IngredientsCannabinol is defined as a phytocannabinoid that is one of the natural compounds derived from the Cannabis sativa L. plant, belonging to the group of C21 terpenophenolic compounds. It is universally abbreviated as CBN, and its systematic IUPAC name is 6,6,9-trimethyl-3-pentyl-6H-benzo[c]chromen-1-ol. CBN has the chemical formula C21H26O2 and a molar mass of 310.43 g/mol. The unstable THC molecule, which has the formula C21H30O2, loses four hydrogen atoms to form CBN.
Chemically, CBN is a benzo[c]chromene derivative with a biphenyl-like core. Structurally, it diverges from THC and cannabidiol (CBD), despite all three deriving from the same cannabis plants. These distinctions in ring system and oxidation pattern explain why CBN acts differently at cannabinoid receptors, particularly the cannabinoid CB1 receptor, and exhibits a different effect profile. As with all other cannabinoids, CBN is a hydrophobic, lipophilic molecule. As well as being soluble in fats, it also dissolves readily in organic solvents such as ethanol or methanol. The melting point of CBN is approximately 77°C (170°F), and the boiling point is 185°C (365°F). At room temperature, CBN is a colourless crystalline solid.
Cannabis (Cannabis sativa L.) is an outstanding source of bioactive natural products, with more than 150 different phytocannabinoids isolated throughout the decades. CBN is one of the most famous phytocannabinoids in C. sativa, and although several phytocannabinoids have been identified in different plants and fungi, CBN has only been identified in cannabis.
CBN is unique in that it does not arise from a pre-existing acidic form, but rather is generated through the oxidation of THC. CBN is unique among phytocannabinoids in that its biosynthetic pathway involves conversion directly from Δ9-THC, rather than from an acidic precursor form. CBN can be found in trace amounts in the cannabis plant, found mostly in cannabis that is aged and stored, allowing for CBN formation through the oxidation of the cannabis plant's main psychoactive and intoxicating chemical, tetrahydrocannabinol (THC). This process of oxidation occurs via exposure to heat, oxygen, and/or light. CBN is found in trace amounts of 0.1%–1.6% dry weight in C. sativa and is derived from THC.
CBN is commercially available in a growing number of product formats. CBN is a minor cannabinoid used in the community in "isolate" products and is claimed to have pro-sleep effects comparable to conventional sleep medications. Common preparations include oral capsules, sublingual tinctures, oil-based drops, edible gummies, and topical preparations. Products often contain minor cannabinoids such as CBN, which are advertised to improve sleep. Products are also available in which CBN is combined with conventional therapies, with a common product containing both CBN and the widely used sleep aid melatonin. CBN isolate and broad-spectrum hemp extracts enriched in CBN are among the most prevalent commercial formats.
CBN was the first cannabinoid to be isolated from cannabis extract in the late 1800s. Specifically, it was discovered by Barlow Wood, Newton Spivey, and Easterfield in 1896. In the early 1930s, CBN's structure was identified by Cahn, marking the first development of a cannabis extract. Wood himself coined the term "cannabinol" for a thick "red oil" from which he extracted CBN alongside other major phytocannabinoids. This discovery was most likely due to rampant degradation of THC to CBN due to poor quality control, and the transportation and storage conditions related to the 19th century.
Its structure and chemical synthesis were achieved by 1940, followed by some of the first preclinical research studies to determine the effects of individual cannabis-derived compounds in vivo. For more than two decades after its discovery, the CBN cannabinoid was thought to be the principal psychoactive component of cannabis. Then, in 1964, Israeli researchers Yechiel Gaoni and Raphael Mechoulam effectively extracted THC from the cannabis plant and found its psychotropic effects.
There is extensive historical evidence that cannabis (Cannabis sativa L.) has been used for different purposes, among them industrial, ornamental, and pharmaceutical (e.g., treating rheumatic pain, constipation, gout, and gynecological disorders) applications. According to Korean and Chinese traditional medical records, the peeled seed of cannabis has been used for constipation, diabetes, pain diseases, menstrual disorders, skin diseases, and dysentery, and cannabis weed (the leaf) has been used for anthelmintic, hair protection, asthma, analgesic, anesthetic, and diuretic purposes. Furthermore, cannabis root has been used to treat difficult births and to relieve blood stasis; cannabis skin has been used for bruises, irritating rashes, and distending pain; and cannabis flower has been used for paralysis, itching.
It should be noted that these traditional preparations used whole cannabis plant materials containing hundreds of compounds. CBN as an isolated entity was not known until 1896; accordingly, traditional references to cannabis medicine cannot be attributed specifically to CBN. The high CBN content of aged or improperly stored cannabis means that some traditional preparations may have incidentally contained higher concentrations of CBN, but this is a post-hoc inference rather than documented traditional practice with the isolated compound.
Over the following decades after CBN's isolation, with the isolation and characterization of major phytocannabinoids, research on CBN was slowly set aside, eclipsed by the important and marked pharmacological activity of two compounds in particular, Δ9-THC and CBD. CBN is one of the least explored of the minor cannabinoids. In recent years, growth of the hemp and medicinal cannabis industries has revived scientific and commercial interest in CBN, particularly for its purported sleep-promoting properties.
CBN is itself the active compound under study; it is not a complex botanical extract but a single defined molecule. However, its pharmacological activity includes action through multiple molecular targets.
Cannabinol (CBN) is a mildly psychoactive phytocannabinoid that acts as a low affinity partial agonist at the CB1 and CB2 receptors of the endocannabinoid system (ECS). Although CBN shares the same mechanism of action as other phytocannabinoids such as THC, it has a lower affinity for CB1 receptors, meaning that much higher doses of CBN are required in order to experience intoxicating effects. Both THC and CBN activate the CB1 (Ki = 211.2 nM) and CB2 (Ki = 126.4 nM) receptors. Each compound acts as a low affinity partial agonist at CB1 receptors with THC demonstrating 5×–10× greater affinity to the CB1 receptor. Like THC, CBN has a higher selectivity for CB2 receptors, which are located throughout the central and peripheral nervous system, but are primarily associated with immune function.
The molecular mechanisms underlying CBN's pharmacological actions involve its interactions with the ECS, modulation of non-cannabinoid receptors, antioxidant and anti-inflammatory properties, and potential antimicrobial activity. A 2025 study published in the Journal of Medicinal Chemistry examined CBN's metabolism and pharmacological effects in detail: using metabolomics, researchers identified CBN-11-OH as the dominant metabolite, with lower levels of CBN-1′-OH and CBN-quinone. Computational simulations reveal CBN's stability at the CYP2C9 active site, driving hydroxy metabolite formation. The study reports the intricate biotransformation of CBN by multiple cytochrome P450 enzymes. Receptor activation assays revealed that CBN-1′-OH acts as a partial CB1 agonist, while CBN and its metabolites antagonize CB1 and CB2 receptors. Notably, CBN and CBN-11-OH elevate intracellular Ca2+ levels in dorsal root ganglia sensory neurons—an effect linked to potential pain relief.
Researchers at the Salk Institute have shown that CBN protected neurons against a form of cell death that is dependent on iron, called oxytosis/ferroptosis, by directly targeting the mitochondria, helping to preserve its key functions. This type of cellular death happens when cells fail to protect themselves against damage from harmful substances. Mitochondria contribute to ferroptosis regulation through their involvement in various metabolic pathways. When mitochondria are not working correctly, ferroptosis can occur. This dysregulation has been linked to diseases that affect the nervous system, including Alzheimer's, Parkinson's, and traumatic brain injury.
Previous research showed that cannabinol (CBN), a minor cannabinoid derived from Δ9-tetrahydrocannabinol, exhibits antioxidant, anti-inflammatory, analgesic, and anti-bacterial effects. Results from transcriptomic analysis revealed that CBN had no negative impact on cell viability at tested concentrations. Instead, it showed a significant effect on stress response and neuroplasticity-related processes.
Background and marketing claims: In recent years, marketers of cannabis products have claimed that cannabinol (CBN) has unique sleep-promoting effects. Despite a plausible mechanism, pre-clinical and clinical research investigating the effects of CBN is dated and limited, with the preponderance of human studies occurring in the 1970–1980s with small sample sizes lacking diversity in sociodemographic characteristics.
Key 2021 Narrative Review (Cannabis and Cannabinoid Research): A 2021 narrative review aimed to answer the question: "Is there sufficient clinical evidence to support claims that CBN has sleep-promoting effects?" A systematic search of PubMed/MEDLINE was performed. The abstracts of 99 human studies were screened for relevance, and eight full-text articles met inclusion criteria for detailed review. The review concluded: pre-clinical and clinical research investigating the effects of CBN is dated and limited. Evidence demonstrating that CBN itself elicits cannabis-like effects in humans is mixed, with the majority of available evidence demonstrating a lack of such an effect. Consequently, there is insufficient published evidence to support sleep-related claims. Randomized controlled trials are needed to substantiate claims made by manufacturers of cannabis products containing CBN. The review further specified that these studies should specifically evaluate effects on sleep through polysomnography, or at minimum through validated sleep questionnaires, and use dosages significantly higher than those found in currently available cannabis products marketed for sleep (typically ≤5 mg).
2024 Animal Polysomnography Study (Neuropsychopharmacology): CBN is a minor cannabinoid used in the community in "isolate" products and is claimed to have pro-sleep effects comparable to conventional sleep medications. However, no study had yet examined whether it impacts sleep architecture using objective sleep measures. The effects of CBN on sleep in rats using polysomnography were therefore examined. CBN increased total sleep time, although there was evidence of biphasic effects with initial sleep suppression before a dramatic increase in sleep. CBN increased both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Regarding clinical translation, the authors noted: results suggest that CBN might be best targeted to patients with sleep maintenance insomnia or early morning awakening insomnia, as CBN had a delayed onset of pro-sleep action that had a longer duration of action than zolpidem. This was a preclinical (animal) study; its findings do not directly establish efficacy in humans.
Human RCT Protocol (CUPID Study): Insomnia is the most prevalent sleep disorder, with few effective pharmacotherapies. Anecdotal reports and recent preclinical research suggest that CBN, a constituent of Cannabis sativa derived from delta-9-tetrahydrocannabinol, could be an effective treatment. Despite this, the isolated effects of CBN on sleep have yet to be systematically studied in humans. A randomised, double-blind, placebo-controlled, single-dose, three-arm, cross-over, proof-of-concept study was designed to investigate the effects of CBN on sleep and next-day function in 20 participants with clinician-diagnosed insomnia disorder and an Insomnia Severity Index Score ≥15. This pilot study investigated the acute effects of oral doses of CBN at 30 and 300 mg in twenty patients with clinician-diagnosed insomnia disorder. Across three treatment sessions, each separated by a two-week washout, participants received two doses of CBN and matched placebo, at random. Participants underwent overnight sleep assessment using in-laboratory polysomnography and next-day neurobehavioral function tests. The primary outcomes were CBN (30 and 300 mg) effects on sleep continuity (wake after sleep onset minutes), compared to placebo, measured using polysomnography. This study was designed to provide novel preliminary data on the effects of CBN on sleep and next-day function in adults living with insomnia disorder, to inform the design of larger clinical trials.
Evidence for CBN + Melatonin Combination (20 mg dose): A randomized, double-blind, placebo-controlled human trial published in Experimental and Clinical Psychopharmacology found significant reductions in nighttime awakenings at a 20 mg nightly dose. Most human studies that have assessed CBN's effects on sleep combined CBN with other phytocannabinoids, and have failed to assess whether CBN has hypnotic effects alone.
Overall evidence assessment: Evidence for CBN as a sleep aid in humans remains preliminary. The most rigorous conclusion from peer-reviewed literature is that studies specifically assessing subjective effects associated with sleep, such as sedation or fatigue, are rare. Most importantly, published clinical trials investigating associations between CBN and validated sleep questionnaires and/or formal polysomnography were not identified in the 2021 review. More recent data (2024–2025) are emerging from both animal polysomnography and small human RCTs, but these do not yet constitute sufficient evidence for established clinical efficacy.
In preclinical models, CBN has been reported to show a number of properties with therapeutic potential such as anti-bacterial, anti-inflammatory, neuroprotection, pain relief, appetite stimulation, and anti-convulsion effects. THC, THCA, and the metabolite cannabinol (CBN) have been described to possess analgesic, anti-inflammatory, and neuroprotective effects.
CBN has been reported to be utilized in the relief of chronic pain, like temporomandibular disorders and fibromyalgia, in rat models for myofascial pain. Compared to cannabidiol (CBD) and Δ9-THC, CBN has an antiallergic effect on airway infections by inhibiting the production of various interleukins and reducing mucus production in mouse models.
In a study using cannabinol in OVA-sensitized and challenged A/J mice, published in Future Medicinal Chemistry in October 2009 as part of "Cannabinoids as novel anti-inflammatory drugs," the compound demonstrated decreased allergen-induced mucus production. CBN is the non-enzymatic oxidation byproduct of THC; it does not show psychotropic properties but exerts sedative, analgesic, anti-inflammatory, and neuroprotective effects.
CBN and its metabolites exhibit mild anti-inflammatory effects in microglial cells, though less potent than cannabigerol and cannabichromene.
Evidence assessment: All pain and anti-inflammatory evidence for CBN is currently preclinical (animal models and in vitro). No published human clinical trials specifically evaluating CBN for pain have been identified in the available peer-reviewed literature.
Scientists at the Salk Institute helped explain how CBN protects the brain against aging and neurodegeneration, then used their findings to develop potential therapeutics. The researchers created four CBN-inspired compounds that were more neuroprotective than the standard CBN molecule — one of which was highly effective in treating traumatic brain injury in a Drosophila fruit fly model. The findings, published in Redox Biology on March 29, 2024, suggest promise for CBN in treating neurological disorders like traumatic brain injury, Alzheimer's disease, and Parkinson's disease.
CBN has been studied for its potential benefit as a neuroprotectant and to prevent Huntington's disease. CBN may also be a powerful neuroprotectant. In one rodent study, researchers used CBN as a treatment for ALS and found that it was able to delay the onset of the condition. While human studies need to be done, this suggests that CBN may provide a powerful tool in the fight against ALS and other neurodegenerative conditions.
In a published article in the Journal of Pharmacology and Experimental Therapeutics in June 2000, a number of cannabinoids including cannabinol were shown to prevent serum-deprived cell death. The study suggests that these cannabinoids act as antioxidants to modulate cell survival.
This antioxidant activity potentially contributes to CBN's neuroprotective effects and may have implications for the treatment of neurodegenerative disorders.
Evidence assessment: Neuroprotection data for CBN are exclusively preclinical (in vitro and animal models including fruit fly and rodent), with no published human clinical trials. Results are scientifically interesting but cannot be translated to clinical recommendations at this stage.
In a research article published in Nature in 2008, five cannabinoids including cannabinol, cannabigerol, THC, CBD, and cannabichromene showed potent antibacterial activity. These five cannabinoids were tested against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains. CBN exhibits potential antimicrobial activity, acting against various bacteria, fungi, and MRSA strains. The underlying mechanisms of this antimicrobial effect are still being elucidated, but may involve disruption of microbial cell membranes and interference with microbial biofilm formation. Compared with other cannabinoids like cannabichromene (CBC) and cannabigerol (CBG), CBN is reported to be effective against methicillin-resistant Staphylococcus aureus (MRSA).
Evidence assessment: Antibacterial findings for CBN are based on laboratory (in vitro) studies only. No human clinical trials have evaluated CBN for the treatment of bacterial infections.
One study evaluated neuroprotective and anti-apoptotic effects of CBN on differentiated mouse retinal ganglion precursor-like cells exposed to elevated pressure conditions mimicking the pathological settings of increased intraocular pressure in glaucoma. Researchers also evaluated the impact of CBN on specific extracellular matrix protein markers and MAPK downstream signaling in primary human trabecular meshwork cells. The results provided evidence for CBN's use as a valid therapeutic intervention in glaucoma treatment, with a potential role in neuroprotection, reduction of IOP, and ECM remodeling.
CBN, unlike CBG, caused conjunctival erythema and hyperemia. A single dose of CBN showed a moderate effect on intraocular pressure after a single dose, and it caused a more significant reduction in ocular tension during chronic administration. Although CBG had similar effects, the response was greater than CBN.
Evidence assessment: Glaucoma-related research on CBN is currently limited to in vitro and animal models. The finding of conjunctival erythema and hyperemia in one study is a noted adverse effect that would require careful evaluation in human trials.
Studies have found that CBN may have appetite-stimulating effects. In a 2012 study done on rodents, CBN reduced the time it took rats to begin eating and increased the amount of food they consumed. This research suggests CBN may have therapeutic potential in situations where low appetite is a factor.
Evidence assessment: Appetite-stimulating effects for CBN are based solely on a rodent study. No human clinical data have been published on this specific effect.
Cannabinol (CBN) helps boost immune function by binding to CB2 receptors rather than CB1 receptors, and also has anti-inflammatory, pain relief, sleep induction, appetite enhancing, and anticonvulsant effects, according to patent and research literature surveys. These anticonvulsant properties have not been substantiated by published human clinical trials, and the evidence base remains preclinical.
CBN has been administered in various forms in research and commercial settings. The following dosages are drawn directly from identified studies:
No established therapeutic dose has been validated by large-scale clinical trials. A scarcity of large-scale, randomized, placebo-controlled human trials and limited data on long-term safety and optimal dosing regimens for various conditions mean that firm dosing recommendations cannot be made on the basis of current evidence.
When taken by mouth, cannabinol is possibly safe for adults when taken at a dose of up to 20 mg daily for up to 7 days. It might cause side effects such as altered taste, headache, and sleepiness. CBN, unlike CBG, caused conjunctival erythema and hyperemia in animal studies examining its ocular effects. Long-term safety data in humans are not available.
The major cannabinoids present in cannabis undergo metabolism primarily through cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) enzymes, and these same enzymes are often involved in the biotransformation of other drugs. Recent studies have been conducted to evaluate the effect of major cannabinoids (THC, CBD, and CBN) and their metabolites on major drug-metabolizing enzymes. Computational simulations reveal CBN's stability at the CYP2C9 active site. CBN undergoes biotransformation by multiple cytochrome P450 enzymes.
A 2025 study published in Basic & Clinical Pharmacology & Toxicology specifically characterized an important pharmacokinetic interaction: products are available in which CBN is combined with the widely used sleep aid melatonin. The combination of CBN and melatonin provides potential for a pharmacokinetic drug–drug interaction, given that cannabinoids are known to inhibit drug-metabolizing enzymes. Indeed, CBN potently inhibited the CYP1A2-mediated metabolism of caffeine. CYP1A2 is the major hepatic enzyme involved in the metabolism of melatonin; thus, researchers examined whether CBN inhibited CYP1A2-mediated metabolism of melatonin in vitro and in vivo. The finding was clinically significant: CBN potently inhibited CYP1A2-mediated metabolism of melatonin and increased the apparent oral bioavailability of melatonin in mice with a four-fold increase in the plasma melatonin exposure. This is a preclinical finding, but it has direct relevance given the widespread commercial availability of CBN+melatonin combination products.
Evidence regarding CBN-induced potentiation of THC effects is mixed. CBN has often been praised for its sedative effects, but it appears that this is usually true when cannabinol is consumed in combination with THC, as is the case with older flower. Also, the terpene profile of a cannabis strain will change with time, leaving more of the sleep-inducing terpenes in the flower. This suggests that the sedative reputation of aged cannabis may be attributable in part to the combined terpene and cannabinoid profile, not CBN alone.
CBN is not listed in the schedules set out by the United Nations' Single Convention on Narcotic Drugs from 1961 nor their Convention on Psychotropic Substances from 1971, so the signatory countries to these international drug control treaties are not required by these treaties to control CBN.
In the United States, the regulatory picture is evolving. Beyond CBD and THC, emerging cannabinoids like CBG (cannabigerol), CBN (cannabinol), and THCV (tetrahydrocannabivarin) are gaining interest for their potential medical benefits. The FDA has not approved CBN for any medical use. The agency has denied approval of cannabinoid-containing food, beverages, or dietary supplements, even when sourced from federally legal hemp. Non-intoxicating hemp products such as most CBD, CBG, and CBN wellness-oriented formulations have been discussed as potentially remaining within legal frameworks following legislative changes enacted in November 2025, though the precise regulatory treatment of CBN under evolving federal hemp policy remains subject to ongoing clarification.
Research on cannabinol is limited and its effects are unclear. When applied to the skin, there is not enough reliable information to know if cannabinol is safe or what the side effects might be. Further research is needed to fully understand the therapeutic potential of CBN and its role in various disease states. The current evidence base does not support statements about CBN's long-term safety profile in humans.
CBN occupies a unique scientific position: it is the oldest-known isolated cannabinoid, yet among the least thoroughly characterized in human clinical research. Among the "minor cannabinoids," cannabinol (CBN) stands out for its important repercussions and implications on the global scientific landscape. It deserves a prominent place within the so-called "cannabinome," with promising pharmacological potential and significant impact on the development of new synthetic methodologies. However, for virtually every proposed therapeutic application — sleep, pain, neuroprotection, antibacterial activity, appetite stimulation, and glaucoma — the evidence base is either exclusively preclinical or consists only of small, early-phase human studies. A scarcity of large-scale, randomized, placebo-controlled human trials, limited data on long-term safety and optimal dosing regimens, and inconsistent standardization across different CBN formulations and products represent the principal limitations of the current evidence.
Health conditions that Cannabinol may help support.
Body systems that Cannabinol may help support.
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