molecular similarity and ease of synthetic conversion, CBD was originally believed to be a natural precursor to THC. However, it is now known that CBD and THC are produced independently in the cannabis plant from the precursor CBG.

  Endocannabinoids

  Anandamide, an endogenous ligand of CB1 and CB2

Endocannabinoids are substances produced from within the body that activate cannabinoid receptors. After the discovery of the first cannabinoid receptor in 1988, scientists began searching for an endogenous ligand for the receptor.

  Types of endocannabinoid ligands

In 1992, in Raphael Mechoulam's lab, the first such compound was identified as arachidonoyl ethanolamine and named anandamide, a name derived from the Sanskrit word for bliss and -amide. Anandamide is derived from the essential fatty acid arachidonic acid. It has a pharmacology similar to THC, although its chemical structure is different. Anandamide binds to the central (CB1) and, to a lesser extent, peripheral (CB2) cannabinoid receptors, where it acts as a partial agonist. Anandamide is about as potent as THC at the CB1 receptor.[31] Anandamide is found in nearly all tissues in a wide range of animals.[32] Anandamide has also been found in plants, including small amounts in chocolate.[33]

Two analogs of anandamide, 7,10,13,16-docosatetraenoylethanolamide and homo-γ-linolenoylethanolamine, have similar pharmacology. All of these are members of a family of signalling lipids called N-acylethanolamines, which also includes the noncannabimimetic palmitoylethanolamide and oleoylethanolamide, which possess anti-inflammatory and orexigenic effects, respectively. Many N-acylethanolamines have also been identified in plant seeds[34] and in molluscs.[35]

Another endocannabinoid, 2-arachidonoyl glycerol, binds to both the CB1 and CB2 receptors with similar affinity, acting as a full agonist at both.[31] 2-AG is present at significantly higher concentrations in the brain than anandamide,[36] and there is some controversy over whether 2-AG rather than anandamide is chiefly responsible for endocannabinoid signalling in vivo.[37] In particular, one in vitro study suggests that 2-AG is capable of stimulating higher G-protein activation than anandamide, although the physiological implications of this finding are not yet known.[38]

In 2001, a third, ether-type endocannabinoid, 2-arachidonyl glyceryl ether (noladin ether), was isolated from porcine brain.[39] Prior to this discovery, it had been synthesized as a stable analog of 2-AG; indeed, some controversy remains over its classification as an endocannabinoid, as another group failed to detect the substance at "any appreciable amount" in the brains of several different mammalian species.[40] It binds to the CB1 cannabinoid receptor (Ki = 21.2 nmol/L) and causes sedation, hypothermia, intestinal immobility, and mild antinociception in mice. It binds primarily to the CB1 receptor, and only weakly to the CB2 receptor.[31]

Discovered in 2000, NADA preferentially binds to the CB1 receptor.[41] Like anandamide, NADA is also an agonist for the vanilloid receptor subtype 1 (TRPV1), a member of the vanilloid receptor family.[42][43]

A fifth endocannabinoid, virodhamine, or O-arachidonoyl-ethanolamine (OAE), was discovered in June 2002. Although it is a full agonist at CB2 and a partial agonist at CB1, it behaves as a CB1 antagonist in vivo. In rats, virodhamine was found to be present at comparable or slightly lower concentrations than anandamide in the brain, but 2- to 9-fold higher concentrations peripherally.[44]

  Function

Endocannabinoids serve as intercellular 'lipid messengers', signaling molecules that are released from one cell and activating the cannabinoid receptors present on other nearby cells. Although in this intercellular signaling role they are similar to the well-known monoamine neurotransmitters, such as acetylcholine and dopamine, endocannabinoids differ in numerous ways from them. For instance, they use retrograde signaling. Furthermore, endocannabinoids are lipophilic molecules that are not very soluble in water. They are not stored in vesicles, and exist as integral constituents of the membrane bilayers that make up cells. They are believed to be synthesized 'on-demand' rather than made and stored for later use. The mechanisms and enzymes underlying the biosynthesis of endocannabinoids remain elusive and continue to be an area of active research.

The endocannabinoid 2-AG has been found in bovine and human maternal milk.[45]

  Retrograde signal

Conventional neurotransmitters are released from a ‘presynaptic’ cell and activate appropriate receptors on a ‘postsynaptic’ cell, where presynaptic and postsynaptic designate the sending and receiving sides of a synapse, respectively. Endocannabinoids, on the other hand, are described as retrograde transmitters because they most commonly travel ‘backward’ against the usual synaptic transmitter flow. They are, in effect, released from the postsynaptic cell and act on the presynaptic cell, where the target receptors are densely concentrated on axonal terminals in the zones from which conventional neurotransmitters are released. Activation of cannabinoid receptors temporarily reduces the amount of conventional neurotransmitter released. This endocannabinoid mediated system permits the postsynaptic cell to control its own incoming synaptic traffic. The ultimate effect on the endocannabinoid-releasing cell depends on the nature of the conventional transmitter being controlled. For instance, when the release of the inhibitory transmitter GABA is reduced, the net effect is an increase in the excitability of the endocannabinoid-releasing cell. On the converse, when release of the excitatory neurotransmitter glutamate is reduced, the net effect is a decrease in the excitability of the endocannabinoid-releasing cell.

  Range

Endocannabinoids are hydrophobic molecules. They cannot travel unaided for long distances in the aqueous medium surrounding the cells from which they are released, and therefore act locally on nearby target cells. Hence, although emanating diffusely from their source cells, they have much more restricted spheres of influence than do hormones, which can affect cells throughout the body.

  U.S. Patent no. 6630507

On October 7, 2003, a U.S. patent number 6630507 entitled "Cannabinoids as Antioxidants and Neuroprotectants" was awarded to the United States Department of Health and Human Services, based on research done at the National Institute of Mental Health (NIMH), and the National Institute of Neurological Disorders and Stroke (NINDS). This patent claims that cannabinoids are "useful in the treatment and prophylaxis of wide variety of oxidation associated diseases such as ischemia, age-related, inflammatory, and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and HIV dementia."[46][47]

On November 17, 2011, in accordance with 35 U.S.C. 209(c)(1) and 37 CFR part 404.7(a)(1)(i), the National Institutes of Health, Department of Health and Human Services, published in the Federal Register, that it is contemplating the grant of an exclusive patent license to practice the invention embodied in U.S. Patent 6,630,507, entitled “Cannabinoids as antioxidants and neuroprotectants” and PCT Application Serial No. PCT/US99/08769 and foreign equivalents thereof, entitled “Cannabinoids as antioxidants and neuroprotectants” [HHS Ref. No. E-287-1997/2] to KannaLife Sciences Inc., which has offices in New York, U.S. This patent and its foreign counterparts have been assigned to the Government of the United States of America. The prospective exclusive license territory may be worldwide, and the field of use may be limited to: The development and sale of cannabinoid(s) and cannabidiol(s) based therapeutics as antioxidants and neuroprotectants for use and delivery in humans, for the treatment of hepatic encephalopathy, as claimed in the Licensed Patent Rights.[48]

  Synthetic and patented cannabinoids

Historically, laboratory synthesis of cannabinoids were often based on the structure of herbal cannabinoids, and a large number of analogs have been produced and tested, especially in a group led by Roger Adams as early as 1941 and later in a group led by Raphael Mechoulam. Newer compounds are no longer related to natural cannabinoids or are based on the structure of the endogenous cannabinoids.

Synthetic cannabinoids are particularly useful in experiments to determine the relationship between the structure and activity of cannabinoid compounds, by making systematic, incremental modifications of cannabinoid molecules.

Medications containing natural or synthetic cannabinoids or cannabinoid analogs:

Other notable synthetic cannabinoids include:

  Table of natural cannabinoids

Cannabigerol-type (CBG)
Chemical structure of cannabigerol.

Cannabigerol
(E)-CBG-C5

Chemical structure of cannabigerol monomethyl ether.

Cannabigerol
monomethyl ether
(E)-CBGM-C5 A

Chemical structure of cannabinerolic acid A.

Cannabinerolic acid A
(Z)-CBGA-C5 A

Chemical structure of cannabigerovarin.

Cannabigerovarin
(E)-CBGV-C3

Chemical structure of cannabigerolic acid A.

Cannabigerolic acid A
(E)-CBGA-C5 A

Chemical structure of cannabigerolic acid A monomethyl ether.

Cannabigerolic acid A
monomethyl ether
(E)-CBGAM-C5 A

Chemical structure of cannabigerovarinic acid A.

Cannabigerovarinic acid A
(E)-CBGVA-C3 A

Cannabichromene-type (CBC)
Chemical structure of cannabichromene.

(±)-Cannabichromene
CBC-C5

Chemical structure of cannabichromenic acid A.

(±)-Cannabichromenic acid A
CBCA-C5 A

Chemical structure of cannabichromevarine.

(±)-Cannabivarichromene,
(±)-Cannabichromevarin
CBCV-C3

Chemical structure of cannabichromevarinic acid A.

(±)-Cannabichromevarinic
acid A
CBCVA-C3 A

Cannabidiol-type (CBD)
Chemical structure of cannabidiol.

(−)-Cannabidiol
CBD-C5

Chemical structure of cannabidiol momomethyl ether.

Cannabidiol
momomethyl ether
CBDM-C5

Chemical structure of cannabidiol-C4

Cannabidiol-C4
CBD-C4

Chemical structure of cannabidivarin.

(−)-Cannabidivarin
CBDV-C3

Chemical structure of cannabidiorcol.

Cannabidiorcol
CBD-C1

Chemical structure of cannabidiolic acid.

Cannabidiolic acid
CBDA-C5

Chemical structure of cannabidivarinic acid.

Cannabidivarinic acid
CBDVA-C3

Cannabinodiol-type (CBND)
Chemical structure of cannabinodiol.

Cannabinodiol
CBND-C5

Chemical structure of cannabinodivarin.

Cannabinodivarin
CBND-C3

Tetrahydrocannabinol-type (THC)
Chemical structure of Δ9-tetrahydrocannabinol.

Δ9-Tetrahydrocannabinol
Δ9-THC-C5

Chemical structure of Δ9-tetrahydrocannabinol-C4

Δ9-Tetrahydrocannabinol-C4
Δ9-THC-C4

Chemical structure of Δ9-tetrahydrocannabivarin.

Δ9-Tetrahydrocannabivarin
Δ9-THCV-C3

Chemical structure of tetrahydrocannabiorcol.

Δ9-Tetrahydrocannabiorcol
Δ9-THCO-C1

Chemical structure of Δ9-tetrahydrocannabinolic acid A.

Δ9-Tetrahydro-
cannabinolic acid A
Δ9-THCA-C5 A

Chemical structure of Δ9-tetrahydrocannabinolic acid B.

Δ9-Tetrahydro-
cannabinolic acid B
Δ9-THCA-C5 B

Chemical structure of Δ9-tetrahydrocannabinolic acid-C4

Δ9-Tetrahydro-
cannabinolic acid-C4
A and/or B
Δ9-THCA-C4 A and/or B

Chemical structure of Δ9-tetrahydrocannabivarinic acid A.

Δ9-Tetrahydro-
cannabivarinic acid A
Δ9-THCVA-C3 A

Chemical structure of Δ9-tetrahydrocannabiorcolic acid.

Δ9-Tetrahydro-
cannabiorcolic acid
A and/or B
Δ9-THCOA-C1 A and/or B

Chemical structure of Δ8-tetrahydrocannabinol.

(−)-Δ8-trans-(6aR,10aR)-
Δ8-Tetrahydrocannabinol
Δ8-THC-C5

Chemical structure of Δ8-tetrahydrocannabinolic acid A.

(−)-Δ8-trans-(6aR,10aR)-
Tetrahydrocannabinolic
acid A
Δ8-THCA-C5 A

Chemical structure of cis-Δ9tetrahydrocannabinol.

(−)-(6aS,10aR)-Δ9-
Tetrahydrocannabinol
(−)-cis9-THC-C5

Cannabinol-type (CBN)
Chemical structure of cannabinol.

Cannabinol
CBN-C5

Chemical structure of cannabinol-C4

Cannabinol-C4
CBN-C4

Chemical structure of cannabivarin.

Cannabivarin
CBN-C3

Chemical structure of cannabinol-C2

Cannabinol-C2
CBN-C2

Chemical structure of cannabiorcol.

Cannabiorcol
CBN-C1

Chemical structure of cannabinolic acid A.

Cannabinolic acid A
CBNA-C5 A

Chemical structure of cannabinol methyl ether.

Cannabinol methyl ether
CBNM-C5

Cannabitriol-type (CBT)
Chemical structure of (-)-trans-cannabitriol.

(−)-(9R,10R)-trans-
Cannabitriol
(−)-trans-CBT-C5

Chemical structure of (+)-trans-cannabitriol.

(+)-(9S,10S)-Cannabitriol
(+)-trans-CBT-C5

Chemical structure of cis-cannabitriol.

(±)-(9R,10S/9S,10R)-
Cannabitriol
(±)-cis-CBT-C5

Chemical structure of trans-cannabitriol ethyl ether.

(−)-(9R,10R)-trans-
10-O-Ethyl-cannabitriol
(−)-trans-CBT-OEt-C5

Chemical structure of trans-cannabitriol-C3

(±)-(9R,10R/9S,10S)-
Cannabitriol-C3
(±)-trans-CBT-C3

Chemical structure of 8,9-dihydroxy-Δ6a(10a)-tetrahydrocannabinol.

8,9-Dihydroxy-Δ6a(10a)-
tetrahydrocannabinol
8,9-Di-OH-CBT-C5

Chemical structure of cannabidiolic acid A cannabitriol ester.

Cannabidiolic acid A
cannabitriol ester
CBDA-C5 9-OH-CBT-C5 ester

Chemical structure of cannabiripsol.

(−)-(6aR,9S,10S,10aR)-
9,10-Dihydroxy-
hexahydrocannabinol,
Cannabiripsol
Cannabiripsol-C5

Chemical structure of cannabitetrol.

(−)-6a,7,10a-Trihydroxy-
Δ9-tetrahydrocannabinol
(−)-Cannabitetrol

Chemical structure of 10-oxo-Δ6a10a-tetrahydrocannabinol.

10-Oxo-Δ6a(10a)-
tetrahydrocannabinol
OTHC

Cannabielsoin-type (CBE)
Chemical structure of cannabielsoin.

(5aS,6S,9R,9aR)-
Cannabielsoin
CBE-C5

Chemical structure of C3-cannabielsoin.

(5aS,6S,9R,9aR)-
C3-Cannabielsoin
CBE-C3

Chemical structure of cannabielsoic acid A.

(5aS,6S,9R,9aR)-
Cannabielsoic acid A
CBEA-C5 A

Chemical structure of cannabielsoic acid B.

(5aS,6S,9R,9aR)-
Cannabielsoic acid B
CBEA-C5 B

Chemical structure of C3-cannabielsoic acid B.

(5aS,6S,9R,9aR)-
C3-Cannabielsoic acid B
CBEA-C3 B

Chemical structure of cannabiglendol-C3

Cannabiglendol-C3
OH-iso-HHCV-C3

Chemical structure of dehydrocannabifuran.

Dehydrocannabifuran
DCBF-C5

Chemical structure of cannabifuran.

Cannabifuran
CBF-C5

Isocannabinoids
Chemical structure of Δ7-trans-isotetrahydrocannabinol.

(−)-Δ7-trans-(1R,3R,6R)-
Isotetrahydrocannabinol

Chemical structure of Δ7-isotetrahydrocannabivarin.

(±)-Δ7-1,2-cis-
(1R,3R,6S/1S,3S,6R)-
Isotetrahydro-
cannabivarin

Chemical structure of Δ7-trans-isotetrahydrocannabivarin.

(−)-Δ7-trans-(1R,3R,6R)-
Isotetrahydrocannabivarin

Cannabicyclol-type (CBL)
Chemical structure of cannabicyclol.

(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclol
CBL-C5

Chemical structure of cannabicyclolic acid A.

(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclolic acid A
CBLA-C5 A

Chemical structure of cannabicyclovarin.

(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclovarin
CBLV-C3

Cannabicitran-type (CBT)
Chemical structure of cannabicitran.

Cannabicitran
CBT-C5

Cannabichromanone-type (CBCN)
Chemical structure of cannabichromanone.

Cannabichromanone
CBCN-C5

Chemical structure of cannabichromanone-C3

Cannabichromanone-C3
CBCN-C3

Chemical structure of cannabicoumaronone.

Cannabicoumaronone
CBCON-C5

  Natural occurrence

A Cannabis Indica plant may have a CBD/THC ratio 4-5 times that of Cannabis Sativa. Marijuana with relatively high ratios of CBD:THC is less likely to induce anxiety than vice versa. This might partial be due to CBD's antagonist effects at the cannabidanoid receptor, compared to THC's partial agonist effect. [50] The relatively large amount of CBD contained in Cannabis Indica, means, compared to a Sativa, the effects are modulated significantly. The effects of Sativa are well known for its cerebral high, hence used daytime as medical cannabis, while Indica is well known for its sedative effects and is often preferred at night.

  The bud of a Cannabis sativa flower coated with trichomes, which can contain up to 4 times more CBD than Cannabis indica

[50]

  See also

  References

  1. ^ a b c Pacher P, Batkai S, Kunos G (2006). "The Endocannabinoid System as an Emerging Target of Pharmacotherapy". Pharmacol Rev. 58 (3): 389–462. DOI:10.1124/pr.58.3.2. PMC 2241751. PMID 16968947. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2241751. 
  2. ^ a b Lambert DM, Fowler CJ (2005). "The endocannabinoid system: drug targets, lead compounds, and potential therapeutic applications". J. Med. Chem. 48 (16): 5059–87. DOI:10.1021/jm058183t. PMID 16078824. 
  3. ^ Roger Pertwee, ed. (2005). Cannabinoids. Springer-Verlag. p. 2. ISBN 3-540-22565-X. 
  4. ^ Begg M, Pacher P, Bátkai S, Osei-Hyiaman D, Offertáler L, Mo FM, Liu J, Kunos G (2005). "Evidence for novel cannabinoid receptors". Pharmacol. Ther. 106 (2): 133–45. DOI:10.1016/j.pharmthera.2004.11.005. PMID 15866316. 
  5. ^ a b Pacher P, Mechoulam R (2011). "Is lipid signaling through cannabinoid 2 receptors part of a protective system?". Prog Lipid Res. 50 (2): 193–211. DOI:10.1016/j.plipres.2011.01.001. PMC 3062638. PMID 21295074. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3062638. 
  6. ^ Núñez E, Benito C, Pazos MR, et al. (2004). "Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study". Synapse 53 (4): 208–13. DOI:10.1002/syn.20050. PMID 15266552. 
  7. ^ a b Woelkart, K.; Salo-Ahen, OM.; Bauer, R. (2008). "CB receptor ligands from plants.". Curr Top Med Chem 8 (3): 173–86. PMID 18289087. 
  8. ^ Perry, NB.; van Klink, JW.; Burgess, EJ.; Parmenter, GA. (Feb 1997). "Alkamide levels in Echinacea purpurea: a rapid analytical method revealing differences among roots, rhizomes, stems, leaves and flowers.". Planta Med 63 (1): 58–62. DOI:10.1055/s-2006-957605. PMID 17252329. 
  9. ^ G. Korte, A. Dreiseitel, P.Schreier, A. Oemhme, S. Locher, S. Geiger, J. Heilmann, P.G. Sand pdf (2010). "Tea catechins’affinity for human cannabinoid receptors". Phytomedicine 17. http://missclasses.com/mp3s/Prize%20CD%202010/Tea/cannaboid.pdf. Retrieved 2012-06-21. 
  10. ^ El-Alfy, Abir T. et. al. "Antidepressant-like effect of [Delta]9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L." Pharmacology Biochemistry and Behavior. 2010 Jun;95(4). ISSN 0091-3057
  11. ^ Bauer, R.; Remiger, P. (Aug 1989). "TLC and HPLC Analysis of Alkamides in Echinacea Drugs1,2.". Planta Med 55 (4): 367–71. DOI:10.1055/s-2006-962030. PMID 17262436. 
  12. ^ Huffman JW (2000). "The search for selective ligands for the CB2 receptor". Curr. Pharm. Des. 6 (13): 1323–37. DOI:10.2174/1381612003399347. PMID 10903395. 
  13. ^ a b Ilan, A. B.; Gevins, A.; Coleman, M.; Elsohly, M. A.; De Wit, H. (2005). "Neurophysiological and subjective profile of marijuana with varying concentrations of cannabinoids". Behavioural Pharmacology 16 (5–6): 487–496. PMID 16148455.  edit
  14. ^ Morgan CJ, Curran HV (April 2008). "Effects of cannabidiol on schizophrenia-like symptoms in people who use cannabis". The British journal of psychiatry : the journal of mental science 192 (4): 306–7. DOI:10.1192/bjp.bp.107.046649. PMID 18378995. 
  15. ^ "Should I Smoke Dope?". http://www.bbc.co.uk/programmes/b009nyxf. Retrieved 2008-05-24. [unreliable source?]
  16. ^ 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. http://www3.interscience.wiley.com/journal/115806131/abstract. 
  17. ^ 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. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2095107. 
  18. ^ 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. 
  19. ^ 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. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2823358. 
  20. ^ 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. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2697769. 
  21. ^ 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. 
  22. ^ 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. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=15845890. 
  23. ^ 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. http://linkinghub.elsevier.com/retrieve/pii/S0028-3908(06)00392-3. 
  24. ^ a b Mechoulam R, Peters M, Murillo-Rodriguez E, Hanuš LO (August 2007). "Cannabidiol--recent advances". Chemistry & Biodiversity 4 (8): 1678–92. DOI:10.1002/cbdv.200790147. PMID 17712814. 
  25. ^ Mahadevan A, Siegel C, Martin BR, Abood ME, Beletskaya I, Razdan RK (October 2000). "Novel cannabinol probes for CB1 and CB2 cannabinoid receptors". Journal of Medical Chemistry 43 (20): 3778–85. DOI:10.1021/jm0001572. PMID 11020293. 
  26. ^ a b Cascio MG, Gauson LA, Stevenson LA, Ross RA, Pertwee R (December 2009). "Evidence that the plant cannabinoid cannabigerol is a highly potent α2-adrenoceptor agonist and moderately potent 5HT1A receptor antagonist". British Journal of Pharmacology 159 (1): 129–41. DOI:10.1111/j.1476-5381.2009.00515.x. PMC 2823359. PMID 20002104. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2823359. 
  27. ^ Baker, P.B., T.A. Gough and B.J. Taylor. 1980. Illicitly imported Cannabis products: some physical and chemical features indicative of their origin. Bulletin on Narcotics 32(2): 31-40.
  28. ^ a b Hillig Karl W., Mahlberg Paul G. (2004). "A chemotaxonomic analysis of cannabinoid variation in Cannabis (Cannabaceae)". American Journal of Botany 91 (6): 966–975. 
  29. ^ "Evidence that the plant cannabinoid Δ9-tetrahydrocannabivarin is a cannabinoid CB1 and CB2 receptor antagonist". British Journal of Pharmacology 146 (7). http://www.nature.com/bjp/journal/v146/n7/abs/0706414a.html. Retrieved 2007-06-24. 
  30. ^ Merkus Frans W.H.M. (1971). "Cannabivarin and tetrahydrocannabivarin, two new constituents of hashish". Nature 232: 579–580. 
  31. ^ a b c Grotenhermen F. (Oct 2005). "Cannabinoids". Current Drug Targets - CNS & Neurological Disorders 4 (5): 507–30. DOI:10.2174/156800705774322111. PMID 16266285. 
  32. ^ Martin BR, Mechoulam R, Razdan RK (1999). "Discovery and characterization of endogenous cannabinoids". Life Sciences 65 (6–7): 573–95. DOI:10.1016/S0024-3205(99)00281-7. PMID 10462059. 
  33. ^ di Tomaso E, Beltramo M, Piomelli D. (Aug 1996). "Brain cannabinoids in chocolate". Nature 382 (6593): 677–8. DOI:10.1038/382677a0. PMID 8751435. 
  34. ^ Chapman, K. D.; Venables, B.; Markovic, R.; Blair Jr, R. W.; Bettinger, C. (1999). "N-Acylethanolamines in Seeds. Quantification of Molecular Species and Their Degradation upon Imbibition". Plant physiology 120 (4): 1157–1164. PMC 59349. PMID 10444099. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=59349.  edit
  35. ^ Sepe, N.; De Petrocellis, L.; Montanaro, F.; Cimino, G.; Di Marzo, V. (1998). "Bioactive long chain N-acylethanolamines in five species of edible bivalve molluscs. Possible implications for mollusc physiology and sea food industry". Biochimica et Biophysica Acta 1389 (2): 101–111. DOI:10.1016/S0005-2760(97)00132-X. PMID 9461251.  edit
  36. ^ Stella N, Schweitzer P, Piomelli D. (Aug 1997). "A second endogenous cannabinoid that modulates long-term potentiation". Nature 388 (6644): 773–8. DOI:10.1038/42015. PMID 9285589. 
  37. ^ Pacher P, Bátkai S, Kunos G (2006). "The Endocannabinoid System as an Emerging Target of Pharmacotherapy". Pharmacological reviews 58 (3): 389–462. DOI:10.1124/pr.58.3.2. PMC 2241751. PMID 16968947. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2241751. 
  38. ^ Savinainen JR, Jarvinen T, Laine K, Laitinen JT. (Oct 2001). "Despite substantial degradation, 2-arachidonoylglycerol is a potent full efficacy agonist mediating CB1 receptor-dependent G-protein activation in rat cerebellar membranes". British Journal of Pharmacology 134 (3): 664–72. DOI:10.1038/sj.bjp.0704297. PMC 1572991. PMID 11588122. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1572991. 
  39. ^ Hanuš L, Abu-Lafi S, Fride E, et al. (2001). "2-Arachidonyl glyceryl ether, an endogenous agonist of the cannabinoid CB1 receptor". Proc. Natl. Acad. Sci. U.S.A. 98 (7): 3662–5. DOI:10.1073/pnas.061029898. PMC 31108. PMID 11259648. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=31108. 
  40. ^ Oka S, Tsuchie A, Tokumura A, Muramatsu M, Suhara Y, Takayama H, Waku K, Sugiura T. (Jun 2003). "Ether-linked analogue of 2-arachidonoylglycerol (noladin ether) was not detected in the brains of various mammalian species". Journal of Neurochemistry 85 (6): 1374–81. DOI:10.1046/j.1471-4159.2003.01804.x. PMID 12787057. 
  41. ^ Bisogno, T., D. Melck, M. Bobrov, N. M. Gretskaya, V. V. Bezuglov, L. De Petrocellis, V. Di Marzo. "N-acyl-dopamines: novel synthetic CB1 cannabinoid-receptor ligands and inhibitors of anandamide inactivation with cannabimimetic activity in vitro and in vivo." The Biochemical Journal. 2000 Nov 1;351 Pt 3:817-24. PMID 11042139
  42. ^ Bisogno T, Ligresti A, Di Marzo V. (Jun 2005). "The endocannabinoid signalling system: biochemical aspects". Pharmacology, Biochemistry, and Behavior 81 (2): 224–38. DOI:10.1016/j.pbb.2005.01.027. PMID 15935454. 
  43. ^ Ralevic V. (July 2003). "Cannabinoid modulation of peripheral autonomic and sensory neurotransmission". European Journal of Pharmacology 472 (1–2): 1–21. DOI:10.1016/S0014-2999(03)01813-2. PMID 12860468. 
  44. ^ Porter AC, Sauer JM, Knierman MD, Becker GW, Berna MJ, Bao J, Nomikos GG, Carter P, Bymaster FP, Leese AB, Felder CC. (June 2002). "Characterization of a Novel Endocannabinoid, Virodhamine, with Antagonist Activity at the CB1 Receptor". The Journal of Pharmacology and Experimental Therapeutics 301 (3): 1020–1024. DOI:10.1124/jpet.301.3.1020. PMID 12023533. http://jpet.aspetjournals.org/cgi/reprint/301/3/1020.pdf. 
  45. ^ Fride E, Bregman T, Kirkham TC. (April 2005). "Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood". Experimental Biology and Medicine 230 (4): 225–234. PMID 15792943. http://www.ebmonline.org/cgi/reprint/230/4/225.pdf. 
  46. ^ US patent 6630507, Hampson, Aidan J.; Axelrod, Julius; Grimaldi, Maurizio, "Cannabinoids as antioxidants and neuroprotectants", issued 2003-10-07 
  47. ^ U.S. Patent 6630507.
  48. ^ [1]
  49. ^ http://www.marijuana.org/mydna10-12-05.htm
  50. ^ a b J.E. Joy, S. J. Watson, Jr., and J.A. Benson, Jr, (1999). Marijuana and Medicine: Assessing The Science Base. Washington D.C: National Academy of Sciences Press. ISBN 0-585-05800-8. http://books.nap.edu/html/marimed/. 

  Further reading

  • Devane WA, Hanuš L, Breuer A, et al. (1992). "Isolation and structure of a brain constituent that binds to the cannabinoid receptor". Science 258 (5090): 1946–9. DOI:10.1126/science.1470919. PMID 1470919. 
  • Hanuš L, Gopher A, Almog S, Mechoulam R (1993). "Two new unsaturated fatty acid ethanolamides in brain that bind to the cannabinoid receptor". J. Med. Chem. 36 (20): 3032–4. DOI:10.1021/jm00072a026. PMID 8411021. 
  • Hanuš L (1987). "Biogenesis of cannabinoid substances in the plant". Acta Universitatis Palackianae Olomucensis Facultatis Medicae 116: 47–53. PMID 2962461. 
  • Hanuš L., Krejčí Z. (1975). "Isolation of two new cannabinoid acids from Cannabis sativa L. of Czechoslovak origin". Acta Univ. Olomuc., Fac. Med 74: 161–166. 
  • Hanuš L., Krejčí Z., Hruban L. (1975). "Isolation of cannabidiolic acid from Turkish variety of cannabis cultivated for fibre". Acta Univ. Olomuc., Fac. Med 74: 167–172. 
  • Mechoulam R, Ben-Shabat S, Hanuš L, et al. (1995). "Identification of an endogenous 2-monoglyceride, present in canine gut, that binds to cannabinoid receptors". Biochem. Pharmacol. 50 (1): 83–90. DOI:10.1016/0006-2952(95)00109-D. PMID 7605349. 
  • Racz, I.; Nadal, X.; Alferink, J.; Baños, J.; Rehnelt, J.; Martín, M.; Pintado, B.; Gutierrez-Adan, A. et al. (2008). "Interferon-gamma is a critical modulator of CB(2) cannabinoid receptor signaling during neuropathic pain". Journal of Neuroscience 28 (46): 12136–12145. DOI:10.1523/JNEUROSCI.3402-08.2008. PMID 19005078.  edit
  • Racz, I.; Nadal, X.; Alferink, J.; Baños, J.; Rehnelt, J.; Martín, M.; Pintado, B.; Gutierrez-Adan, A. et al. (2008). "Crucial role of CB(2) cannabinoid receptor in the regulation of central immune responses during neuropathic pain". Journal of Neuroscience 28 (46): 12125–12135. DOI:10.1523/JNEUROSCI.3400-08.2008. PMID 19005077.  edit

  External links

  Cannabinoid information

  Cannabinoid research organizations


   
               

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