Cannabinol
Also known asCannabinolo · Cannabinolum · Cannabinolo [DCIT] · Cannabinol (CBN) · Cannabinolum [INN-Latin] · Cannabinol (6CI) · CANNABINOL [MI] · CANNABINOL [INN]
6,6,9-trimethyl-3-pentylbenzo[c]chromen-1-ol
- PubChem CID
- 2543
- ChEMBL
- CHEMBL74415
- Measurements
- 25
- InChIKey
- VBGLYOIFKLUMQG-UHFFFAOYSA-N
I · Summary
What is known
Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.
What it is
Cannabinol (CBN) is a physiologically inactive constituent of Cannabis sativa.
cannabinol has been reported in Cannabis sativa with data available.
Cannabinol is a cannabinoid isolated from the plant Cannabis that is a metabolite of tetrahydrocannabinol (THC), with potential immunosuppressive and anti-inflammatory activities. Cannabinol preferentially binds to the cannabinoid G-protein coupled receptor CB2, which is mainly expressed on a variety of immune cells, such as T-cells, B-cells, macrophages and dendritic cells. Stimulation of CB2 receptors by cannabinol may both trigger apoptosis in these cells and inhibit the production of a variety of cytokines. Cannabinol exerts minimal affinity for CB1 and has a weak effect on the central nervous system.
A physiologically inactive constituent of Cannabis sativa L.
History, discovery and cultural use
— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when Cannabinol was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.
Histories of this field
Scholarship on psychedelics generally, not on Cannabinol specifically. Whether any of these treats this compound is a question for the book, not for this page.
Mescaline: A Global History of the First Psychedelic
Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.
Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.
Expanding Mindscapes: A Global History of Psychedelicsopen access
Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.
Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.
Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers
Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.
Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.
Psychonauts: Drugs and the Making of the Modern Mind
The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.
Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.
Ancient Psychoactive Substances
Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.
Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.
A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.
Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.
Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.
Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.
Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.
Institutional archives
- Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
- Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.
The rest of this dossier
- Affinity — 25 measurements in this archive, equilibrium constants kept apart from functional readouts.
- Toxicology — nothing published for Cannabinol. An absent record is an absence of study, not evidence of safety.
- Legal — no DEA record is held here — which is not a finding that this compound is uncontrolled.
- Systems — where this compound’s targets are transcribed, by brain region and tissue.
Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Cannabinol is the history note, which says so on its face and carries a reference for every claim in it.
II · Identity
Structure and descriptors
Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.
- Formula
- C21H26O2R
- Molecular weight
- 310.44g/molR
- Exact mass
- 310.1933DaR
- cLogP
- 5.73R
- TPSA
- 29.5ŲR
- H-bond donors
- 1R
- H-bond acceptors
- 2R
- Rotatable bonds
- 4R
- Aromatic rings
- 2R
- Heavy atoms
- 23R
- Fraction sp³
- 0.429R
- Formal charge
- 0R
Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.
Bemis–Murcko scaffold
c1ccc2c(c1)COc1ccccc1-2
No other compound in this archive shares it. All families
III · Behavior
Behavioral summary
Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.
Classification
MeSH indexes no pharmacological class for this compound.
Duration of acute subjective effects
—
No controlled human trial reporting a duration for this compound is cited here. The archive holds no other record of one either. A duration is not inferred from a chemical relative.
Plasma elimination half-life
How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.
No half-life is published for this compound in the sources this site reads.
Primary pharmacological drivers
ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.
Nothing about this compound’s pharmacology is published with a citation in the sources this site reads. The measured binding data below is what the archive can show.
IV · Clinical
Clinical description
Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.
No diagnostic chapter is shown for this compound. Either PubChem records no MeSH pharmacological class for it, or the class it records is not one of the substance classes ICD-11 gives a chapter to. Inferring a chapter from the compound’s name or its binding profile would be a diagnosis this archive is in no position to make.
How much has been written about each domain
The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.
None of the 0 records this archive holds for this compound uses a term from any of the clinical domains. That is a statement about the literature recorded here, not about the compound.
V · Systems
Systems physiology
Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.
Brain
basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.
Measured but not drawn — this anatomogram has no outline for them: spinal cord 18.8, pituitary gland 17.3, midbrain 15.5, retina 12.0.
Body
Square-root ramp · shared scale across both plates
Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.
Brain regions
Regions where this compound's measured targets are transcribed. Linked from the plate above.
basal ganglia
20.7 nTPMspinal cord
18.8 nTPMcerebral cortex
18.6 nTPMcerebellum
18.3 nTPMpituitary gland
17.3 nTPMmidbrain
15.5 nTPMamygdala
13.3 nTPMhippocampal formation
13.2 nTPMretina
12.0 nTPMhypothalamus
12.0 nTPM
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
liver
1507.9 nTPMheart muscle
83.9 nTPMsmall intestine
78.5 nTPMurinary bladder
32.8 nTPMsmooth muscle
32.8 nTPMduodenum
32.1 nTPMspleen
25.7 nTPMskeletal muscle
23.7 nTPMkidney
22.5 nTPMsalivary gland
18.1 nTPMcolon
17.9 nTPMlung
15.8 nTPMstomach 1
14.7 nTPMadrenal gland
11.3 nTPMthyroid gland
8.5 nTPMpancreas
6.8 nTPM
Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.
2 of this compound’s targets could not be resolved to a gene and are absent from both columns: Transient receptor potential cation channel subfamily A member 1, Transient receptor potential cation channel subfamily V member 2.
Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.
VI · Profile
Affinity rosette
The strongest measurement at each of 11 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.
VII · Toxicology
Toxicological profile
What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.
Measured in this archive
Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.
Cytochrome P450 inhibition 6
Inhibition of a drug-metabolising enzyme, which is how interactions arise — the harmala alkaloids' MAO inhibition is the same kind of fact, and appears with the measurements above.
- Cytochrome P450 1B1Ki148nMCHEMBL4035358
- Cytochrome P450 2A6Ki1,000nMCHEMBL5096668
- Cytochrome P450 2B6Ki2,550nMCHEMBL5096670
- Cytochrome P450 2J2IC5019,000nMCHEMBL5096666
- Cytochrome P450 2A6IC5030,400nMCHEMBL5096667
- Cytochrome P450 2B6Ki39,000nMCHEMBL5096669
Published toxicology
— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Cannabinol. They index compounds that have been studied for decades, so most of this archive has no entry. An absent record is an absence of study, not evidence of safety.
Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.
VIII · Evidence
Every measurement
One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.
Equilibrium binding constants 10
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| CB2 | Cannabinoid receptors | Ki | 96.00 | 7.02 | Homo sapiens | CHEMBL658959 |
| CB1 | Cannabinoid receptors | Ki | 100 | 7.00 | Homo sapiens | CHEMBL6083332 |
| Cytochrome P450 1B1 | Enzymes | Ki | 148 | 6.83 | Homo sapiens | CHEMBL4035358 |
| CB1 | Cannabinoid receptors | Ki | 308 | 6.51 | RAT | PMID 11408610 |
| CB1 | Cannabinoid receptors | Ki | 308 | 6.51 | Homo sapiens | CHEMBL657905 |
| CB1 | Cannabinoid receptors | Ki | 392 | 6.41 | Rattus norvegicus | CHEMBL658895 |
| Cytochrome P450 2A6 | Enzymes | Ki | 1,000 | 6.00 | Homo sapiens | CHEMBL5096668 |
| CB1 | Cannabinoid receptors | Ki | 1,100 | 5.96 | Homo sapiens | CHEMBL5096660 |
| Cytochrome P450 2B6 | Enzymes | Ki | 2,550 | 5.59 | Homo sapiens | CHEMBL5096670 |
| Cytochrome P450 2B6 | Enzymes | Ki | 39,000 | 4.41 | Homo sapiens | CHEMBL5096669 |
Functional readouts 15
IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.
- P
- PubChem
- C
- ChEMBL
- R
- Computed here with RDKit
- D
- Derived here from the stored measurement
IX · Trials
Registered clinical trials
Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.
6T
Registered studies
1T
Open or ongoing
6T
With a phase recorded
By phase
A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.
- Phase 11
- Phase 23
- Phase 31
- Not applicable3
By status
The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.
- Completed4
- Not yet recruiting1
- Unknown status1
Every matched study
Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.
- NCT07821840Not yet recruiting · Not applicable
CannaRiver CBD Calm for Anxiety, Sleep, and Well-Being in Adults With Generalized Anxiety Disorder
- Enrollment
- 60Testimated
- Started
- 2026-11-01
- Sponsor
- Associação Pan-Americana Multidisciplinar de Endocanabinologia
Conditions Generalized Anxiety Disorder
Matched “Cannabinol (CBN)” in the study’s intervention “Cannabidiol (CBD) With Cannabinol (CBN) and Cannabigerol (CBG) Oral Tincture (CannaRiver CBD Calm)”
- NCT05344170Completed · Phase 1 / Phase 2
Cannabinol Use in Patients With Insomnia Disorder
- Enrollment
- 20Tactual
- Started
- 2022-08-24
- Sponsor
- Woolcock Institute of Medical Research
Conditions Insomnia Disorder
Matched “Cannabinol (CBN)” in the study’s intervention “30 mg Cannabinol (CBN)”
- NCT05212402Completed · Not applicable
Assessing the Effects of a Cannabidiol Derived From Hemp Supplement in Healthy Adults
- Enrollment
- 56Tactual
- Started
- 2022-01-18
- Sponsor
- University of South Carolina
Conditions Healthy · Safety Issues
Matched “Cannabinol” in the study’s intervention “Cannabinol”
- NCT04908215Completed · Phase 2
INM-755 (Cannabinol) Cream for Treatment of Epidermolysis Bullosa
- Enrollment
- 19Tactual
- Started
- 2021-12-28
- Sponsor
- InMed Pharmaceuticals Inc.
Conditions Epidermolysis Bullosa Simplex · Epidermolysis Bullosa, Junctional · Epidermolysis Bullosa Dystrophica · Kindler Syndrome
Matched “Cannabinol” in the study’s intervention “INM-755 (cannabinol) cream”
- NCT03675971Unknown status · Phase 2 / Phase 3
COPE: Cannabinoids to Obviate Pain Experiment After Knee Replacement
- Enrollment
- 220Testimated
- Started
- 2020-05-01
- Sponsor
- Unity Health Toronto
Conditions Arthroplasty, Replacement, Knee
Matched “Cannabinol” in the study’s intervention “Cannabinol”
- NCT00270803Completed · Not applicable
The Effects of Marijuana on Orientation and Motor Coordination and Brain Metabolism in Regular Smokers of Marijuana
- Enrollment
- 12Tactual
- Started
- 2004-07
- Sponsor
- Tel-Aviv Sourasky Medical Center
Conditions Marijuana Dependence
Matched “Cannabinol” in the study’s intervention “Tetra Hydro Cannabinol (THC)”
Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.
Searched as Cannabinol · Cannabinolo · Cannabinolum. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.
A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Cannabinol worked.
X · Legal
Controlled-substance status
United States federal scheduling, read from the DEA records this archive holds. Not legal advice, and an absent record is not a finding that a compound is uncontrolled.
An absent DEA record is not a finding that Cannabinol is legal. It means this archive holds no DEA passage for it. The Controlled Substances Analogue Enforcement Act reaches substances that appear on no schedule by name, and many compounds here are ring-substituted analogues of scheduled drugs. Nothing on this plate should be read as saying a compound may lawfully be made, held or supplied.
United States federal status only. State law differs, and so does the law of every other country — none of it is represented here. Scheduling changes, and this reflects the DEA records held by PubChem descriptive sections when the monograph was last harvested, not necessarily today. This is a record of what a database publishes, not legal advice.
XI · Literature
Sources behind this dossier
The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.
Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.
- 01
Evidence for a new G protein-coupled cannabinoid receptor in mouse brain
Breivogel CS, Griffin G, Di Marzo V et al. · Molecular pharmacology 2001
- · 1 measurement at 1 target (Ki), strongest CB1 at 6.51 pX