(To clarify the scientific nomenclature, the following three phytocannabinoid acids and their neutral forms are referred to as "primary phytocannabinoids" since they are the only phytocannabinoids to be enzymatically-produced directly from the CBGA/CBGVA "parent" precursors.)
Science has discovered nearly 150 phytocannabinoids naturally produced in Cannabis sativa L. (the official taxonomic binomial name for Hemp) . Phytocannabinoids are formed as aromatic carboxylic acids, and are classified as terpenophenolic compounds or "meroterpenes" . Phytocannabinoids are of the few natural exogenous compounds (compounds made outside the body) capable of modulating the receptors and enzymes comprising the Endocannabinoid System of humans and other vertebrates . More details on this fascinating core physiological system can be found in our Endocannabinoid System science and information page.
Interestingly, other species of higher plants, liverworts and fungi produce compounds of similar structure to the phytocannabinoids produced in Hemp, which also interact with vertebrate cannabinoid receptors and have been categorized as phytocannabinoids [1, 2]. Yet, with the exception of Helichrysum umbraculigerum that naturally produces CBG-type compounds at around 0.2% of its weight (or microorganisms and other life genetically modified to produce cannabinoids), Cannabis sativa seems to be the sole natural source of the unique cannabinoids it produces in prolific measure . (Rest assured, CANNACEA products are Non-GMO as Nature intends!)
Close-up of Cannabis flower showing forest of glandular trichomes where phytocannabinoids and phytoterpenes get produced.
This rare dance of cannabis phytochemical genesis takes place within the glandular trichomes, resinous structures emanating across the aerial surface and throughout the lifecycle of the plant . First, olivetolic acid (OA) and geranyl pyrophosphate (GPP) condense to form the initial phytocannabinoid, Cannabigerolic Acid (CBGA) [1-2, 4].
CBGA has a 5-carbon sidechain and is the precursor of "conventional" phytocannabinoids, which likewise have 5-carbon sidechains. In cannabis varieties with high levels of divarinolic acid (DA), which is identical to OA except for its 3-carbon sidechain instead of OA's 5-carbon sidechain, GPP can condense with DA to produce significant levels of Cannabigerovarinic Acid (CBGVA). CBGVA is CBGA's homolog, differing only by having a 3-carbon sidechain instead of CBGA's 5-carbon sidechain. CBGVA is the precursor of "varin" cannabinoids, which likewise have 3-carbon sidechains. [1-2, 4]
Next, CBGA and CBGVA get metabolized into the remaining acid-form primary phytocannabinoids by their respective synthase enzymes endogenously produced by Cannabis sativa, which conversion takes place exclusively within the glandular trichomes [1-4]. In effect, CBGA and its sidechain homologs are the "parent phytocannabinoids"!
CBGA is enzymatically transformed into the “conventional” primary phytocannabinoid acids:
- Cannabidiolic Acid (CBDA)
- Tetrahydrocannabinolic Acid (THCA)
- Cannabichromenic Acid (CBCA)
CBGVA is enzymatically transformed into the “varin-type” primary phytocannabinoid acids:
- Cannabidivarinic Acid (CBDVA)
- Tetrahydrocannabivarinic Acid (THCVA)
- Cannabichromevarinic Acid (CBCVA)
Onwards, these primary phytocannabinoid acids transform by heat, light or oxygen into their neutral forms by shedding their carboxylic acid group, a process known as "decarboxylation" [1-4]. Fresh cannabis plants contain relatively low levels of decarboxylated primary phytocannabinoids (increasing with time and degradation):
"Conventional" Decarboxylated Phytocannabinoids
- Cannabigerol (CBG)
- Cannabidiol (CBD)
- delta-9 Tetrahydrocannabinol (THC)
- Cannabichromene (CBC)
"Varin" Decarboxylated Phytocannabinoids
- Cannabigerovarin (CBGV)
- Cannabidivarin (CBDV)
- Tetrahydrocannabivarin (THCV)
- Cannabichromevarin (CBCV)
Finally, nonenzymatic degradation pathways act on the enzymatically-produced primary phytocannabinoids to form all remaining known "secondary phytocannabinoids" and their isomeric structural analogs through the influence of heat, light or oxygen. This is how delta-9 THC degrades non-enzymatically into CBN or delta-8 THC, for example. [1-4]
Biosynthesis of CBDA, THCA, and CBCA from CBGA through the phytocannabinoid synthase pathways. Degradation of the CBD-, THC-, and CBC-type phytocannabinoids leads to CBE-, CBN-, and CBL-type phytocannabinoids. *This compound was not identified in cannabis by this study. From Hartsel et al, 2016 
Structure/Function Effects of Key Phytocannabinoids
In the following exploration of pioneering phytocannabinoid science, the "major" phytocannabinoids refers to CBD and its acid-form precursor CBDA, which together comprise over 80% of the phytocannabinoid mass in most phytocannabinoid-rich hemp varieties.
The “minor” phytocannabinoids refers to a wide sea of all remaining phytocannabinoids, detectable and undetectable, found in Hemp at significantly lower levels than the major phytocannabinoids CBD/CBDA. These include CBG, CBC, THC, CBN, CBGV, CBDV, and THCV with their acid-form precursors CBGA, CBCA, THCA, CBNA, CBGVA, CBDVA and THCVA, respectively. Besides these, the many remaining minor phytocannabinoids range from low to trace levels and are only beginning to be studied. [1-6]
We shall be discussing the most well-studied phytocannabinoids, with some interesting but less-studied phytocannabinoids covered at the end. While many of the following phytocannabinoids can be detected in our full spectrum hemp oils, please visit our Lab Results to discover which phytocannabinoids are quantified in our products.
CBD is the main phytocannabinoid present in our products. CBD is a relative "late-bloomer on the scene" compared with its sister primary phytocannabinoid, THC. Initially, it seems non-psychotropic CBD didn't garner as much attention as THC, even if CBD was identified and isolated from Cannabis sativa in 1940 by Adams, Hunt and Clark before THC was isolated or synthesized [7-9].
While CBD is one of the main phytocannabinoids in Cannabis sativa, it is almost always the main phytocannabinoid in Hemp. This is because Hemp is defined to have a limited concentration of THC in most jurisdictions (0.3% THC limit in USA) due to THC's psychotropic effects when found at higher levels, while non-psychotropic CBD enjoys no limitations on either side of the Hemp divide. The only time CBD is not the main phytocannabinoid in Hemp is in specialized Hemp varieties where the "parent CBGA" phytocannabinoid is only slightly metabolized into the remaining phytocannabinoid types we know, in which case CBGA and its decarboxylate CBG become the main phytocannabinoids present.
CBD has low in vitro binding affinity and functional activity at the two primary cannabinoid receptors in the human body, CB1 and CB2 [10-11]. However, CBD appears to be a potent "negative allosteric modulator" at both the CB1 receptor  and the CB2 receptor , meaning it suppresses the activating effects of other compounds at these cannabinoid receptors, hence why CBD has been shown to suppress various effects of THC [14, 56, 67-68].
CBD is an antagonist at the G-protein-coupled receptor 55 (GPR55), a novel endocannabinoid receptor discovered in 1999, and was shown to significantly help regulate bone growth functionality in mice .
CBD is a potent inhibitor of fatty acid amide hydrolase (FAAH), an enzyme responsible for degrading one of the major endocannabinoids naturally produced in our bodies, anandamide (AEA), and is also a potent inhibitor of the cellular re-uptake of anandamide, thereby increasing levels of anandamide through two simultaneous pathways [16-17].
Beyond the cannabinoid receptors, CBD has numerous biological targets resulting in a variety of physiological effects. These include the ability to help regulate various immune functions, cellular functions, inflammatory functions, and cardiac rhythmic functioning .
Particularly by acting as an agonist of the 5-HT1A serotonin receptor, multiple in vivo studies demonstrated how CBD helps regulate acute autonomic responses related to psychological function, and the functioning of nausea and vomiting responses .
CBD activates and desensitizes the transient receptor potential TRPA1 channel , as well as TRPV1, TRPV2, and TRPV3 channels , with especially high efficacy and potency at TRPV3 . Confirming these in vitro results with the help of rats, CBD dose-dependently stimulated antinociceptive pathways and caused analgesia in vivo .
CBD was found to be potent in its activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance, with no significant difference in such antibacterial activity compared with CBG, CBC, CBN and THC .
Taken orally by humans, CBD is primarily metabolized by the liver, and somewhat the GI tract, into active 7-OH-CBD that gets converted to inactive 7-COOH-CBD. Taken in oil form, CBD is subjected to significant first-pass liver metabolism before entering the blood, having ~80% transformed into 7-COOH-CBD, ~10% into 7-OH-CBD, with ~10% remaining as parent CBD. [69-71]
Together with the millennia that humans have safely used Hemp as a food and dietary supplement, there is substantial modern in vitro and in vivo clinical evidence, in both humans and animals, that CBD has a favorable safety profile when taken at levels corresponding with those provided by the suggested use of our supplements. [21-27]
CBDA is the carboxylic acid precursor of CBD, losing its additional CO2 to become CBD via "decarboxylation" by heating or light-exposure [1-4]. Like CBD, CBDA does not produce any psychotropic effects [3, 6]. Unlike CBD, however, CBDA exhibits poor penetration into the brain through the blood-brain barrier like all acid-form phytocannabinoids . CBDA is normally found only at unquantifiable trace levels in our decarboxylated full spectrum hemp oils, but it is still lovely introducing you to the precursor phytocannabinoid of CBD!
CBDA has no significant in vitro activity or affinity for the CB1 receptor of the Endocannabinoid System, however it does enhance 5-HT1A serotonin receptor activation . Furthermore, particularly within a full spectrum phytocannabinoid profile, CBDA is both a potent inhibitor of monoacylglycerol lipase (MAGL), an enzyme responsible for degrading one of the major endocannabinoids naturally produced in our bodies, 2-AG, as well as a potent inhibitor of the cellular re-uptake of anandamide, thereby increasing levels of the endocannabinoids through multiple pathways . CBDA is also a potent inhibitor of the pro-inflammatory cyclooxygenase-2 (COX-2) .
CBDA was found to help regulate psychological function and the functioning of nausea and vomiting responses in shrews and rats [29, 31-32].
CBG is the neutral form of CBGA, the acid form "parent phytocannabinoid" of all 100+ phytocannabinoids in Cannabis. Like all other neutral phytocannabinoids, CBG is formed by the decarboxylation of CBGA. CBG is usually found at low levels in hemp since the majority of it will have been converted onwards to other major and minor phytocannabinoids, unless it is a rare variety lacking onward synthase enzymes. [1-4]
CBG has been proven to be non-psychotropic in vivo , as expected with its in vitro affinity and activity at both CB1 and CB2 receptors being several orders of magnitude lower than psychotropic THC's [11, 34]. However, CBG has been found to regulate signaling of other cannabinoids at the CB1 and CB2 receptors in vitro .
CBG, particularly within a full spectrum phytocannabinoid profile, also affects endocannabinoid tone by inhibiting FAAH, MAGL, and NAAA, enzymes responsible for degrading the key endocannabinoids anandamide and 2-AG, while also inhibiting anandamide cellular reuptake [16-17].
In vitro, CBG has been shown to act as a potent alpha-2 adrenoceptor agonist, as well as a moderate antagonist of 5-HT1A serotonin receptor agonists . This is in opposition to the effect CBD has at 5-HT1A, mentioned above, and could be why CBG is able to antagonize the effects CBD has on the functioning of nausea and vomiting responses in rats and shrews .
As do many phytocannabinoids, CBG interacts with various TRP channels, showing potent agonist activity at TRPA1, weak agonist activity at TRPV1 and TRPV2, with potent antagonism at TRPM8 in vitro .
CBG was found to be potent in its activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance, with no significant difference in such antibacterial activity compared with CBD, CBC, CBN and THC .
CBC is the neutral form of CBCA from which it is derived by decarboxylation [1-4]. It was first discovered in 1966 simultaneously by Claussen and colleagues alongside Gaoni and Mechoulam .
While CBC was initially found to be sedative in dogs and caused slight muscular coordination effects in rats, it was subsequently found to be non-psychoactive in humans and rhesus monkeys .
CBC has 1-2 orders of magnitude lower in vitro affinity and activity at the CB1 and CB2 receptors compared with THC . However, particularly within a full spectrum phytocannabinoid profile, CBC affects endocannabinoid tone by inhibiting FAAH, MAGL, and NAAA, enzymes responsible for degrading the key endocannabinoids anandamide and 2-AG, while also inhibiting anandamide cellular reuptake [16-17].
CBC has been shown to be antinociceptive in rats . Of all the primary and secondary phytocannabinoids tested through one in vitro study, CBC was the most potent agonist at TRPA1 channels, also activating TRPV3 and TRPV4 channels, while strongly desensitizing all three of these TRP channels .
CBC has also been shown to raise the viability of adult mouse neural stem/progenitor cells (NSPCs) during differentiation .
CBC was reported as outperforming the other primary phytocannabinoids in terms of anti-bacterial and anti-fungal functionality , though there was no significant difference compared with CBD, CBG, CBN and THC in their high potency of activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance .
CBN is the neutral form of CBNA from which it can be derived by decarboxylation [1-4]. CBN is the degradation byproduct of THC, once the latter phytocannabinoid is exposed to oxygen and light [1-6], in the same manner as CBNA gets derived from THCA. Hence, CBN and CBNA are considered non-enzymatically-produced "secondary phytocannabinoids". Importantly, the levels of CBN and CBNA are often used as general markers in assessing the age and storage quality of a cannabis sample.
CBN was the first-ever cannabinoid to be isolated in 1896 by Wood, Spivey and Easterfield, using charas resin from cannabis grown near the banks of the Yamuna River in Northern India .
CBN has been shown to have 10% the psychotropic effect of THC in humans . This is related to how CBN has lower binding affinity than THC does at the CB1 and CB2 receptors, normally by one order of magnitude or more in various in vitro assays, though both phytocannabinoids share similar functional activity at these receptors [17, 34]. While CBN has been shown to have a small potentiating effect on THC’s physiological and psychological effects in humans , when CBN is added to THC the effects are not significantly additive in terms of in vitro CB1 receptor affinity .
CBN is a potent agonist and desensitizer of TRPA1 channels, while potently blocking TRPM8 channels .
CBN has been shown to help regulate involuntary muscular functions in mice , inflammatory functions in rats , as well as immunological functions in various animal models .
CBN was found to be potent in its activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance, with no significant difference in such antibacterial activity compared with CBD, CBG, CBC and THC .
CBDV is the neutral form of CBDVA from which it is derived by decarboxylation [1-4]. CBDV was first isolated by Vollner and colleagues in 1969 .
While most Cannabis sativa varieties from around the World contain detectable amounts of the “varin-type” phytocannabinoids (CBDV, CBDVA, THCV, THCVA, CBGV, CBGVA, etc), these varin-types are normally only found at significant levels in varieties native to Asia and Africa, the highest levels being found in feral varieties from India and Nepal [48-49].
CBDV is virtually identical to CBD, except that CBDV has 3 carbons on its sidechain compared with the 5-carbon sidechain of its more ubiquitous homolog CBD, due to CBDVA being biosynthesized in the cannabis plant from CBGVA instead of CBGA [1-4].
Like CBD, CBDV is non-psychotropic and has been shown to help regulate involuntary muscular functions [50-51]. CBDV also affects endocannabinoid tone by inhibiting FAAH and NAAA, two enzymes responsible for degrading the key endocannabinoid anandamide, while also inhibiting anandamide cellular reuptake .
CBDV is a potent agonist at TRPA1 channels, and a less potent agonist at TRPV1 and TRPV2 channels, while antagonizing calcium ion elevation at TRPM8 . CBDV is also an agonist at TRPV3 channels .
THC is the neutral form of THCA from which it is derived by decarboxylation [1-4]. THC was first isolated by Wollner, Matchett, Levine and Loewe in 1942 , followed almost a quarter-century later by Gaoni and Mechoulam isolating and partially synthesizing THC in 1964 . THC's psychotropic effects are arguably one of the major reasons cannabis became quite famous (and infamous) across recorded human history.
THC displays partial agonist activity at both CB1 and CB2 receptors . THC with its analogs, homologs and degradation products are the only phytocannabinoids having significant, detectable psychotropic or psychotomimetic effects, since their binding affinities to the CB1 receptor are one or more orders of magnitude greater than those of the other phytocannabinoids [17, 34]. The CB1 receptor, found primarily in the central nervous system (brain), mediates most of the psychotropic effects of THC .
Clinical studies demonstrate that 2.5 mg is the Lowest Observed Effect Level (LOEL) dose for THC taken alone for the majority of naive users . Our supplement formulations and suggested serving sizes are designed so the LOEL of THC is neither reached nor breached , even before accounting for how CBD suppresses various side effects of THC when CBD is taken at a higher dose than THC [14, 56, 67-68].
Beyond the cannabinoid receptors, THC displays a wide variety of physiological effects in vitro on various other human receptors and enzymes in the low micro-molar range and below, including at G-protein-coupled receptors GPR55 and GPR18, peroxisome proliferator-activated receptor gamma (PPARγ), transient receptor potential (TRP) channels, and cytochrome P450 (CYP) enzymes .
THC has also displayed significant 5-HT3A serotonin receptor antagonism and allosterism, hence its well-established ability to help regulate the functioning of nausea and vomiting responses [57-58].
THC was found to be potent in its activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance, with no significant difference in such antibacterial activity compared with CBD, CBG, CBC and CBN .
Taken orally by humans, THC is metabolized into active 11-OH-THC that gets converted to inactive 11-COOH-THC. Similarly to CBD, taken in oil-form, THC is subjected to significant first-pass liver metabolism before entering the blood, with ~80% transformed into 11-COOH-THC, ~10% into 11-OH-THC, and ~10% remaining as parent THC. 
CBE is the primary degradation product of CBD by pyrolysis (heat) or photo-oxidation [1, 3, 59].
CBL is the primary degradation product of CBC by pyrolysis (heat) or photo-oxidation [1, 3, 59].
CBT is one of the phytocannabinoids found within Cannabis sativa [1, 3, 59], having been first discovered by Ludwig Bercht and colleagues in a sample from Lebanese cannabis .
Not much else was known about CBT until recently, when nuclear magnetic resonance and associated molecular structure analyses were performed on CBT by Jared Wood and colleagues. Their research not only firmly established its atomic configuration, but also suggests CBT is a secondary phytocannabinoid formed non-enzymatically as a byproduct of primary phytocannabinoid transformation. Furthermore, they suggest CBT is a natural transformational byproduct of CBC. 
Not to be confused with Cannabitriol that is often given the same acronym "CBT".
The decarboxylation product of THCVA, THCV is the 3-carbon sidechain "varin" homolog of THC (THC has a 5-carbon sidechain like all "conventional" cannabinoids). [1-6]
THCV has approximately 20% - 25% the potency and psychoactivity of THC . This is probably due to it having lower binding affinity and functional activity at the CB1 and CB2 receptors than THC, though the affinity of THCV at these receptors is within one order of magnitude of THC's [17, 34].
Interestingly, in opposition to THC’s appetite-inducing effects, THCV has demonstrated appetite suppression in rats while also helping regulate the functioning of nausea responses .
d8THC is a degradation product of THC, of which it is an analog [1-6]. d8THC has been shown to be 2/3rds as potent and psychoactive as THC .
Cannabidibutol (CBDB) & Tetrahydrocannabutol (THCB):
CBDB and THCB are the 4-carbon sidechain homologs of CBD and THC, respectively, and are naturally produced at low levels in cannabis [63-64].
Cannabidiphorol (CBDP) & Tetrahydrocannabiphorol (THCP):
CBDP and THCP, recently-discovered in 2019 by Citti, Linciano and colleagues, are the 7-carbon sidechain homologs of CBD and THC, respectively, and are naturally produced at low levels in cannabis . 7-carbon sidechain homologs of CBD and THC were not thought to naturally occur in cannabis until this discovery.
Cannabinoid structural and functional research indicates the 7-carbon sidechain increases binding affinity at the CB1 and CB2 receptors compared with the 5-carbon sidechain of "conventional" phytocannabinoids, thereby increasing potency of their effects at these receptors . This allows THCP to be considered a potent "full agonist" at the CB1 receptor whereas THC is considered a "partial agonist" with its lower CB1 binding affinity.
Note: We exist to help you optimize the greatest health, joy, and success, yet we have not mentioned potential effects that the phytocannabinoids in our products may have on specific diseases. Supplements are restricted from declaring the ability to diagnose, treat, cure or prevent any disease, irrespective of the quality of supporting scientific evidence. Still, supplements are at least allowed to inform about their structural or functional effects as supported by science. Your trusted physician should be the source for specific health recommendations. There are also plenty of peer-reviewed studies available online for you to independently research. Our mission is simply to produce the finest hemp supplements possible with exemplary safety and efficacy, while providing some education and inspiration along the way!
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