Editing Cannabinol (section)

====Putative receptor targets====
The table highlights several common cannabinoids along with putative receptor targets and therapeutic properties. Exogenous (plant-derived) phytocannabinoids are identified with an asterisk while remaining chemicals represent well-known [[Endocannabinoid system|endocannabinoids]] (i.e., endogenously produced cannabinoid receptor [[Ligand (biochemistry)|ligands]]).

{| class="wikitable"
! Full Name
! Known Receptor Targets
! Putative Therapeutic Properties
|- style="vertical-align: top;"
| Cannabichromene (CBC)
|
* Agonist at CB2,<ref name="Sampson-2021">{{cite journal | vauthors = Sampson PB | title = Phytocannabinoid Pharmacology: Medicinal Properties of ''Cannabis sativa'' Constituents Aside from the "Big Two" | journal = Journal of Natural Products | volume = 84 | issue = 1 | pages = 142–160 | date = January 2021 | pmid = 33356248 | doi = 10.1021/acs.jnatprod.0c00965 | s2cid = 229694293 }}</ref> TRPV3, and most potent phytocannabinoid at TRPA1<ref name="Sampson-2021" /><ref name="Muller-2019" />
* Very low efficacy at TRPV1 and TRPV4, but may reduce expression of TRPV4 in the presence of inflammation<ref name="Muller-2019" />
* High affinity for CB1 but no observed functional activity<ref name="Sampson-2021" />
* Antagonist at TRPM8<ref name="Muller-2019" />
|
* Antimicrobial and anti-inflammatory<ref name="Sampson-2021" />
* Potential neuroprotective effects<ref name="Sampson-2021" />
* Potential efficacy in treatment of inflammatory pain<ref name="Sampson-2021" />
|- style="vertical-align: top;"
| Cannabidiol (CBD)
|
* Very weak affinity for CB1 and CB2<ref name="Cherkasova-2022">{{cite journal | vauthors = Cherkasova V, Wang B, Gerasymchuk M, Fiselier A, Kovalchuk O, Kovalchuk I | title = Use of Cannabis and Cannabinoids for Treatment of Cancer | journal = Cancers | volume = 14 | issue = 20 | pages = 5142 | date = October 2022 | pmid = 36291926 | pmc = 9600568 | doi = 10.3390/cancers14205142 | doi-access = free }}</ref>
* Conflicting reports but generally described as negative allosteric modulator at CB1 & CB2, altering THC activity when THC & CBD are coadministered<ref name="Cherkasova-2022" />
* Agonist at TRPA1,<ref name="Muller-2019" /> TRPV1 (high potency at this “capsaicin receptor” without ablative effects<ref name="Muller-2019" />), TRPV2, TRPV3, PPARγ, 5-HT1A, A2 and A1 adenosine receptors<ref name="Cherkasova-2022" />
* Highest potency at TRPV1<ref name="Muller-2019" />
* Antagonist at GPR55, GPR18, 5-HT3A,<ref name="Cherkasova-2022" /> with highest potency as antagonist at TRPM8<ref name="Muller-2019" />
* Inverse agonist at GPR3, GPR6, and GPR12<ref name="Cherkasova-2022" />
|
* Anti-inflammatory<ref name="Mead-2019">{{cite journal | vauthors = Mead A | title = Legal and Regulatory Issues Governing Cannabis and Cannabis-Derived Products in the United States | journal = Frontiers in Plant Science | volume = 10 | pages = 697 | date = 2019-06-14 | pmid = 31263468 | pmc = 6590107 | doi = 10.3389/fpls.2019.00697 | doi-access = free }}</ref><ref name="Muller-2019" />
* Anti-convulsant<ref name="Mead-2019" />
* Potential efficacy in treatment of inflammatory and chronic pain<ref name="Muller-2019" />
|- style="vertical-align: top;"
| Cannabigerol (CBG)
|
* Low affinity agonist and partial agonist at CB1 and CB2, respectively<ref name="Sampson-2021" />
* Agonist at α2adrenoceptor<ref name="Sampson-2021" /> and TRP channels such as TRPA1, TRPV2, and TRPV3, with highest potency as agonist at TRPV1<ref name="Muller-2019" />
* Readily desensitizes but low affinity for TRPV4<ref name="Muller-2019" />

* Antagonist at 5-HT1A<ref name="Sampson-2021" /> and TRPM8<ref name="Muller-2019" />
|
* Anti-microbial, anti-inflammatory, and anti-nociceptive effects<ref name="Sampson-2021" />
* Neuroprotective properties via mitigation of oxidative stress<ref name="Sampson-2021" />
* Potential anti-tumor agent<ref name="Sampson-2021" />
* Potential efficacy in treatment of chemotherapy-induced muscle atrophy and weight loss<ref name="Sampson-2021" />
|- style="vertical-align: top;"
| Cannabinol (CBN)
|
* Agonist at CB1 and CB2, with some evidence of slightly higher affinity at CB2<ref name="Sampson-2021" />
* Low affinity agonist at TRPV1, TRPV2, TRPV3, TRPV4, and TRPA1,<ref name="Muller-2019" /> but readily desensitizes TRPV4<ref name="Muller-2019" />
* Antagonist at TRPM8<ref name="Muller-2019" />
|
* Antimicrobial and anti-inflammatory / immunosuppressive effects<ref name="Sampson-2021" />
* Potential efficacy in treatment of ocular disease and epidermolysis bullosa<ref name="Sampson-2021" />
* Reported neuroprotective effects (synergistic if coadministered with other cannabinoids)<ref name="Sampson-2021" />
* Relevance to pain, itch, and inflammation via TRP channel activity<ref name="Sampson-2021" />
|- style="vertical-align: top;"
| Tetrahydrocannabinol (THC) / Delta-9-Tetrahydrocannabinol (Δ<sup>9</sup>-THC)
|
* Agonist at CB1 and CB2, as well as GPR55, GPR18, PPARγ, and TRPA1<ref name="Muller-2019" /><ref name="Cherkasova-2022" />
* Antagonist at TRPM8<ref name="Muller-2019" /><ref name="Cherkasova-2022" /> and 5-HT3A<ref name="Cherkasova-2022" />
* Differing activity across TRP channels: highest potency phytocannabinoid at TRPV2; modest activity at TRPV3, TRPV4, TRPA1, and TRPM8; no activity observed at TRPV1<ref name="Muller-2019" />
* Importantly, 11-OH-THC, the active metabolite generated via first-pass-metabolism of THC, demonstrates different binding profile at TRP channels<ref name="Muller-2019" />
|
* Potential relevance to sleep induction (e.g., increased adenosine levels<ref name="Cherkasova-2022" />) and increased quality of sleep<ref name="Muller-2019" />
* Dose-dependent anxiolytic effects,<ref name="Muller-2019" /> with anxiogenic effects at high doses
* Appetite stimulation<ref name="Muller-2019" /><ref name="Legare-2022" />
* Anti-nausea<ref name="Muller-2019" /><ref name="Legare-2022" />
* In combination with CBD, potential efficacy in treatment of spasticity, neuropathic pain and muscle spasticity (see Sativex: THC-containing therapeutic approved in Europe as treatment for Multiple Sclerosis)
|- style="vertical-align: top;"
| 2-Arachidonoylglycerol (2-AG)
|
* Partial agonist at CB1 (e.g., on lysosomal surface, increasing lysosomal integrity) and CB2<ref name="Cherkasova-2022" />
* Agonist at GPR55, GPR18, GPR119, PPAR, and robust activation at TRPV4<ref name="Muller-2019" /><ref name="Cherkasova-2022" />
|
* Anti-oxidative properties<ref name="Cherkasova-2022" />
* Increased lysosomal stability & integrity<ref name="Cherkasova-2022" />
* Attenuation of mitochondrial damage during cell stress<ref name="Cherkasova-2022" />
|- style="vertical-align: top;"
| Anandamide (AEA)
|
* Agonist at GPR18, GPR119, and PPAR, with robust activation at TRPV4, and very high efficacy at TRPA1<ref name="Muller-2019" /><ref name="Cherkasova-2022" />
* Potent partial agonist at GPR55<ref name="Cherkasova-2022" /><ref name="Legare-2022" />
* Low-affinity full agonist at TRPV1,<ref name="Muller-2019" /><ref name="Legare-2022" /> with similar but less potent affinity as compared to capsaicin<ref name="Muller-2019" />
* Antagonist at TRPM8<ref name="Muller-2019" />
| Anti-oxidative properties<ref name="Cherkasova-2022" />
|}