Not something the plant sets out to make — CBN is what Δ9-THC turns into as it ages. It is also sold, at scale, as the sleep cannabinoid. Three trials have tested that claim in people, and both of the ones that pre-specified a primary endpoint missed it. The largest study of all is a null. Every dose that produced any signal is 4–60× what a retail capsule contains. Here is that record, in full.
Every other compound pillar on this platform sits on the enzymatic tree that starts at CBGA, the mother acid: a dedicated synthase commits substrate to each branch. CBN has no such branch. It is what happens to that tree's products when they sit in a jar — as Δ9-THC and THCA meet oxygen, light and time, they oxidise to CBN. Two routes reach the same place, and neither involves an enzyme dedicated to the job.
CBN is the only compound with a pillar on this platform that the plant does not make with a dedicated enzyme. THCA synthase, CBDA synthase and CBCA synthase each convert the mother acid CBGA into a branch acid. There is no equivalent step for CBN: it appears as Δ9-THC and THCA oxidise on contact with air, light and time. That is why CBN accumulates in aged, oxidised or poorly stored material and why fresh plants hold only traces of it — and it is why every claim on this page is about a degradation product, not a biosynthetic one.
Stated plainly, because the alternative is worse. The gated CBG Atlas registry contains no graded CBN record, and no biosynthesis record underwrites an oxidation pathway — so unlike /cbdv or /cbga, this page rests on no registry-graded citation at all. Every paper below is real, published and checkable, and every one of them is ungraded here. Dressing a loosely-related record up as an anchor would buy a badge this page has not earned.
A first-class reference is as clear about its limits as its knowledge. For most minor cannabinoids the limit is that nobody has looked. For CBN it is stranger than that: people looked, carefully, in trials built to answer the question — and the endpoints those trials chose in advance came back null.
Read the right-hand column carefully, because it holds two different states. The sleep-efficacy rows describe questions that were tested and whose pre-specified endpoints came back null — those are results. The ≤5 mg retail dose and long-term safety are genuine absences: nobody has run those studies at all. An absence of evidence and a negative result are not the same thing, and this page keeps them in separate rows. We do not write a miss as “mixed”, as “promising”, as “trending toward significance”, or as a call for more research — and equally, our evidence ladder reserves Not-supported for evidence weighing against a claim, which is a judgement for the gated pipeline rather than for this page.
Three published trials have given CBN to people specifically to test it for sleep. They are ordered by design standing, not by how encouraging they sound — the largest and most positive is last, because it is the weakest of the three in every respect that determines whether a result can be trusted. Each entry leads with what was actually tested and carries a paired shows / does not show that cannot be separated from it.
These papers are real, checkable, and not graded entries in the CBG Atlas registry — the gated pipeline has not ingested them, so none carries a rung on our evidence ladder and nothing here is asserted on their authority. The badges name each study's design, which is not a grade and is deliberately rendered in the neutral chip. If and when these enter the registry through the gated pipeline, they will appear graded and cited like every other record.
What was actually tested: A double-blind, randomised, placebo-controlled study run remotely between May and November 2022, registered as NCT05839964. Five arms — placebo, 20 mg CBN, and 20 mg CBN plus 10, 20 or 100 mg CBD — taken for seven consecutive nights. Participants were 18–55 years old and rated their own past-week sleep quality as “poor” or “very poor”. ⚠ THE REGISTRATION LISTS THE CONDITION AS “HEALTHY ADULTS” and records the study as enrolling healthy volunteers: this is a self-rated poor-sleep population, NOT a population with diagnosed insomnia. Modified intent-to-treat analysis, n = 293.
⚠ THE PRIMARY ENDPOINT WAS NOT MET. Sleep quality on 20 mg CBN versus placebo: odds ratio 2.26, 95% CI [0.93, 5.52], p = .082 — the interval crosses 1. Two secondary endpoints did reach significance: number of awakenings (p = .025) and overall sleep disturbance (p = .023). ⚠ AND THREE SECONDARIES WERE NULL: there was no difference from placebo for sleep-onset latency, for wake after sleep onset, or for daytime fatigue (all p > .05). Adding CBD did not improve on CBN alone at any of the three CBD doses.
What it shows: That 20 mg of CBN taken nightly for a week, in adults who rate their own sleep as poor, reduced self-reported night-time awakenings and overall sleep disturbance relative to placebo — both secondary measures — without changing daytime fatigue.
What it does NOT show: That CBN improved sleep quality: the endpoint the trial pre-specified to answer that question did not reach significance. It also does not show any effect on how long people took to fall asleep or how long they were awake in the night — both were measured, and both were null. And it says nothing about the ≤5 mg found in retail products; the dose here was 20 mg.
Read it with this: ⚠ SPONSOR STUDY, WITH NO INDEPENDENT AUTHOR. Every listed author is affiliated with Canopy Growth Corporation except one, who is at Wana Brands — a cannabis-products company. No results have been posted to the trial registration, so the published paper is the whole public record of a trial run entirely by industry. Read the endpoint table below before reading any summary of this trial elsewhere.
What was actually tested: A randomised, double-blind, placebo-controlled, three-arm, SINGLE-NIGHT crossover trial in 20 adults aged 25–65 with physician-diagnosed insomnia disorder (DSM-5 and ICSD-3 criteria, Insomnia Severity Index ≥ 15), run at the Woolcock Institute of Medical Research in Sydney. Each participant received a single oral dose of 30 mg CBN, 300 mg CBN and matched placebo, in randomised order, with a two-week washout between nights. Sleep was measured by overnight in-laboratory POLYSOMNOGRAPHY. Registered as NCT05344170 — the registration carries the acronym CUPID, which is the trial's name and not this paper's title. ⚠ Twenty participants, one night per arm: this is a proof-of-concept study and the registration says so.
⚠ THE PRIMARY ENDPOINT WAS NOT MET. Wake after sleep onset did not change significantly at either dose — 300 mg: −6.3 minutes, 95% CI [−18.2, +5.5], p = 0.29; 30 mg: −4.0 minutes, 95% CI [−15.9, +7.9], p = 0.50. At 300 mg the paper reports significant results on other measures: more NREM-2 sleep (p = 0.03) and shorter sleep-onset latency (p = 0.004), which the registration ranks as SECONDARY outcomes; and better subjective sleep quality (p = 0.005) and a lower EEG arousal index (p = 0.02), which the registration ranks as TERTIARY outcomes. The abstract reports these effects for 300 mg; it reports no corresponding 30 mg result.
What it shows: That a single 300 mg dose of CBN altered several measurable features of one night's sleep in twenty adults with diagnosed insomnia, and that participants rated that night better.
What it does NOT show: That CBN reduced time spent awake in the night — the objective measure this trial existed to test, recorded in a sleep laboratory, did not move at either dose. It also shows nothing about repeated use: every participant took each dose once. ⚠ AND THE POSITIVES CANNOT BE PROMOTED INTO THE HOLE THE PRIMARY LEFT. “It felt better” is a tertiary outcome; the primary was the objective one, and it was null.
Read it with this: ⚠ 247 MILD-TO-MODERATE ADVERSE EVENTS were recorded across the arms of a twenty-person, three-night study. None were serious, and the authors call for larger and longer trials. ⚠ The registration also lists next-day simulated driving, postural sway, reaction time and memory consolidation as safety outcomes; the published abstract does not report them, so this page states nothing about next-day function — that needs the full text. This is the academic trial of the three: the sponsor is the Woolcock Institute of Medical Research, with the University of Sydney as collaborator.
What was actually tested: A randomised, double-blind, placebo-controlled study of a hemp-derived CBN sleep aid, TruCBN™, at 25 mg (n = 206), 50 mg (n = 205) and 100 mg (n = 203), against placebo (n = 204) and against 4 mg melatonin (n = 202) — 1,020 participants across five arms. Sleep quality was measured with the PROMIS Sleep Disturbance 8A questionnaire. Stress, anxiety, pain and well-being were exploratory measures. ⚠ THE PUBLISHED REPORT NAMES NO TRIAL REGISTRATION, so there is no public protocol against which a pre-specified primary endpoint can be checked. ⚠ It is indexed in PubMed as a journal article, NOT as a randomised controlled trial — unlike the other two trials on this page.
All three CBN doses and the melatonin group improved on sleep quality relative to placebo. ⚠ AND THE COMPARISON THAT MATTERS IS A NULL: the paper reports “no significant differences between any group and the melatonin group”, and states again that there was no significant difference in sleep-quality improvement between any treatment group and 4 mg melatonin. Of the exploratory measures, only stress at the 100 mg dose differed from placebo; anxiety, pain, well-being and the frequency of side effects did not.
What it shows: That in a large, blinded, placebo-controlled comparison, 25, 50 and 100 mg of this manufacturer's CBN improved a self-reported sleep-disturbance score more than placebo did.
What it does NOT show: ⚠ THAT CBN IS “AS GOOD AS MELATONIN”. The paper reports a NON-SIGNIFICANT DIFFERENCE from the melatonin arm. A non-significant difference is not equivalence — no non-inferiority margin was pre-specified, and a study is not designed to prove sameness by failing to find a difference. It also does not show a pre-specified benefit of any kind, because no registered primary endpoint exists to check the analysis against.
Read it with this: ⚠ FUNDING AND STAFFING, BOTH. The study was funded by FloraWorks, the manufacturer of the TruCBN™ ingredient it tested, and six of the eight authors are employed by Radicle Science, the contract research organisation that ran it. ⚠ The abstract closes by calling orally ingested CBN “a safe and effective alternative for the improvement of sleep”. That is the sponsor's framing of an unregistered study whose active comparator it did not beat, and CBG Atlas does not echo it. The dosing duration is not stated in the published abstract and is therefore not stated here.
A trial names one outcome, in advance, as the one that will answer its question. Everything else is secondary or tertiary, and a positive further down the list does not fill the hole a missed primary leaves. Below is every outcome each trial registered, in the rank the registration gave it, with what happened to it. The ranks are transcribed from ClinicalTrials.gov, not from the papers' own summaries.
Registration: NCT05839964. Registered condition: “Healthy Adults”; the registration records the study as enrolling healthy volunteers. No results have been posted. Funding: Canopy Growth Corporation — every author but one, who is at Wana Brands.
| Registered rank | Pre-specified outcome | What happened |
|---|---|---|
| PrimaryNot met | Median sleep quality rating during the dosing week (Consensus Sleep Diary, completed within an hour of waking each morning) | NOT MET. 20 mg CBN vs placebo — odds ratio 2.26, 95% CI [0.93, 5.52], p = .082. The confidence interval crosses 1. |
| SecondarySignificant | Number of awakenings after sleep onset | Reduced versus placebo, p = .025. |
| SecondarySignificant | Overall sleep disturbance (PROMIS) | Reduced versus placebo, p = .023. |
| SecondaryNull | Mean latency to sleep onset | No difference from placebo (p > .05). |
| SecondaryNull | Mean time spent awake after sleep onset | No difference from placebo (p > .05). |
| SecondaryNull | Mean daytime fatigue | No difference from placebo (p > .05). |
| Tertiary / otherNot reported | Early-morning awakening; depression, anxiety and stress subscales; irritability; perceived stress; adverse events | Registered as other outcomes. Not reported in the published abstract, and no results are posted to the registration — so this page states nothing about them. |
The line that travels is “clinically shown to reduce night-time awakenings”. Awakenings is a SECONDARY endpoint. The endpoint this trial pre-specified as the one that would decide the question — sleep quality — did not reach significance, and three of the five secondaries, including how long people took to fall asleep, were null.
Registration: NCT05344170 (acronym: CUPID). Registered as a Phase 1/2 proof-of-concept crossover study in 20 adults with clinician-diagnosed insomnia disorder. Sponsor: Woolcock Institute of Medical Research; collaborator: University of Sydney. Funding: Academic. This is the trial on this page with no industry sponsor.
| Registered rank | Pre-specified outcome | What happened |
|---|---|---|
| PrimaryNot met | Wake after sleep onset (WASO), in minutes, by overnight in-laboratory polysomnography | NOT MET, at either dose. 300 mg: −6.3 min, 95% CI [−18.2, +5.5], p = 0.29. 30 mg: −4.0 min, 95% CI [−15.9, +7.9], p = 0.50. |
| SecondarySignificant | Traditional sleep staging (proportion of the night in wake, N1, N2, N3 and REM) | 300 mg increased NREM-2 sleep, p = 0.03. |
| SecondarySignificant | Sleep onset latency, by polysomnography | 300 mg reduced it, p = 0.004. |
| SecondaryNot reported | Absolute EEG power during NREM sleep | Registered as secondary; not reported in the published abstract. |
| Tertiary / otherSignificant | EEG arousal index (registered, in the trial's own words, as a tertiary outcome) | 300 mg reduced it, p = 0.02. |
| Tertiary / otherSignificant | Next-day post-wake subjective sleep evaluation (LSEQ and RCSQ — the registration's only subjective sleep measures, both registered as tertiary outcomes) | 300 mg improved subjective sleep quality, p = 0.005. |
| Tertiary / otherNot reported | Sleep spindles; EEG power in REM; next-day simulated driving, postural sway, reaction time and memory consolidation | Registered as tertiary, exploratory or safety outcomes. Not reported in the published abstract — so this page states nothing about next-day function. |
The lines that travel are “CBN improved sleep quality in a polysomnography trial” and “CBN cut night-time arousals”. BOTH ARE TERTIARY OUTCOMES. This trial existed to ask whether CBN reduces time spent awake in the night, measured objectively in a sleep laboratory — and the answer was no, at 30 mg and at 300 mg. A subjective rating cannot be promoted into the hole an objective primary left.
Registration: None named in the published report. ⚠ The paper carries no trial-registration identifier, so no protocol is publicly available and no analysis can be checked against a pre-specification. It is indexed in PubMed as a journal article, not as a randomised controlled trial. Funding: FloraWorks — the manufacturer of the TruCBN™ ingredient under test. Six of the eight authors are employed by Radicle Science, the contract research organisation that ran the study.
| Registered rank | Pre-specified outcome | What happened |
|---|---|---|
| PrimaryNot assessable | None publicly pre-specified | ⚠ NOT ASSESSABLE. With no registration there is no public record of what this study set out to measure before it measured it. Every result below is therefore reported without a pre-specification behind it — which is a limit on the whole study, not a footnote to one row. |
| SecondarySignificant | Sleep quality (PROMIS Sleep Disturbance 8A) versus placebo | All three CBN doses and the 4 mg melatonin group improved significantly relative to placebo. |
| SecondaryNull | Sleep quality versus 4 mg melatonin — the active comparator | NO SIGNIFICANT DIFFERENCE between any group and the melatonin group. ⚠ That is a null, not equivalence: no non-inferiority margin was pre-specified. |
| Tertiary / otherSignificant | Stress (exploratory) | 100 mg showed a larger decrease than placebo. |
| Tertiary / otherNull | Anxiety, pain, well-being, and the frequency of side effects (exploratory) | No significant difference from placebo for any of them. |
The line that travels is “as effective as melatonin”. THE PAPER REPORTS NO SIGNIFICANT DIFFERENCE FROM MELATONIN — a failure to detect a difference, in a study with no pre-specified non-inferiority margin and no registration at all. It is the weakest kind of positive result on this page and it is the one most often quoted as the strongest.
Because in a paragraph it does not survive. “Sleep quality improved” and “the primary endpoint was sleep quality and it was not significant” cannot sit in the same sentence without one of them winning, and the one that wins is always the shorter, happier one. Here the rank is a column, so a result cannot be lifted away from the rank it was registered under. Two of these three trials pre-specified a primary endpoint and missed it. The third never publicly pre-specified one at all.
This one is kept apart from the three above on purpose. It is not a CBN trial: it compared six active formulations, with no placebo arm and no CBN-only arm, so it cannot tell you what CBN does on its own. What it can tell you — and it is the largest study in the entire CBN literature — is what happens when you add CBN to something that already works. Nothing measurable happened.
What was actually tested: 1,793 adults with sleep disturbance, randomised to one of six capsule formulations for four weeks: 15 mg CBD or 5 mg melatonin, each alone or combined with minor cannabinoids including 15 mg CBN and 5 mg CBC. Sleep disturbance was measured weekly with the PROMIS Sleep Disturbance SF 8A. ⚠ THERE IS NO PLACEBO ARM AND NO CBN-ONLY ARM. All six arms were active, so every within-group improvement is uncontrolled; the only controlled comparisons the study can make are between formulations. Run by Radicle Science.
⚠ THE CBN RESULT IS A NULL. Adding 15 mg CBN to 15 mg CBD — alone or together with 5 mg CBC — produced NO SIGNIFICANT DIFFERENCE versus CBD isolate. Nothing beat 5 mg melatonin either: formulations containing melatonin, alone or with CBD and CBN, did not differ from CBD isolate, and the authors conclude that the effects observed “do not exceed that of 5 mg melatonin” and that “the addition of low doses of CBN and CBC may not improve the effect of formulations containing CBD or melatonin isolate”. All formulations were well tolerated: 12% of participants reported a side effect and none were severe.
What it shows: That in the largest study in the CBN literature, adding CBN to a CBD formulation added nothing measurable to a sleep-disturbance score over four weeks.
What it does NOT show: Anything about CBN taken on its own — there was no CBN-only arm. And because there was no placebo arm, the improvements every group reported cannot be attributed to any of the products; only the differences BETWEEN formulations are controlled, and the CBN difference was not significant.
Read it with this: ⚠ THIS STUDY IS ROUTINELY LEFT OUT OF CBN SUMMARIES, INCLUDING BRIEFS WRITTEN FOR THIS PAGE. It is the largest study of all, and it is the one that says adding CBN changed nothing. A reference that publishes the three CBN trials and quietly omits the 1,793-participant null is running a selection filter, which is the thing this platform exists not to do.
Products marketed for sleep typically contain ≤5 mg of CBN. The lowest dose in any published trial is 15 mg, and that arm was a null. Every dose that produced any signal at all sits between 4× and 60× the retail amount. This is the single most important number on the page, so it is a table rather than a sentence.
| Dose | vs retail | Study | What happened |
|---|---|---|---|
| ≤ 5 mg | 1× — the retail dose | The typical CBN content of products marketed for sleep (Corroon 2021) | ⚠ NEVER TESTED. No published CBN trial has given a dose this low. Nothing anywhere on this page describes what a ≤5 mg product does, because nobody has measured it. |
| 15 mg, added to 15 mg CBD | 3× | Saleska 2024 — n = 1,793, four weeks | No significant difference from CBD isolate alone. The lowest dose anyone has studied is also the clearest null. |
| 20 mg | 4× | Bonn-Miller 2024 — n = 293, seven nights | Primary endpoint (sleep quality) not significant, p = .082. Two secondaries moved; sleep-onset latency, wake after sleep onset and daytime fatigue did not. |
| 25 / 50 / 100 mg | 5–20× | Kolobaric 2024 — n = 1,020, manufacturer-funded, unregistered | All three doses improved a sleep-disturbance score versus placebo — and none separated from 4 mg melatonin. No pre-specified primary endpoint exists to check. |
| 30 mg | 6× | Lavender 2026 — n = 20, one night | Primary endpoint (wake after sleep onset, by polysomnography) not significant, p = 0.50. The abstract reports the trial's significant secondary and tertiary results for 300 mg only. |
| 300 mg | 60× | Lavender 2026 — n = 20, one night | Primary endpoint not significant, p = 0.29. Secondary outcomes (NREM-2 sleep, sleep-onset latency) and tertiary outcomes (arousal index, subjective sleep quality) did move. |
The whole CBN sleep story starts there — old cannabis feels more sedating, old cannabis has more CBN, therefore CBN is sedating. No study has ever attributed that drowsiness to CBN, and aged material differs from fresh material in many ways at once: terpenes evaporate, Δ9-THC degrades, CBN rises. Rising CBN is a marker of ageing, not a demonstrated cause of anything ageing produces. The 2021 review that examined the question described the sleep claims as possibly “rooted in cannabis lore”. Then the trials that reviewer asked for were run — at 20 to 300 mg — and the two that pre-specified a primary endpoint missed it.
What was actually tested: A single-author narrative review asking one question: “Is there sufficient clinical evidence to support claims that CBN has sleep-promoting effects?” Ninety-nine human study abstracts were screened and eight full-text articles met the inclusion criteria. ⚠ IT WAS PUBLISHED IN AUGUST 2021 AND THEREFORE ASSESSED NONE OF THE THREE MODERN CBN SLEEP TRIALS — the earliest of them had not finished dosing.
The review found the CBN literature “dated and limited”, with most human work done in the 1970s–1980s in small samples, and no clinical trial linking CBN to validated sleep questionnaires or to polysomnography. Its conclusion, verbatim: there is “insufficient published evidence to support sleep-related claims”. It called for randomised controlled trials using polysomnography or validated questionnaires, at doses — verbatim — “significantly higher than those found in currently available cannabis products marketed for sleep (typically ≤5 mg)”. It also notes that evidence CBN itself produces cannabis-like effects in people is mixed, with most of it showing no such effect.
What it shows: That as of 2021 no clinical trial supported CBN sleep claims, and — the part that has not aged and is the anchor of this page — that products marketed for sleep typically contain ≤5 mg of CBN, far below any dose that had been studied.
What it does NOT show: Anything about the three trials that came after it. This review cannot be quoted as a verdict on Bonn-Miller 2024, Lavender 2026 or Kolobaric 2024 — those are published above, in full, on their own terms. ⚠ Note what happened next, though: the trials the reviewer asked for were run, at 20–300 mg, and the two that pre-specified a primary endpoint missed it.
CBN and melatonin are sold together, routinely, in the same capsule. The only published evidence about that combination is a drug-interaction signal in mice — and it is the most consumer-relevant thing in this entire file. Every signal below is tied to the study it came from, and the preclinical ones are labelled preclinical without being softened for it.
What was actually tested: Laboratory enzyme work on CYP1A2 — the main liver enzyme that clears melatonin — followed by dosing in MICE to measure melatonin in blood. The study exists because of a specific commercial fact the authors name themselves: products combining CBN with melatonin are widely sold, and cannabinoids are known to inhibit drug-metabolising enzymes.
CBN potently inhibited the CYP1A2-mediated metabolism of melatonin in the laboratory assay, and in mice it increased melatonin's apparent oral bioavailability — a FOUR-FOLD increase in plasma melatonin exposure. The authors present it as an additional example of a potential drug–drug interaction involving melatonin.
What it shows: That CBN can block the enzyme that clears melatonin, and that in an animal this raises how much melatonin reaches the bloodstream from the same dose.
What it does NOT show: What happens in a person. No CBN–melatonin interaction study in people has been published, so the size of this effect at a human dose is unknown, and nothing here says the combination is dangerous — or that it is safe. It is a reason to raise a CBN-plus-melatonin product with a prescriber or pharmacist rather than to assume the two ingredients simply add up.
Read it with this: ⚠ The practical point survives the species limit: this is a preclinical finding about a combination that is already on shelves in a single capsule. A reference that publishes CBN's sleep trials and not this paper would be publishing the half a seller likes.
CBN strongly inhibited the CYP1A2 enzyme that clears melatonin, and in mice it produced a roughly four-fold increase in melatonin exposure in the blood (Anderson 2025, PMID 39722474). ⚠ CBN AND MELATONIN ARE SOLD TOGETHER IN THE SAME CAPSULE, ROUTINELY. This is a preclinical finding — cells and mice, not people — and no interaction study in people has been published, so the size of the effect in a person is unknown. It is the reason to raise a CBN product with a pharmacist rather than assume the combination is inert.
The polysomnography trial recorded 247 mild-to-moderate adverse events across its three arms, in twenty participants dosed on three separate nights (Lavender 2026, PMID 41698831). None were serious. This is a tolerability signal, not a safety alarm — but a compound whose primary endpoint was null still produced that many recorded events, and the trial's own authors call for larger and longer studies.
The manufacturer-funded study reported no significant difference in the frequency of side effects between any CBN dose and placebo (Kolobaric 2024, PMID 39204082), and the 1,793-participant formulation study reported side effects in 12% of participants with none severe (Saleska 2024, PMID 37162192). Both are short, self-reported and industry-run. Reassuring at that scale and duration; not a characterised safety profile.
The trials that gave CBN on its own ran for SEVEN NIGHTS (Bonn-Miller 2024) and for a SINGLE NIGHT per dose (Lavender 2026). The four-week exposure was CBN inside a CBD formulation (Saleska 2024). Kolobaric 2024 does not state its dosing duration in the published abstract, so this page does not state it either. Nobody has followed people taking CBN for months.
Work in human liver preparations identifies CYP2C9 and CYP3A4 as the main enzymes that process CBN (Watanabe 2007, PMID 17303175). Those enzymes handle a great many prescription medicines, which is the general reason cannabinoid–medicine interactions are plausible. No CBN interaction study in people has been published. If you take prescription medicines, discuss any cannabinoid product with your prescriber or pharmacist.
In a 1984 study, CBN lowered eye pressure in cats — but also caused conjunctival redness and hyperaemia, and in rats given CBN systemically it produced polyspike discharges on the electrocorticogram. Cannabigerol, tested alongside it in the same paper, lowered eye pressure without either effect (Colasanti 1984, PMID 6499952). Animal findings from four decades ago, reported because they are the toxicity half of a study usually cited only for its eye-pressure half.
⚠ NO CBN-PRODUCT-SPECIFIC RESIDUAL-THC STUDY EXISTS, so this is stated as an ANALOGY and never as a CBN finding. In an Argentine survey of 500 commercial cannabis oils, 13 of the 17 products labelled “THC-free” tested positive for Δ9-THC — 76.5% of a very small subgroup (Fernández 2023, PMID 37392612). Those were cannabis oils, not CBN products, and the number rests on seventeen items. What it supports is a labelling caution, not a measurement: because CBN is formed from THC, a CBN product's route of manufacture makes residual THC a question worth asking of a certificate of analysis. It supports no claim about any specific product.
CBN has no approved use in any jurisdiction and is not a treatment for insomnia or any other sleep disorder. Nothing here diagnoses, treats, cures or prevents any disease, and nothing here is a recommendation to take CBN or a dose at which to take it. Nobody should change or stop a prescribed sleep medication on the strength of this page, and persistent sleep problems are worth raising with a clinician, because they can have causes a supplement will not address. If you take prescription medicines — melatonin included — discuss any cannabinoid product with your prescriber or pharmacist. See safety & reporting and how we grade.
Laboratory and animal work on how CBN might act, kept separate from the trial record on purpose: a receptor fact and a clinical outcome are answered by different study designs, and merging them is how a lab result becomes a health claim. Mechanism detail is researcher-tier on this platform; switch to Researcher depth for the cited record.
In plain terms: in rats, CBN does change sleep as measured objectively — but not simply. Sleep is suppressed first and increases afterwards, which is not what “sedating” describes. The researchers also found that most of the cannabinoid-receptor activity after a CBN dose belongs to something the body makes from CBN rather than to CBN itself. All of that is in rats, and the trials in people are published above, where the primary endpoints were missed. Switch to Researcher depth for the cited detail.
What was actually tested: Polysomnography in RATS, with brain and plasma concentrations measured, plus cannabinoid-receptor assays. Rodents throughout — no people at any point in this study.
CBN increased total sleep time in rats, raising both non-REM and REM sleep. ⚠ THE EFFECT WAS BIPHASIC: there was initial sleep SUPPRESSION before the increase. Following a CBN dose, its metabolite 11-hydroxy-CBN reached brain concentrations comparable to CBN itself. ⚠ AND THIS IS A MEASURED FINDING, NOT A HYPOTHESIS: in the receptor assays 11-hydroxy-CBN was active at cannabinoid CB1 receptors with potency and efficacy comparable to Δ9-THC, while CBN itself had much lower activity. The metabolite also influenced sleep architecture, with some differences from CBN. On non-REM sleep the magnitude of CBN's effect was comparable to the sleep aid zolpidem, though — unlike CBN — zolpidem did not change REM sleep.
What it shows: That in rats CBN changes objectively measured sleep architecture, that the change is biphasic rather than simple sedation, and that a metabolite of CBN — not CBN itself — carries most of the CB1 activity.
What it does NOT show: Anything about people. The zolpidem comparison in particular is a rat measurement and is NOT a statement that CBN performs like a prescription hypnotic in a person; the trials that asked that question in people are published above, and their primary endpoints were missed. ⚠ It also does not show that humans experience this metabolite the way rats do: Watanabe 2007 shows human liver enzymes form 11-hydroxy-CBN, but nobody has measured its brain exposure or its effects in a person. Joining the two studies is an inference across species, and it is labelled as one here.
Read it with this: ⚠ THE BIPHASIC EFFECT IS PART OF THE FINDING AND IS NOT DROPPED WHEN THE RESULT IS SUMMARISED. “CBN increases total sleep time in rats” omits that sleep was initially suppressed. Reported here because a compound sold to be taken at bedtime having an early sleep-suppressing phase in an animal model is exactly the kind of detail a summary sheds.
What was actually tested: Human hepatic microsomes and recombinant human cytochrome P450 enzymes, in the test tube. Human TISSUE, not human participants — the distinction matters and is why this is not in the human record above.
CBN was metabolised mainly to 11-hydroxy-CBN and 8-hydroxy-CBN. The 11-hydroxylation was catalysed principally by CYP2C9 and the 8-hydroxylation by CYP3A4, with selective inhibitors of each enzyme family blocking the corresponding reaction. Catalytic rate figures are reported in the source and are deliberately not reproduced on this consumer surface.
What it shows: That human liver enzymes convert CBN into 11-hydroxy-CBN, and which two enzymes do most of the work — the human-tissue basis for expecting CBN to interact with medicines handled by CYP2C9 and CYP3A4.
What it does NOT show: What that metabolite then does in a person. This study measures formation, not effect, not brain exposure and not behaviour. The rat work above is the only place a CB1 activity comparison for the metabolite exists, and it is a rat result.
What was actually tested: A review of the molecular pharmacology of the seven most thoroughly investigated phytocannabinoids — Δ9-THC, Δ9-THCV, cannabinol, cannabidiol, cannabidivarin, cannabigerol and cannabichromene — covering targets inside and outside the endocannabinoid system. A secondary source: it reports other people's experiments.
CBN is one of the seven compounds characterised. The framing is the useful part for a reader here: the review states that “slight structural differences can elicit diverse and competing physiological effects”, which is precisely why CBN cannot be reasoned about as though it were a milder THC despite arising from it.
What it shows: That CBN has been characterised pharmacologically alongside the other major phytocannabinoids, and that structural similarity between cannabinoids does not imply similar effects.
What it does NOT show: Any clinical effect. A molecular-pharmacology review describes what a compound binds and modulates in laboratory systems; it does not establish what it does in a person. It also predates every trial on this page.
Read it with this: Secondary source, and binding constants for these compounds are researcher-tier figures that are deliberately not reproduced on this consumer surface.
Put the first two records together and the temptation is obvious: human liver enzymes form 11-hydroxy-CBN (Watanabe 2007); in rats that metabolite reaches high brain concentrations and is active at CB1 comparably to Δ9-THC (Arnold 2025); therefore people who take CBN are producing a THC-like agent in the brain. Nobody has measured that. One study measures formation in human tissue; the other measures brain exposure and receptor activity in rats. Joining them is an inference across species, and this page labels it as one rather than publishing it as a finding. What is measured, and what the page therefore states, is that CBN itself had much lower CB1 activity than its metabolite in those assays — which is also why CBN cannot be reasoned about as a milder THC, the point the 2017 review makes directly.
CBN has a second literature that has nothing to do with sleep: eye pressure and the retina. None of it is clinical, one of the studies delivered CBN by injection into the eye, and the older one contains a toxicity finding that is usually left behind when its eye-pressure result travels.
What was actually tested: Mouse retinal ganglion precursor-like cells under elevated hydrostatic pressure, human trabecular meshwork cells, and a rat model of glaucoma made by laser photocoagulation of the episcleral vein. ⚠ CBN WAS DELIVERED BY INTRAVITREAL INJECTION — directly into the eye. That is not a route any consumer product uses, and it is not comparable to swallowing a capsule.
CBN protected the cultured cells from pressure-induced toxicity in a dose-dependent way, reduced changes in extracellular-matrix proteins in the trabecular meshwork cells, and — injected into the eye — improved pattern electroretinogram amplitudes and lowered intraocular pressure in the rat model.
What it shows: A preclinical, multi-target signal for CBN in eye tissue and in a rodent glaucoma model, when CBN is injected directly into the eye.
What it does NOT show: Any clinical effect in glaucoma. There is no CBN trial in people for glaucoma, and this study cannot be read as one. Glaucoma causes irreversible vision loss and is managed by an ophthalmologist; nothing here is a treatment, and no CBN product should be used in place of prescribed care.
Read it with this: ⚠ ONE THING WE DELIBERATELY DO NOT ASSERT. Three authors are affiliated with InMed Pharmaceuticals, and that affiliation is printed on the paper. The company's cannabinol eye programme, INM-088, is NEVER NAMED in this publication — so CBG Atlas does not link the two. Naming a development programme the paper itself does not name would be inventing a fact from an affiliation, which is a different thing from reporting the affiliation, and only the second is defensible.
What was actually tested: Cannabinol or cannabigerol applied topically to cats' eyes as a single drop, or delivered continuously for nine days by osmotic minipump; and cannabinol or cannabigerol given systemically to rats with electrocorticogram recording. Animals only.
Both compounds lowered intraocular pressure in cats, with the larger effect on chronic dosing, and cannabigerol's chronic response was the greater of the two. ⚠ AND THE HALF THAT USUALLY GETS DROPPED: cannabinol — but NOT cannabigerol — caused conjunctival redness and hyperaemia; and systemic cannabinol produced 8–13 Hz polyspike discharges on the rat electrocorticogram during wakefulness and REM sleep, which cannabigerol did not. The authors' own conclusion is that cannabinol, like cannabis and Δ9-THC, produced both ocular and neurotoxicity, while cannabigerol's pressure-lowering effect appeared dissociable from those adverse effects.
What it shows: That in animals four decades ago both compounds lowered eye pressure, and that in the same experiments CBN produced two adverse effects that CBG did not.
What it does NOT show: Anything about people, and nothing about treatment. It is included in full because the eye-pressure half of this paper circulates on its own, and the toxicity half is in the same abstract.
Four things circulate as CBN evidence and are refused here. Each refusal carries its reason, so nobody has to re-derive it the next time one is pasted back in — stating a boundary once is cheaper than defending it forever.
⚠ WE DO NOT PUBLISH THIS RATIO. It is repeated across cannabis writing and we could not trace it to a primary source that measures it; the 1996 receptor-binding paper it is usually credited to characterises binding at the CB2 receptor, not a CB1 potency ratio. We do not print an identifier for that paper either, because publishing a citation in order to knock it down would put a real identifier next to a claim it does not support — the precise error this page exists to avoid. The defensible measured statement is the one in the mechanism section: in rats, CBN itself had much lower CB1 activity than its metabolite, which was comparable to Δ9-THC (Arnold 2025).
A 2021 randomised crossover trial of the sublingual cannabinoid medicine ZTL-101 improved insomnia symptoms in 23 of 24 participants over two weeks (Walsh 2021, PMID 34115851) — and it supports NO CBN CLAIM WHATEVER. ZTL-101 is a MULTI-CANNABINOID EXTRACT. The trial had no CBN-only arm, no CBN comparison and no way to attribute any part of its result to CBN. Its milligram composition is not stated in the published abstract and is not reproduced here. A positive trial of a mixture is evidence about the mixture.
This is folklore, and it is the origin of the whole CBN sleep story. No study has attributed drowsiness from aged cannabis to CBN; the 2021 review that examined the question describes the sleep claims as possibly “rooted in cannabis lore” (Corroon 2021, PMID 34468204). Aged material differs from fresh material in many ways at once — terpenes evaporate, THC degrades — and CBN rising is a marker of that ageing, not a demonstrated cause of any effect it produces.
None exists. The nearest published evidence is an analogy from a survey of commercial cannabis oils, and it is published on this page explicitly as an analogy with its denominator attached — 13 of 17 products labelled “THC-free” tested THC-positive (Fernández 2023, PMID 37392612). Stating that as a CBN finding, or quoting the 76.5% without its seventeen-item base, would be a fabricated fact wearing a real citation.
Three columns, so the difference is structural rather than rhetorical. CBG and CBDV are reference chemistry here, not pillars of this page — and neither column's record transfers to CBN.
| Property | CBG (made by the plant) | CBDV (made by the plant) | CBN (this page — a degradation product) |
|---|---|---|---|
| Where it comes from | Made by the plant. CBGA is the mother acid; heat removes CO₂ to give neutral CBG. | Made by the plant, on the varin branch. CBDA synthase converts CBGVA to CBDVA, which decarboxylates to CBDV. | NOT made by the plant as an end product. CBN appears as Δ9-THC and THCA oxidise with air, light and time. |
| Is there a dedicated enzyme? | Yes — CBGA is the substrate the three branch synthases compete for. | Yes — CBDA synthase, characterised for the pentyl reaction and inferred for the varin one. | NO. THERE IS NO CBN SYNTHASE. Oxidation and heat, not enzymology. This is the single most-misunderstood fact about CBN. |
| Molecular formula | C₂₁H₃₂O₂ · ≈ 316.48 g/mol | C₁₉H₂₆O₂ · ≈ 286.4 g/mol | C₂₁H₂₆O₂ · ≈ 310.43 g/mol — six hydrogens lighter than CBG, because it is oxidised |
| What its level on a certificate of analysis tells you | Chemotype and harvest timing — how much the plant made, and how much converted onward. | Chemotype — whether the plant runs the propyl branch at all. | AGE AND STORAGE. Closer to a freshness measurement than a cultivar one. |
| The caution that travels with it | Blood pressure — CBG is an α2-adrenoceptor agonist, so a cardiovascular caution travels with it wherever its effects are discussed. | Liver enzymes — transaminase elevations appeared in two independent CBDV studies. | Melatonin. CBN inhibited the enzyme that clears melatonin and raised melatonin exposure four-fold in mice, and the two are sold in the same capsule. |
| Trials in people | See the CBG monograph — the deepest graded record on this platform. Not summarised as a count here, because that count is derived from the gated registry rather than typed into a page. | Four published, including a Phase 2 randomised controlled trial in focal epilepsy. No primary efficacy endpoint was met. | Three that tested CBN for sleep. Both trials that pre-specified a primary endpoint MISSED IT; the third names no registration at all. |
| What it was tested FOR | A range of indications — see the monograph and the gap map. | Seizures, HIV-associated neuropathic pain, and autism-related brain imaging. | Sleep, and essentially nothing else. Every modern trial of CBN in people is a sleep trial. |
| Approved medicine | None. | None, in any jurisdiction. | None, in any jurisdiction. There is no approved CBN hypnotic. |
| The characteristic misreading | That a precursor's importance to the plant transfers to a person. | That CBDV inherits CBD's clinical standing because the names and scaffolds are close. | That “the sleep cannabinoid” has a sleep indication behind it — and that a trial's secondary or tertiary positive is the same thing as its primary endpoint. |
| Does the neighbouring column transfer? | NO. | NO. | NO. Being a cannabinoid is a structural fact, not shared evidence. Each of these three has its own record, and CBN's is the sleep record above. |
Each of these three has its own file, built from its own studies, and none inherits another's standing. CBN's file is the sleep record above: three trials, two missed primaries, one unregistered positive that did not separate from 4 mg melatonin, and a 1,793-participant null. That is the whole of it — and it is still more than most minor cannabinoids have.
The consumer question corpus for CBN, kept on this page rather than moved elsewhere. Identity and chemistry are stated as fact with a grade; effect claims — especially sleep, sedation and relaxation — are reported as the claims of others, not affirmed. These answer the practical questions the evidence sections above do not: legality, product formats, drug testing, buying and labelling.
40 questions are answered here. 30 carry a verified grade on the six-rung evidence ladder. 10 are marked with an evidence state rather than a rung — most often no primary evidence, which means our registry holds nothing on that question. That is not the same claim as not supported, and we do not render it as one.
The question corpus below was written before the modern CBN sleep trials were catalogued here, and several of its answers describe controlled human sleep and dosing studies as lacking or absent. That is no longer accurate: three such trials are published in full above, with their pre-specified endpoints and their results. Where the two disagree, the evidence sections above are authoritative. The corpus is generated from a source file this page does not own, and the corrections have been reported for the next regeneration rather than patched here — because a page that silently edits a generated corpus is a page whose corpus can no longer be regenerated.
Cannabinol (CBN) is a minor, non-intoxicating cannabinoid found in cannabis and hemp, best known for forming as THC ages. It appears only in trace amounts in fresh plants and accumulates in older, stored, or heat- and light-exposed material. It is the oxidative breakdown product of THC.
"Cannabinol" is the common name for this specific molecule — one of the first cannabinoids ever isolated from cannabis. "Cannabi" marks it as a cannabinoid; the "-ol" ending reflects its chemistry. Today CBN refers to the aromatic compound that forms when THC oxidizes with age.
Essentially, yes. CBN is the oxidative degradation product of THC: as THC meets oxygen, heat, light, and time, it slowly converts to CBN. That's why aged or poorly stored cannabis contains more CBN than fresh flower. Fresh plants hold only trace amounts.
CBN is naturally occurring — it forms in the cannabis plant as THC ages and oxidizes, with no lab synthesis required. Commercial CBN may be extracted from aged hemp or converted from THC under controlled oxidation, but the molecule itself is the same natural degradation product.
Not the way THC does. CBN is considered non-intoxicating to, at most, weakly intoxicating; it does not produce THC's characteristic high. Some people report mild relaxation, but CBN is not classified as a strongly psychoactive cannabinoid, and its cannabinoid-receptor activity is weak.
CBN is generally classed as non-intoxicating to, at most, weakly intoxicating — "psychoactive" and "intoxicating" are not the same word. CBN does not cause THC's high, and shows only weak cannabinoid-receptor activity in laboratory studies. Any subjective mental effects in humans are mild and not well characterized.
CBN is widely marketed as "sedating," and some users report feeling drowsy. Three controlled trials have now given CBN to people, but none measured sedation itself as an outcome, and one found no difference from placebo in next-day fatigue (Bonn-Miller 2024). The reputation may owe more to aged cannabis than to CBN. Individual experiences vary. (Not medical advice.)
No trial has ranked them. Relaxation has not been a pre-specified outcome in any CBN trial, and where CBD was added to CBN it changed nothing on the sleep measures that were tested (Bonn-Miller 2024). Claims that one "relaxes" more than the other are marketing, not a measured comparison. (Not medical advice.)
Generally yes in the US, with state-level exceptions. As of 2026, hemp-derived CBN is federally legal in the United States under the 2018 Farm Bill when the product contains no more than 0.3% delta-9 THC by dry weight. State laws vary and the rules are changing. General information, not legal advice — verify locally.
The 2018 Farm Bill legalized hemp and its derivatives containing no more than 0.3% delta-9 THC by dry weight, which is generally read to cover hemp-derived CBN. Evolving "total-THC" interpretations add some uncertainty. As of 2026 — general information, not legal advice.
It depends on your state: CBN's status varies, and some states restrict or ban hemp-derived cannabinoids even where federal rules are permissive. We can't determine your specific state's current status here. Check your state's up-to-date laws or a qualified attorney. As of 2026 — general information, not legal advice.
Outside the US, CBN falls under each jurisdiction's own cannabis and novel-food laws, not the US Farm Bill. Canada regulates CBN under the Cannabis Act; the UK and EU regulate cannabinoids through controlled-substance and novel-food frameworks, under which CBN is not specifically authorised as a food. Status varies and changes — general information, not legal advice.
No benefit of CBN is established in people. CBN has real laboratory activity — a potent TRPA1 agonist/desensitiser, and antibacterial (anti-MRSA) in vitro (De Petrocellis 2011; Appendino 2008) — but its marketed benefit, sleep, has been tested in people, and both trials that pre-specified a primary endpoint missed it (Bonn-Miller 2024; Lavender 2026). That is graded Not-supported: tested, and the pre-specified endpoint was not met. CBN has no approved use in any jurisdiction. (Not medical advice.)
CBN is sold mainly in "sleep" and relaxation products, often blended with melatonin, CBD, or other cannabinoids. These are marketing uses, not established medical ones: CBN has no approved therapeutic indication anywhere, and the sleep claim has been tested in controlled trials whose pre-specified primary endpoints were missed. We present these claims for information only. (Not medical advice.)
Not on the evidence: CBN's sleep claim has been tested in people, and the endpoints those trials pre-specified were missed. In 293 self-rated poor sleepers, 20 mg nightly for a week did not significantly improve sleep quality (Bonn-Miller 2024); in a sleep laboratory, 30 mg and 300 mg did not reduce time spent awake at night (Lavender 2026). Lower-ranked outcomes did move, but they do not fill the hole a missed primary endpoint leaves, which is why CBN and sleep is graded Not-supported here. (Not medical advice.)
Yes — and that is the point. Three published trials have given CBN to people for sleep, at 20 mg, at 25/50/100 mg, and at 30 mg and 300 mg (Bonn-Miller 2024; Kolobaric 2024; Lavender 2026). Both trials that registered a primary endpoint missed it, and the third names no registration at all. The evidence exists; where it was pre-specified, it is negative.
Short-term safety was measured in the trials: side-effect frequency did not differ from placebo in a 1,020-person study (Kolobaric 2024), while a 20-person laboratory trial recorded 247 mild-to-moderate adverse events across its arms, none serious (Lavender 2026). Long-term safety, and any interaction study in people, remain unpublished. Consult a qualified professional before use, especially if pregnant, nursing, or on medication. (Not medical advice.)
Grogginess has actually been measured: next-day fatigue on 20 mg did not differ from placebo (Bonn-Miller 2024). A single-night laboratory trial at 30 mg and 300 mg recorded 247 mild-to-moderate adverse events, none serious (Lavender 2026). Many "sleep" products also contain melatonin or other cannabinoids, so any effect may not be CBN's alone. Stop use if you feel unwell. (Not medical advice.)
No safe dose or toxicity threshold for CBN has been defined in humans, so there's no reliable "safe maximum," and we don't provide dosing guidance. Trials have given single doses as high as 300 mg and nightly doses of 20 to 100 mg; those are research doses, reported here as record and not as an amount to take. More is not better; consult a qualified healthcare professional. (Not medical advice.)
No interaction study in people has been published. Human liver preparations show CBN is processed by major drug-metabolising enzymes (Watanabe 2007), and in mice CBN blocked the enzyme that clears melatonin and raised melatonin exposure about four-fold (Anderson 2025) — a preclinical finding, but CBN and melatonin are routinely sold in the same capsule. Talk with your doctor or pharmacist before combining products. (Not medical advice.)
Possibly — and this is a real risk. Standard tests screen for THC and its metabolites, and because CBN is chemically related to THC it can cross-react with some immunoassay tests, potentially producing a positive result. CBN products may also contain trace THC. Weigh this carefully before use if you're tested.
Pure CBN is a distinct molecule — the oxidation product of THC, not THC itself — so it isn't THC. However, because CBN forms from THC in cannabis and hemp, CBN products can contain trace amounts of residual THC and other cannabinoids. Check the product's third-party lab report.
Yes — it's a real risk. Two things drive it: CBN can cross-react with the THC immunoassays used in standard screening, and CBN products can carry trace THC that tests are designed to detect. No study has measured residual THC in CBN products specifically, so that second route is plausible rather than quantified. If you're subject to drug testing, the cautious choice is to avoid CBN products.
CBN is sold as oils and tinctures held under the tongue, gummies and other edibles, and capsules — often blended with melatonin, CBD, or other cannabinoids in "sleep" formulas. Route affects how quickly effects begin and how long they last. We describe formats only and give no dosing advice.
CBN is sold as oils and tinctures, gummies and edibles, capsules or softgels, and vape products — frequently marketed as "sleep" blends combined with melatonin, CBD, or terpenes. Products vary widely in purity and actual CBN content, so a third-party lab report matters. We don't endorse any brand.
There is no established or clinically validated CBN dose — for sleep or anything else — and we don't give dosing recommendations. Doses of 20 mg, 25 to 100 mg, and 30 to 300 mg have been given in controlled trials; none met a pre-specified primary endpoint for sleep, and the 5 mg or less typical of retail products has never been tested at all. Discuss any use with a qualified healthcare professional. (Not medical advice.)
There's no evidence-based timing for CBN. Controlled trials have dosed CBN — nightly for a week, and as single doses in a sleep laboratory — but none compared timings, and CBN's pharmacokinetics in people are unpublished. Onset and duration also depend on format, since edibles act slower than sublingual oils, and vary by person. We give no dosing or timing guidance. (Not medical advice.)
Neither has been shown better. CBN's own sleep trials missed their pre-specified primary endpoints, and in the largest study of any CBN formulation — 1,793 people — adding 15 mg CBN to 15 mg CBD was no different from CBD alone (Saleska 2024). No published trial has compared CBN alone against CBD alone. They are different molecules: CBN forms as THC degrades, CBD is made by the plant. (Not medical advice.)
CBN is the oxidative breakdown product of THC: as THC ages, it becomes CBN. The key difference is intoxication — THC is strongly intoxicating, while cannabis-like effects from CBN have been mixed and mostly not observed in people (Corroon 2021). CBN is not a milder version of THC; it is a chemically different, fully aromatised molecule. Same origin, very different compound.
Both are non-intoxicating minor cannabinoids, but their origins and lab pharmacology differ. CBG is made by the plant from CBGA (the "mother" cannabinoid); CBN forms as THC degrades, with no enzyme dedicated to making it. They act at different receptor targets in vitro. Neither has an established human sleep benefit — and for CBN that is now a tested result, not an open question.
CBN and melatonin have been compared head to head, twice. Against 4 mg melatonin, no CBN dose — 25, 50 or 100 mg — differed significantly from the melatonin group (Kolobaric 2024); and in a 1,793-person study nothing beat 5 mg melatonin (Saleska 2024). CBN was not shown better. A non-significant difference is also not equivalence, so "as good as melatonin" is not supported either. (Not medical advice.)
CBN's molecular formula is C₂₁H₂₆O₂, with a molecular weight of about 310.43 g/mol (CAS 521-35-7; PubChem CID 2543). It is the fully aromatic, oxidized relative of THC — that extra oxidation and aromatization are exactly what make it CBN rather than THC.
Yes. CBN forms directly from THC through oxidation: exposure to oxygen, heat, and light over time aromatizes THC into CBN. Unlike most cannabinoids, it isn't built by a plant enzyme from CBGA — it's a degradation product, which is why aged cannabis accumulates it.
Yes — this is CBN's defining feature. It is the oxidative degradation (breakdown) product of THC, forming as THC ages with exposure to oxygen, heat, and light. It isn't synthesized by a dedicated plant enzyme like most cannabinoids; it accumulates as fresh, THC-rich material gets older.
Not primarily, no — unlike CBD or THC, CBN is not mainly made from a CBGA-derived acid via a synthase. A cannabinolic acid (CBNA) does exist — it arises as THCA oxidizes with age and can decarboxylate to CBN — but CBN's defining route is the oxidation of neutral THC. It's fundamentally a degradation product.
CBN is sold by hemp and cannabinoid retailers online and, where legal, in dispensaries and specialty stores — usually as "sleep" oils, gummies, or capsules. Availability depends on your local laws (see the legality answers). Because quality varies, buy only from sellers who provide third-party lab testing. We don't endorse vendors.
CBN occurs only in trace amounts in fresh cannabis — it accumulates slowly as THC degrades — so producing it requires aged material or controlled oxidation of THC, plus extraction and purification. That low natural abundance and extra processing make CBN scarcer and costlier than mainstream cannabinoids like CBD.
Look for a current Certificate of Analysis (COA) from an independent, third-party lab. It should confirm the actual CBN content matches the label, show THC levels (important for drug-test and legality reasons), and screen for contaminants like pesticides, solvents, and heavy metals. No COA is a red flag.
That's your call, and here is what is checkable about CBN. Its headline selling point — better sleep — has been tested, and the pre-specified primary endpoints were missed; no dose has been shown to meet one; the 5 mg or less typical of retail products has never been tested at all; and CBN can affect drug tests. Discuss it with a qualified healthcare professional first. (Not medical advice.)
Prioritize transparency: a recent third-party COA verifying CBN content and screening for contaminants, clear labeling of all cannabinoid amounts (including any THC), and a reputable, contactable seller. Match the product to your local laws, and be skeptical of sleep claims that outrun the evidence.
Not an empty box, and not a request for work that has already been done. A clear specification of the evidence that would move CBN off a missed primary — any of which would enter through the gated pipeline and appear here, graded and cited.
Two of the three CBN sleep trials pre-specified a primary endpoint and missed it; the third names no registration, so nothing in it was publicly pre-specified. What would move CBN off a null is a registered trial, in a defined population, that hits a pre-specified primary endpoint. Until one exists, no sleep claim is available at any dose.
Every dose that produced any signal is 4–60× the ≤5 mg typical of products marketed for sleep, and the closest anyone has come to a retail dose — 15 mg, inside a CBD formulation — was a null. Nobody has tested what is on the shelf. Until someone does, the trial record cannot be read as evidence about the product a reader is holding.
Two of the three trials are industry-authored, and the largest positive was funded by the manufacturer of the ingredient it tested and run by a contracted research organisation. Independent, registered replication would settle far more than another sponsor study. Two specific human measurements are missing and would matter more than another questionnaire: pharmacokinetics for CBN AND for its 11-hydroxy metabolite, because nobody should be inferring a person's exposure from rodent brain concentrations; and a study of the CBN–melatonin interaction, which is a mass-market pairing whose only evidence is in mice.
Every CBN-specific paper cited above: real, published, checkable, and ungraded here. There is no second list of graded records on this page, because there is nothing to put in one — the gated registry holds no CBN study yet, and that is stated rather than disguised.
Randomised, placebo-controlled · in people · primary endpoint missed
Crossover · polysomnography · in people · primary endpoint missed
Manufacturer-funded · unregistered · not indexed as an RCT
n = 1,793 · six active arms · no placebo · formulation null for CBN
Narrative review · published 2021, BEFORE all three CBN sleep trials
Preclinical · liver enzymes in vitro + mice · not people
Preclinical · rat polysomnography + receptor assays · not people
In vitro · human liver microsomes and recombinant enzymes
Review · secondary source · molecular pharmacology
Preclinical · cells + rats · intravitreal delivery only
Preclinical · cats and rats · 1984
Walsh 2021 — “Treating insomnia symptoms with medicinal cannabis: a randomized, crossover trial of the efficacy of a cannabinoid medicine compared with placebo”, Sleep 2021;44(11):zsab149, PMID 34115851, doi:10.1093/sleep/zsab149 — a trial of the multi-cannabinoid extract ZTL-101, with no CBN-only arm and no CBN comparison. Supports no CBN claim.
Fernández 2023 — “An assessment of qualitative and quantitative cannabinoids analysis in selected commercially available cannabis oils in Argentina”, Forensic Science International 2023;349:111762, PMID 37392612, doi:10.1016/j.forsciint.2023.111762 — cannabis oils, not CBN products; cited on this page as a labelling analogy, with its denominator (13 of 17) attached.
For the compound this platform holds its deepest graded record on, see the CBG monograph; for the other pillar built on a set of missed primary endpoints, see CBDV; and for how a claim earns a rung here, see how we grade. Peregrine Biopharma funds the platform and holds no editorial authority.
Seven compounds, each with its own monograph. The line under each one is what the verified registry actually holds for it — including where that is nothing yet.
The mother cannabinoid. CBGa decarboxylates to CBG, and both occur in the plant — it is CBGa that the three synthases branch into THC, CBD and CBC. The best-evidenced compound on this platform.
The acid CBG comes from, and the shared substrate the three branch synthases compete for. Decarboxylates to CBG with heat.
The propyl (varin) analogue of CBG — a three-carbon side chain instead of five.
Non-intoxicating, and one of the three branch products off the shared CBGA substrate.
The propyl analogue of CBD, and the varin with the largest published human trial record.
The propyl analogue of THC, with receptor behaviour that differs from it in laboratory work.