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]
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]
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.
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]
| Type |
Skeleton |
Cyclization |
Cannabigerol-type
CBG |
 |
 |
Cannabichromene-type
CBC |
 |
 |
Cannabidiol-type
CBD |
 |
 |
Tetrahydrocannabinol-
and
Cannabinol-type
THC, CBN |
 |
 |
Cannabielsoin-type
CBE |
 |
 |
iso-
Tetrahydrocannabinol-
type
iso-THC |
 |
 |
Cannabicyclol-type
CBL |
 |
 |
Cannabicitran-type
CBT |
 |
 |
| 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]
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).
At least 85 different cannabinoids have been isolated from the Cannabis plant.[9] At least 25 different cannabinoids have been isolated from Echinacea species.[10] 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 (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.[11]
Delta-9-Tetrahydrocannabinol (Δ9-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 high associated with cannabis by binding to the CB1 cannabinoid receptors in the brain.
Main article:
CannabidiolCannabidiol (CBD) is not particularly psychoactive in and of itself, and was thought not to affect the psychoactivity of THC.[12] However, recent evidence shows that smokers of cannabis with a higher CBD/THC ratio were less likely to experience schizophrenia-like symptoms.[13] 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).[14] Cannabidiol has little affinity for CB1 and CB2 receptors but acts as an indirect antagonist of cannabinoid agonists.[15] Recently it was found to be an antagonist at the putative new cannabinoid receptor, GPR55, a GPCR expressed in the caudate nucleus and putamen.[16] Cannabidiol has also been shown to act as a 5-HT1A receptor agonist,[17] an action that is involved in its antidepressant,[18][19] anxiolytic,[19][20] and neuroprotective[21][22] effects.
It appears to relieve convulsion, inflammation, anxiety, and nausea.[23] CBD has a greater affinity for the CB2 receptor than for the CB1 receptor.[23]
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 (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.[24]
Main article:
CannabigerolCannabigerol (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.[25] It also binds to the CB2 receptor.[25]
Tetrahydrocannabivarin (THCV) is prevalent in certain central Asian and southern African strains of Cannabis.[26] [27] It is an antagonist of THC at CB1 receptors and attenuates the psychoactive effects of THC.[28]
Main article:
CannabidivarinAlthough 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. [29][27]
Cannabichromene (CBC) is non-psychoactive and does not affect the psychoactivity of THC .[12]
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.
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.
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 usually determined by gas chromatography (GC), or more reliably by gas chromatography combined with mass spectrometry (GC/MS). Liquid chromatography (LC) techniques are also possible, although these are often only semi-quantitative or qualitative. 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.
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.
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.)
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.
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 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.
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.[30] Anandamide is found in nearly all tissues in a wide range of animals.[31] Anandamide has also been found in plants, including small amounts in chocolate.[32]
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[33] and in molluscs.[34]
Another endocannabinoid, 2-arachidonoyl glycerol, binds to both the CB1 and CB2 receptors with similar affinity, acting as a full agonist at both.[30] 2-AG is present at significantly higher concentrations in the brain than anandamide,[35] and there is some controversy over whether 2-AG rather than anandamide is chiefly responsible for endocannabinoid signalling in vivo.[36] 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.[37]
In 2001, a third, ether-type endocannabinoid, 2-arachidonyl glyceryl ether (noladin ether), was isolated from porcine brain.[38] 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.[39] 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.[30]
Discovered in 2000, NADA preferentially binds to the CB1 receptor.[40] Like anandamide, NADA is also an agonist for the vanilloid receptor subtype 1 (TRPV1), a member of the vanilloid receptor family.[41][42]
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.[43]
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.[44]
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.
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.
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."[45][46]
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.[47]
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:
- Dronabinol (Marinol), is Δ9-tetrahydrocannabinol (THC), used as an appetite stimulant, anti-emetic, and analgesic
- Nabilone (Cesamet), a synthetic cannabinoid and an analog of Marinol. It is Schedule II unlike Marinol, which is Schedule III
- Sativex, a cannabinoid extract oral spray containing THC, CBD, and other cannabinoids used for neuropathic pain and spasticity in 22 countries including England, Canada and Spain. Sativex develops whole-plant cannabinoid medicines
- Rimonabant (SR141716), a selective cannabinoid (CB1) receptor inverse agonist used as an anti-obesity drug under the proprietary name Acomplia. It is also used for smoking cessation
Other notable synthetic cannabinoids include:
- JWH-018, a potent synthetic cannabinoid agonist discovered by Dr. John W. Huffman at Clemson University. It is being increasingly sold in legal smoke blends collectively known as "spice". Several countries and states have moved to ban it legally.
- CP-55940, produced in 1974, this synthetic cannabinoid receptor agonist is many times more potent than THC.
- Dimethylheptylpyran
- HU-210, about 100 times as potent as THC[48]
- HU-331 a potential anti-cancer drug derived from cannabidiol that specifically inhibits topoisomerase II.
- SR144528, a CB2 receptor antagonist
- WIN 55,212-2, a potent cannabinoid receptor agonist
- JWH-133, a potent selective CB2 receptor agonist
- Levonantradol (Nantrodolum), an anti-emetic and analgesic but not currently in use in medicine
- AM-2201, a potent cannabinoid receptor agonist.
| Cannabigerol-type (CBG) |
Cannabigerol
(E)-CBG-C5
|
Cannabigerol
monomethyl ether
(E)-CBGM-C5 A
|
Cannabinerolic acid A
(Z)-CBGA-C5 A
|
Cannabigerovarin
(E)-CBGV-C3
|
|
|
Cannabigerolic acid A
(E)-CBGA-C5 A
|
Cannabigerolic acid A
monomethyl ether
(E)-CBGAM-C5 A
|
Cannabigerovarinic acid A
(E)-CBGVA-C3 A
|
|
|
| Cannabichromene-type (CBC) |
(±)-Cannabichromene
CBC-C5
|
(±)-Cannabichromenic acid A
CBCA-C5 A
|
(±)-Cannabivarichromene,
(±)-Cannabichromevarin
CBCV-C3
|
(±)-Cannabichromevarinic
acid A
CBCVA-C3 A
|
|
| Cannabidiol-type (CBD) |
(−)-Cannabidiol
CBD-C5
|
Cannabidiol
momomethyl ether
CBDM-C5
|
Cannabidiol-C4
CBD-C4
|
(−)-Cannabidivarin
CBDV-C3
|
Cannabidiorcol
CBD-C1
|
Cannabidiolic acid
CBDA-C5
|
Cannabidivarinic acid
CBDVA-C3
|
|
|
|
| Cannabinodiol-type (CBND) |
Cannabinodiol
CBND-C5
|
Cannabinodivarin
CBND-C3
|
|
|
|
| Tetrahydrocannabinol-type (THC) |
Δ9-Tetrahydrocannabinol
Δ9-THC-C5
|
Δ9-Tetrahydrocannabinol-C4
Δ9-THC-C4
|
Δ9-Tetrahydrocannabivarin
Δ9-THCV-C3
|
Δ9-Tetrahydrocannabiorcol
Δ9-THCO-C1
|
|
Δ9-Tetrahydro-
cannabinolic acid A
Δ9-THCA-C5 A
|
Δ9-Tetrahydro-
cannabinolic acid B
Δ9-THCA-C5 B
|
Δ9-Tetrahydro-
cannabinolic acid-C4
A and/or B
Δ9-THCA-C4 A and/or B
|
Δ9-Tetrahydro-
cannabivarinic acid A
Δ9-THCVA-C3 A
|
Δ9-Tetrahydro-
cannabiorcolic acid
A and/or B
Δ9-THCOA-C1 A and/or B
|
(−)-Δ8-trans-(6aR,10aR)-
Δ8-Tetrahydrocannabinol
Δ8-THC-C5
|
(−)-Δ8-trans-(6aR,10aR)-
Tetrahydrocannabinolic
acid A
Δ8-THCA-C5 A
|
(−)-(6aS,10aR)-Δ9-
Tetrahydrocannabinol
(−)-cis-Δ9-THC-C5
|
|
|
| Cannabinol-type (CBN) |
Cannabinol
CBN-C5
|
Cannabinol-C4
CBN-C4
|
Cannabivarin
CBN-C3
|
Cannabinol-C2
CBN-C2
|
Cannabiorcol
CBN-C1
|
Cannabinolic acid A
CBNA-C5 A
|
Cannabinol methyl ether
CBNM-C5
|
|
|
|
| Cannabitriol-type (CBT) |
(−)-(9R,10R)-trans-
Cannabitriol
(−)-trans-CBT-C5
|
(+)-(9S,10S)-Cannabitriol
(+)-trans-CBT-C5
|
(±)-(9R,10S/9S,10R)-
Cannabitriol
(±)-cis-CBT-C5
|
(−)-(9R,10R)-trans-
10-O-Ethyl-cannabitriol
(−)-trans-CBT-OEt-C5
|
(±)-(9R,10R/9S,10S)-
Cannabitriol-C3
(±)-trans-CBT-C3
|
8,9-Dihydroxy-Δ6a(10a)-
tetrahydrocannabinol
8,9-Di-OH-CBT-C5
|
Cannabidiolic acid A
cannabitriol ester
CBDA-C5 9-OH-CBT-C5 ester
|
(−)-(6aR,9S,10S,10aR)-
9,10-Dihydroxy-
hexahydrocannabinol,
Cannabiripsol
Cannabiripsol-C5
|
(−)-6a,7,10a-Trihydroxy-
Δ9-tetrahydrocannabinol
(−)-Cannabitetrol
|
10-Oxo-Δ6a(10a)-
tetrahydrocannabinol
OTHC
|
| Cannabielsoin-type (CBE) |
(5aS,6S,9R,9aR)-
Cannabielsoin
CBE-C5
|
(5aS,6S,9R,9aR)-
C3-Cannabielsoin
CBE-C3
|
(5aS,6S,9R,9aR)-
Cannabielsoic acid A
CBEA-C5 A
|
(5aS,6S,9R,9aR)-
Cannabielsoic acid B
CBEA-C5 B
|
(5aS,6S,9R,9aR)-
C3-Cannabielsoic acid B
CBEA-C3 B
|
Cannabiglendol-C3
OH-iso-HHCV-C3
|
Dehydrocannabifuran
DCBF-C5
|
Cannabifuran
CBF-C5
|
|
|
| Isocannabinoids |
(−)-Δ7-trans-(1R,3R,6R)-
Isotetrahydrocannabinol
|
(±)-Δ7-1,2-cis-
(1R,3R,6S/1S,3S,6R)-
Isotetrahydro-
cannabivarin
|
(−)-Δ7-trans-(1R,3R,6R)-
Isotetrahydrocannabivarin
|
|
|
| Cannabicyclol-type (CBL) |
(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclol
CBL-C5
|
(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclolic acid A
CBLA-C5 A
|
(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclovarin
CBLV-C3
|
|
|
| Cannabicitran-type (CBT) |
Cannabicitran
CBT-C5
|
|
|
|
|
| Cannabichromanone-type (CBCN) |
Cannabichromanone
CBCN-C5
|
Cannabichromanone-C3
CBCN-C3
|
Cannabicoumaronone
CBCON-C5
|
|
|
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. [49] 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.
[49]
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Cannabinoids
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| Phytocannabinoids |
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| Cannabinoid metabolites |
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| Endogenous cannabinoids |
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Synthetic cannabinoid
receptor agonists |
Classical cannabinoids
(Dibenzopyrans) |
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| Nonclassical cannabinoids |
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| Benzoylindoles |
|
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| Naphthoylindoles |
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| Naphthylmethylindoles |
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| Phenylacetylindoles |
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| Naphthoylpyrroles |
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| Eicosanoids |
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| Others |
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Allosteric modulators of
cannabinoid receptors |
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Endocannabinoid
activity enhancers |
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Cannabinoid receptor
antagonists and
inverse agonists |
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-trans-cannabitriol.png)
-trans-cannabitriol.png)
-tetrahydrocannabinol.png)
-tetrahydrocannabinol.png)
