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A cannabinoid is one of a class of diverse chemical compounds that acts on cannabinoid receptors in cells that alter neurotransmitter release in the brain. Ligands for these receptor proteins include the endocannabinoids (produced naturally in the body by animals),^[1] the phytocannabinoids (found in cannabis and some other plants), and synthetic cannabinoids (manufactured artificially). The most notable cannabinoid is the phytocannabinoid tetrahydrocannabinol (THC), the primary psychoactive compound in cannabis.^[2][3] Cannabidiol (CBD) is another major constituent of the plant.^[4] There are at least 113 different cannabinoids isolated from cannabis, exhibiting varied effects.^[5]

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 arylsulfonamides, as well as eicosanoids related to endocannabinoids.^[2]

Cannabinoid receptors[edit]

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.^[6] 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.^[7] The human brain has more cannabinoid receptors than any other G protein-coupled receptor (GPCR) type.^[8]

Cannabinoid receptor type 1[edit]

CB₁ receptors are found primarily in the brain, more specifically in the basal ganglia and in the limbic system, including the hippocampus ^[1] and the striatum. 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. CB1 is also found in the human anterior eye and retina.^[9]

Cannabinoid receptor type 2[edit]

CB₂ receptors are predominantly found in the immune system, or immune-derived cells^[10] 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.^[11] CB₂ receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis seen in animal models.^[10]

Cannabis-derived cannabinoids[edit]

The classical cannabinoids are concentrated in a viscous resin produced in structures known as glandular trichomes. At least 113 different cannabinoids have been isolated from the Cannabis plant^[5] To the right, the main classes of cannabinoids from Cannabis are shown. The best studied cannabinoids include tetrahydrocannabinol (THC), cannabidiol (CBD) and cannabinol (CBN).

Types[edit]

All classes derive from cannabigerol-type compounds and differ mainly in the way this precursor is cyclized.^[12] The classical cannabinoids are derived from their respective 2-carboxylic acids (2-COOH) by decarboxylation (catalyzed by heat, light, or alkaline conditions).^[13]

• CBG (Cannabigerol)
• CBC (Cannabichromene)
• CBL (Cannabicyclol)
• CBV (Cannabivarin)
• THCV (Tetrahydrocannabivarin)
• CBDV (Cannabidivarin)
• CBCV (Cannabichromevarin)
• CBGV (Cannabigerovarin)
• CBGM (Cannabigerol Monomethyl Ether)
• THC (Tetrahydrocannabinol)
• THCA (Tetrahydrocannbinolic acid)
• CBD (Cannabidiol)
• CBDA (Cannabidiolic Acid)

Tetrahydrocannabinol[edit]

Tetrahydrocannabinol (THC) is the primary psychoactive component of the Cannabis plant. Delta-9-tetrahydrocannabinol (Δ⁹-THC, THC) and delta-8-tetrahydrocannabinol (Δ⁸-THC), mimic the actions of anandamide and 2-arachidonoylglycerol neurotransmitters produced naturally in the body. These cannabinoids produce the effects associated with cannabis by binding to the CB₁ cannabinoid receptors in the brain.

Cannabidiol[edit]

Cannabidiol (CBD) is non-psychotropic. Recent evidence shows that the compound counteracts cognitive impairment associated with the use of cannabis.^[14] Cannabidiol has little affinity for CB₁ and CB₂ receptors but acts as an indirect antagonist of cannabinoid agonists.^[15] 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-HT_1A receptor agonist.^[17] CBD can interfere with the uptake of adenosine, which plays an important role in biochemical processes, such as energy transfer. It may play a role in promoting sleep and suppressing arousal.^[18]

CBD shares a precursor with THC and is the main cannabinoid in CBD-dominant Cannabis strains. CBD has been shown to play a role in preventing the short-term memory loss associated with THC.^[19]

There is tentative evidence that CBD had an anti-psychotic effect, but research in this area is limited.^[20][14]

Cannabinol[edit]

Cannabinol (CBN) is the primary product of THC degradation, and there is usually little of it in a fresh plant.^{[citation needed]} CBN content increases as THC degrades in storage, and with exposure to light and air.^{[citation needed]} It is only mildly psychoactive. Its affinity to the CB₂ receptor is higher than for the CB₁ receptor.^[21]

Cannabigerol[edit]

Cannabigerol (CBG) is non-psychoactive but still affects the overall effects of Cannabis. CBG has been shown to promote apoptosis in cancer cells and inhibit tumor growth in mice.^[22] It acts as an α₂-adrenergic receptor agonist, 5-HT_1A receptor antagonist, and CB₁ receptor antagonist.^[23] It also binds to the CB₂ receptor.^[23]

Tetrahydrocannabivarin[edit]

Tetrahydrocannabivarin (THCV) is prevalent in certain central Asian and southern African strains of Cannabis.^[24][25] It is an antagonist of THC at CB₁ receptors and attenuates the psychoactive effects of THC.^[26]

Cannabidivarin[edit]

Although cannabidivarin (CBDV) is usually a minor constituent of the cannabinoid profile, enhanced levels of CBDV have been reported in feral cannabis plants from the northwest Himalayas, and in hashish from Nepal.^[25][27]

Cannabichromene[edit]

Cannabichromene (CBC) is non-psychoactive and does not affect the psychoactivity of THC.^[28] CBC has shown antitumor effects in breast cancer xenoplants in mice.^[29] More common in tropical cannabis varieties.

Biosynthesis[edit]

Cannabinoid production starts when an enzyme causes geranyl pyrophosphate and olivetolic acid to combine and form CBGA. Next, CBGA is independently converted to either CBG, THCA, CBDA or CBCA by four separate synthase, FAD-dependent dehydrogenase enzymes. There is no evidence for enzymatic conversion of CBDA or CBD to THCA or THC. For the propyl homologues (THCVA, CBDVA and CBCVA), there is an analogous pathway that is based on CBGVA from divarinolic acid instead of olivetolic acid.

Double bond position[edit]

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[edit]

Most classical cannabinoids 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.

Cannabinoids in other plants[edit]

Phytocannabinoids are known to occur in several plant species besides cannabis. These include Echinacea purpurea, Echinacea angustifolia, Acmella oleracea, Helichrysum umbraculigerum, and Radula marginata.^[30] The best-known cannabinoids that are not derived from Cannabis are the lipophilic alkamides (alkylamides) from Echinacea species, most notably the cis/trans isomers dodeca-2E,4E,8Z,10E/Z-tetraenoic-acid-isobutylamide.^[30] At least 25 different alkylamides have been identified, and some of them have shown affinities to the CB₂-receptor.^[31][32] In some Echinacea species, cannabinoids are found throughout the plant structure, but are most concentrated in the roots and flowers.^[33][34] Yangonin found in the Kava plant has significant affinity to the CB1 receptor.^[35] Tea (Camellia sinensis) catechins have an affinity for human cannabinoid receptors.^[36] A widespread dietary terpene, beta-caryophyllene, a component from the essential oil of cannabis and other medicinal plants, has also been identified as a selective agonist of peripheral CB₂-receptors, in vivo.^[37] Black truffles contain anandamide.^[38]

Most of the phytocannabinoids are nearly insoluble in water but are soluble in lipids, alcohols, and other non-polar organic solvents.

Cannabis plant profile[edit]

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[edit]

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.^[39] Thus supplementing with CYP 2C9 inhibitors leads to extended intoxication.^[39]

Some is also stored in fat in addition to being metabolized in the liver. Δ⁹-THC is metabolized to 11-hydroxy-Δ⁹-THC, which is then metabolized to 9-carboxy-THC.^[40] 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 or others, 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. This is because they are fat-soluble, lipophilic molecules that accumulate in fatty tissues.^[41]

Separation[edit]

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. Once extracted, isolated components can be separated using wiped film vacuum distillation or other distillation techniques.

History[edit]

Cannabinoids were first discovered in the 1940s, when CBD and CBN were identified. The structure of THC was first determined in 1964.^{[citation needed]}

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.^{[citation needed]}

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.^[6][42]

Types of endocannabinoid ligands[edit]

Arachidonoylethanolamine (Anandamide or AEA)[edit]

Anandamide was the first such compound was identified as arachidonoyl ethanolamine. The name is derived from the Sanskrit word for bliss and -amide. It has a pharmacology similar to THC, although its structure is quite 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.^[43] Anandamide is found in nearly all tissues in a wide range of animals.^[44] Anandamide has also been found in plants, including small amounts in chocolate.^[45]

Two analogs of anandamide, 7,10,13,16-docosatetraenoylethanolamide and homo-γ-linolenoylethanolamine, have similar pharmacology. All of these compounds 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^[46] and in molluscs.^[47]

2-Arachidonoylglycerol (2-AG)[edit]

Another endocannabinoid, 2-arachidonoylglycerol, binds to both the CB₁ and CB₂ receptors with similar affinity, acting as a full agonist at both.^[43] 2-AG is present at significantly higher concentrations in the brain than anandamide,^[48] and there is some controversy over whether 2-AG rather than anandamide is chiefly responsible for endocannabinoid signalling in vivo.^[1] 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.^[49]

2-Arachidonyl glyceryl ether (noladin ether)[edit]

In 2001, a third, ether-type endocannabinoid, 2-arachidonyl glyceryl ether (noladin ether), was isolated from porcine brain.^[50] 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.^[51] It binds to the CB₁ cannabinoid receptor (K_i = 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.^[43]

N-Arachidonoyl dopamine (NADA)[edit]

Discovered in 2000, NADA preferentially binds to the CB₁ receptor.^[52] Like anandamide, NADA is also an agonist for the vanilloid receptor subtype 1 (TRPV1), a member of the vanilloid receptor family.^[53][54]

Virodhamine (OAE)[edit]

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.^[55]

Lysophosphatidylinositol (LPI)[edit]

Recent evidence has highlighted lysophosphatidylinositol as the endogenous ligand to novel endocannabinoid receptor GPR55, making it a strong contender as the sixth endocannabinoid.^[56]

Function[edit]

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 dopamine, endocannabinoids differ in numerous ways from them. For instance, they are used in retrograde signaling between neurons. 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.^[57]

Retrograde signal[edit]

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.^{[citation needed]}

Range[edit]

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.^{[citation needed]}

Synthetic cannabinoids[edit]

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.^[58]

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.^[59]

When synthetic cannabinoids are used recreationally, they present significant health dangers to users.^[60] In the period of 2012 through 2014, over 10,000 contacts to poison control centers in the United States were related to use of synthetic cannabinoids.^[60]

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, Canemes), a synthetic cannabinoid and an analog of Marinol. It is Schedule II unlike Marinol, which is Schedule III
• Rimonabant (SR141716), a selective cannabinoid (CB₁) receptor inverse agonist once used as an anti-obesity drug under the proprietary name Acomplia. It was also used for smoking cessation

Other notable synthetic cannabinoids include:

• JWH-018, a potent synthetic cannabinoid agonist discovered by 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.
• JWH-073
• 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^[61]
• 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

Table of plant cannabinoids[edit]

Table of plant cannabinoids[show]

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

See also[edit]

• Cannabinoid receptor antagonist
• Endocannabinoid enhancer
• Endocannabinoid reuptake inhibitor
• Cancer and nausea § Cannabinoids

References[edit]