Cannabinol

Cannabinol at a Glance

Cannabinol (CBN) is not made by the plant in any quantity — it is what THC becomes when it oxidises in air, so its concentration is a record of how the material was handled rather than of what the plant was.

It is mildly psychoactive, far weaker than THC, and it is marketed heavily as a sleep cannabinoid.

That reputation is the interesting part, because the evidence behind it is surprisingly thin — it traces largely to old studies of CBN given with THC, where the sedation is attributable to the THC.

It was also the first cannabinoid anyone isolated, in 1896, and for forty years it was mistaken for the active principle of the plant.

The First Cannabinoid

CBN was isolated from charas — Indian hemp resin — by Thomas Barlow Wood, W. T. Newton Spivey and Thomas Hill Easterfield at Cambridge in 1896 ^{6Reference 6Wood TB et al. · 1896XL.—CharasView study →}, and described in detail three years later in a paper simply titled Cannabinol, Part I ^{7Reference 7Wood TB et al. · 1899III.—CannabinolView study →}. It was the first cannabinoid anyone obtained pure, and for the next four decades it was widely taken to be the compound responsible for cannabis’s effects.

That was wrong, and it took a long time to correct. R. S. Cahn established cannabinol’s correct structure in 1932 ^{8Reference 8Cahn RS · 1932Cannabis indica resinView study →}, and Roger Adams confirmed it by total synthesis in 1940 ^{9Reference 9Adams R et al. · 1940Structure of cannabinolView study →}. But the actual psychoactive principle, THC, was not isolated and characterised until 1964 ^{13Reference 13Gaoni Y · 1964Isolation, structure, and partial synthesis of an active constituent of hashishView study →} — sixty-eight years after CBN.

The reason for the confusion is chemical rather than careless. Nineteenth- and early-twentieth-century work was done on aged resin, in which much of the THC had already oxidised to CBN. The compound that crystallised most readily out of old charas was the degradation product, not the active one. Anyone studying cannabis before chromatography was, in effect, studying what was left.

That history matters for how the modern claims are read. CBN’s reputation as the sedating cannabinoid is older than the knowledge that THC exists, and it was formed at a time when “cannabinol” was a name for whatever in cannabis did things.

An Ageing Marker, Not a Plant Product

Cannabis does not make cannabinol in any quantity. CBN is what THC becomes when it oxidises, so a CBN figure on a certificate of analysis is a record of the material’s history rather than of its genetics.

The classic storage study is more specific than the folklore. Fairbairn and colleagues stored solutions of pure cannabinoids and eleven samples of herbal and resin cannabis under controlled conditions and found that exposure to light was the single greatest cause of cannabinoid loss — but that light-driven loss of THC did not produce a corresponding increase in cannabinol. Air oxidation in the dark did ^{10Reference 10Fairbairn JW et al. · 1976The stability of cannabis and its preparations on storageView study →}. Temperature up to 20 °C mattered little, and carefully prepared material kept in the dark at room temperature was reasonably stable for one to two years, because the intact glandular trichomes act as “well filled, well closed containers” ^{10Reference 10Fairbairn JW et al. · 1976The stability of cannabis and its preparations on storageView study →}.

So the useful reading of a CBN number is narrower than “this is old”. It says the material has been exposed to air, with the trichomes broken or the flower ground, rather than simply stored a long time or left in the light.

Two practical consequences follow. Freshly harvested and well-cured cannabis contains very little CBN, and in seized samples it stays under about 1% even where THC exceeds 10% ^{11Reference 11ElSohly MA et al. · 2024ObservationalA 10-year trend in cannabis potency (2013–2022) in different geographical regions of the United States of America — observationalView study →}. And most CBN sold as a product is not harvested — it is made, by deliberately oxidising THC, which is a manufacturing choice rather than a botanical one.

What It's Used For

Cannabinol is not really made by the plant so much as left behind by it: CBN forms as THC oxidises on contact with air, so ground, broken or long-open material is higher in it ^{10Reference 10Fairbairn JW et al. · 1976The stability of cannabis and its preparations on storageView study →}.

It’s a weak partial agonist at CB1 and at most mildly intoxicating ^{4Reference 4Pertwee RG · 2008ReviewThe diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: Δ9-tetrahydrocannabinol, cannabidiol and Δ9-tetrahydrocannabivarin — reviewView study →}.

Its commercial identity is “the sleep cannabinoid” — but that reputation runs well ahead of the evidence, and pinning down a real hypnotic effect for CBN alone is the central research question here.

Evidence by IndicationStrength of support · Beta

01SleepShaky42%One small industry-funded human RCT (subjective) + objective rat polysomnography ^{1,2Reference 1Bonn-Miller MO et al. · 2024RCTA double-blind, randomized, placebo-controlled study of the safety and effects of CBN with and without CBD on sleep quality — randomised controlled trial (human)View study →Reference 2Arnold JC et al. · 2025AnimalA sleepy cannabis constituent: cannabinol and its active metabolite influence sleep architecture in rats — rat polysomnography modelView study →}

02Appetite stimulationShaky35%Rat feeding study; CB1-mediated ^{3Reference 3Farrimond JA et al. · 2012AnimalCannabinol and cannabidiol exert opposing effects on rat feeding patterns — rat modelView study →}

Mechanisms

Clinical trials

CBN has a single completed sleep RCT and little else; interest is largely commercial, ahead of the clinical evidence.

Last checked: July 2026.

Pharmacokinetics

There is essentially no human pharmacokinetic data for CBN. What is known comes from rodents and from the cannabinoid class.

The one finding that matters is metabolic. Rat polysomnography work traced much of CBN’s effect on sleep architecture not to CBN itself but to 11-hydroxy-CBN, a metabolite that is a considerably more potent CB1 agonist than the parent ^{2Reference 2Arnold JC et al. · 2025AnimalA sleepy cannabis constituent: cannabinol and its active metabolite influence sleep architecture in rats — rat polysomnography modelView study →} — the same pattern as THC’s 11-hydroxy metabolite. If that holds in people, then oral CBN’s activity would depend heavily on first-pass metabolism, and route would change the effect rather than just its timing.

Like the other cannabinoids CBN is highly lipophilic and would be expected to distribute into fat with a long terminal half-life, but this has not been measured in humans at any dose.

Isolate vs. Plant Studies

Every result for CBN comes from the isolate, and for this molecule the distinction is unusually clean: because the compound is a degradation product rather than a chemotype marker, there is no “CBN-rich cannabis” in the way there is CBD-rich hemp. Nobody has run a trial of a plant preparation and attributed the result to CBN.

The human trial used 20 mg of purified CBN in a defined nightly dose ^{1Reference 1Bonn-Miller MO et al. · 2024RCTA double-blind, randomized, placebo-controlled study of the safety and effects of CBN with and without CBD on sleep quality — randomised controlled trial (human)View study →}. The rat sleep and feeding work used purified compound ^{2,3Reference 2Arnold JC et al. · 2025AnimalA sleepy cannabis constituent: cannabinol and its active metabolite influence sleep architecture in rats — rat polysomnography modelView study →Reference 3Farrimond JA et al. · 2012AnimalCannabinol and cannabidiol exert opposing effects on rat feeding patterns — rat modelView study →}.

The historical literature is where the isolate/plant confusion actually bites, and it runs backwards from the usual direction. The older “CBN is sedative” reports were largely made on aged plant material and on CBN given alongside THC — and where the two were separated, CBN alone was weakly active while the combination was not ^{5Reference 5Takahashi RN · 1975AnimalPharmacologic interaction between cannabinol and Δ9-tetrahydrocannabinol — animal modelView study →}. So the plant-level observation that produced the reputation was an observation about THC in disguise.

Its Role in Plants

CBN has no biosynthetic role, no dedicated enzyme and no known function for the plant. It is not one of the three products the cannabinoid pathway makes from cannabigerolic acid — those are THCA, CBDA and CBCA ^{14Reference 14Sirikantaramas S et al. · 2004The gene controlling marijuana psychoactivity: molecular cloning and heterologous expression of Δ1-tetrahydrocannabinolic acid synthase from Cannabis sativa LView study →} — and there is no cannabinolic acid synthase.

Its acid form, cannabinolic acid (CBNA), does occur, and arises the same way: by oxidation of THCA rather than by synthesis. The cannabinoid pathway builds; CBN is what happens afterwards.

Prevalence in Nature

CBN occurs wherever THC has been left in contact with air, which in practice means everywhere cannabis is stored, and nowhere else. It is one of the hundred-plus phytocannabinoids catalogued from the plant ^{12Reference 12Hanuš LO et al. · 2016ReviewPhytocannabinoids: a unified critical inventory — reviewView study →}, and no other genus is a source.

Its concentration is a function of handling rather than of genotype — the exception among the cannabinoids, and the reason it is useless as a chemotype marker. In the DEA survey of seized cannabis from 2013 to 2022, CBN was, with CBG, one of only two cannabinoids besides THC to exceed 0.5% of dried material, reaching up to about 1% ^{11Reference 11ElSohly MA et al. · 2024ObservationalA 10-year trend in cannabis potency (2013–2022) in different geographical regions of the United States of America — observationalView study →}. In freshly cured flower it is far lower.

A purchased CBN product is usually manufactured. Isolating meaningful quantities from plant material would require deliberately degrading it, so commercial CBN is generally produced by oxidising THC or by synthesis, not extracted as such.

Major Natural Sources

Source	Part	Level	Note
Aged or air-exposed cannabis (Cannabis sativa)	dried flower, resin	up to ~1% in seized samples	rises with air exposure, not with time in the dark 10,11Reference 10Fairbairn JW et al. · 1976The stability of cannabis and its preparations on storageView study →Reference 11ElSohly MA et al. · 2024ObservationalA 10-year trend in cannabis potency (2013–2022) in different geographical regions of the United States of America — observationalView study →
Freshly cured cannabis	dried flower	very low	intact trichomes are stable for 1–2 years in the dark 10Reference 10Fairbairn JW et al. · 1976The stability of cannabis and its preparations on storageView study →
Charas / hashish, historically	aged resin	high enough to crystallise out	the source of the 1896 isolation 6Reference 6Wood TB et al. · 1896XL.—CharasView study →
Commercial CBN products	isolate	variable	usually made by oxidising THC rather than extracted

Discovery & Synthesis

The history is set out above: isolated from charas in 1896 by Wood, Spivey and Easterfield ^{6,7Reference 6Wood TB et al. · 1896XL.—CharasView study →Reference 7Wood TB et al. · 1899III.—CannabinolView study →}, correctly structured by Cahn in 1932 ^{8Reference 8Cahn RS · 1932Cannabis indica resinView study →}, and confirmed by Adams’s total synthesis in 1940 ^{9Reference 9Adams R et al. · 1940Structure of cannabinolView study →} — which makes CBN one of the earliest cannabinoids to be made in a laboratory as well as the first to be isolated.

Production today is oxidation, not extraction or biosynthesis. Because the plant does not accumulate CBN in useful amounts, commercial material is made by converting THC — a route that is chemically simple and economically obvious, and which is worth knowing when reading a CBN product’s provenance claims.

Patents: not yet researched (future patent-loop pass).

Toxicity & Safety

CBN is mildly active and regarded as well tolerated, with drowsiness the most commonly described effect. Because human study is minimal, its full safety profile and drug-interaction potential are not established — and since its effects appear partly mediated by a CB1-active metabolite, caution with other sedatives is sensible. Commercial CBN products vary in purity and labelled content, and much of the CBN on the market is deliberately oxidised THC — so residual THC content is a reasonable thing to ask about, since it would be both intoxicating and, in many jurisdictions, a legal problem.

Dosage

The only human dose with any evidence behind it is the 20 mg nightly used in the sleep RCT ^{1Reference 1Bonn-Miller MO et al. · 2024RCTA double-blind, randomized, placebo-controlled study of the safety and effects of CBN with and without CBD on sleep quality — randomised controlled trial (human)View study →} — a single, small, industry-funded study, so this is a studied dose, not a recommendation. No dose is established for any other use, and animal doses do not translate to humans.

References

1. Bonn-Miller MO, Feldner MT, Bynion TM, et al. (2024). A double-blind, randomized, placebo-controlled study of the safety and effects of CBN with and without CBD on sleep quality — randomised controlled trial (human). Experimental and Clinical Psychopharmacology. https://pubmed.ncbi.nlm.nih.gov/37796540/
2. Arnold JC, Occelli Hanbury-Brown CV, Anderson LL, et al. (2025). A sleepy cannabis constituent: cannabinol and its active metabolite influence sleep architecture in rats — rat polysomnography model. Neuropsychopharmacology. https://pubmed.ncbi.nlm.nih.gov/39528623/
3. Farrimond JA, Whalley BJ, Williams CM (2012). Cannabinol and cannabidiol exert opposing effects on rat feeding patterns — rat model. Psychopharmacology (Berl). https://pubmed.ncbi.nlm.nih.gov/22543671/
4. Pertwee RG (2008). The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: Δ9-tetrahydrocannabinol, cannabidiol and Δ9-tetrahydrocannabivarin — review. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/17828291/
5. Takahashi RN, Karniol IG (1975). Pharmacologic interaction between cannabinol and Δ9-tetrahydrocannabinol — animal model. Psychopharmacologia. https://pubmed.ncbi.nlm.nih.gov/168604/
6. Wood TB, Spivey WTN, Easterfield TH (1896). XL.—Charas. The resin of Indian hemp. Journal of the Chemical Society, Transactions. https://doi.org/10.1039/ct8966900539
7. Wood TB, Spivey WTN, Easterfield TH (1899). III.—Cannabinol. Part I. Journal of the Chemical Society, Transactions. https://doi.org/10.1039/ct8997500020
8. Cahn RS (1932). Cannabis indica resin. Part III. The constitution of cannabinol. Journal of the Chemical Society. https://doi.org/10.1039/jr9320001342
9. Adams R, Baker BR, Wearn RB (1940). Structure of cannabinol. III. Synthesis of cannabinol, 1-hydroxy-3-n-amyl-6,6,9-trimethyl-6-dibenzopyran. Journal of the American Chemical Society. https://doi.org/10.1021/ja01865a083
10. Fairbairn JW, Liebmann JA, Rowan MG (1976). The stability of cannabis and its preparations on storage. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/6643/
11. ElSohly MA, Majumdar CG, Chandra S, et al. (2024). A 10-year trend in cannabis potency (2013–2022) in different geographical regions of the United States of America — observational. Frontiers in Public Health. https://pubmed.ncbi.nlm.nih.gov/39421827/
12. Hanuš LO, Meyer SM, Muñoz E, et al. (2016). Phytocannabinoids: a unified critical inventory — review. Natural Product Reports. https://pubmed.ncbi.nlm.nih.gov/27722705/
13. Gaoni Y, Mechoulam R (1964). Isolation, structure, and partial synthesis of an active constituent of hashish. Journal of the American Chemical Society. https://doi.org/10.1021/ja01062a046
14. Sirikantaramas S, Morimoto S, Shoyama Y, et al. (2004). The gene controlling marijuana psychoactivity: molecular cloning and heterologous expression of Δ1-tetrahydrocannabinolic acid synthase from Cannabis sativa L. Journal of Biological Chemistry. https://pubmed.ncbi.nlm.nih.gov/15190053/

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