Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
+1 more
TerpenoidCannabichromene
CBC (cannabichromene) is a naturally-occurring cannabinoid of the benzopyran class. It is the third major phytocannabinoid in cannabis, alongside THC and CBD, distinguished by its complete lack of intoxicating effects. It acts on pain-sensing nerve fibers and enhances inhibitory brain signaling,[1][2] without engaging the receptor pathway responsible for cannabis intoxication.[3][4]
CBC (cannabichromene) is a naturally-occurring cannabinoid of the benzopyran class. It is the third major phytocannabinoid in cannabis alongside THC and CBD, distinguished by its complete lack of intoxicating effects. CBC is a TRPA1 channel agonist and GABA_A positive allosteric modulator,[1][2] producing its effects by desensitizing pain-sensing neurons and enhancing inhibitory signaling.
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
+1 more
TerpenoidCBC was first isolated in 1966 by two independent research groups working simultaneously on cannabis plant material.[5] Early studies found it was the second most abundant cannabinoid in drug-type cannabis, with anti-inflammatory activity exceeding standard pain medications.[6] Despite renewed scientific interest since the 2010s, no completed human clinical trial has been conducted, and the sole registered Phase 1 study remains suspended.
Subjective effects include, based on animal models only, analgesia, reduced inflammation, and anti-seizure action — whether any of these produce a noticeable human experience remains genuinely unknown. CBC does not cause intoxication or altered consciousness; it produces none of the high associated with cannabis.[3][4] No adverse subjective effects have been reported in any study.
No dependence or withdrawal has been documented, consistent with CBC's negligible activity at the receptor pathway that drives cannabis addiction. The dominant risk is co-administration with sedative drugs — alcohol, benzodiazepines, or opioids — which CBC amplifies through direct pharmacological action.[7] The evidence base rests entirely on cell and animal studies — no human pharmacokinetic, dose-response, or safety data exist for isolated CBC.
History[edit]
Discovery
Cannabichromene was isolated in 1966 by two independent groups working simultaneously. Yechiel Gaoni and Raphael Mechoulam identified it in Egyptian hashish,[5] extending Mechoulam's 1964 work on THC to a second major cannabinoid class. Concurrently, Ulrich Claussen, Friedrich Von Spulak, and Friedrich Korte extracted CBC from hemp, establishing it as the third recognized phytocannabinoid.
Scientific significance
The first systematic biological study, by Turner and ElSohly in 1981, found CBC was the second most abundant cannabinoid in drug-type cannabis and that its anti-inflammatory activity exceeded the NSAID phenylbutazone.[6] That profile — pharmacologically potent but non-intoxicating — took decades to fully investigate.
Modern research
Scientific interest revived in the 2010s when CBC was identified as a potent activator of pain-sensing TRPA1 channels[1] and later as a modulator of inhibitory brain signaling.[2] As of 2026, CBC remains one of the most characterized phytocannabinoids to have never completed a human clinical trial.
The name "cannabichromene" combines "cannabis" with "chromene," the benzopyran ring that defines its chemical structure and distinguishes it from THC. CBC has no street names, no recreational identity, and no cultural narrative — historically the second most abundant cannabinoid in drug-type cannabis, yet almost entirely unknown outside pharmacological research.
Chemistry[edit]
Structural class
CBC belongs to the benzopyran (chromene) subclass of phytocannabinoids.[8] All major cannabinoids share the same C₂₁ molecular starting material, but CBC's final biosynthetic assembly produces a chromene ring rather than THC's cyclohexane — the structural reason it produces no intoxication. Its molecular formula is C₂₁H₃₀O₂ (314.46 g/mol). The pentyl side chain and chromene structure underlie its antibacterial activity.[9]
Natural occurrence
In cannabis, CBC forms when cannabichromenic acid (CBCA) decarboxylates. CBCA is the first cannabinoid to appear in young seedlings,[10] suggesting a developmental role in the plant. CBC was historically the second most abundant cannabinoid in drug-type cannabis,[6] though modern high-THC cultivation has reduced its share.[11] It degrades to cannabicyclol under acid or UV light[12] and is absorbed primarily via the lymphatic system after oral dosing.[13]
Pharmacology[edit]
Mechanism of action
CBC has negligible activity at the CB1 — the receptor responsible for cannabis intoxication — which is why it produces no high.[3][4] Its primary action is activating TRPA1 channels on pain-sensing nerve fibers, producing initial excitation followed by prolonged silencing.[1] This desensitization underlies its analgesic and anti-inflammatory effects, including a calming effect on intestinal spasms.[14]
CBC also enhances the brain's main inhibitory signaling — GABA — by binding to a novel site on GABA receptors, separate from where benzodiazepines act.[2] This accounts for anti-seizure effects in animal models.[15] In mice, CBC also suppressed an enzyme that breaks down natural mood-related compounds, producing antidepressant-like behavioral effects comparable to imipramine.[16]
Pharmacokinetics
No human pharmacokinetic data exist for isolated CBC. In rats, oral CBC is absorbed primarily through the lymphatic system — a consequence of its fat-soluble structure.[13] Co-administration with CBD raises plasma levels of both compounds in rats.[17] CBC does not significantly block liver metabolic enzymes,[7] making it less likely than CBD to interfere with other medications.
Neuroscience[edit]
Where it acts
CBC acts on two systems outside the classical cannabinoid pathway. On pain-sensing nerve fibers, it activates then silences TRPA1 channels, functionally switching off pain signals.[1] It also modulates brainstem regions that regulate how strongly pain signals are perceived.[18]
At GABA receptors, CBC strengthens inhibitory signaling through a binding site distinct from both benzodiazepines and neurosteroids.[2] In animal models, this produces measurable reductions in seizure activity.[15]
Why it matters
CBC achieves stronger effects at lower doses when combined with other cannabinoids[19] and synergizes with the terpene β-caryophyllene.[20][21] This means CBC in full-spectrum cannabis products may behave very differently from isolated CBC.
Whether CBC crosses the blood-brain barrier in humans is unknown — all CNS effects have been demonstrated only in rodents. The contribution of individual CBC enantiomers to neural activity is entirely unstudied.[22]
Subjective Effects[edit]
CBC is non-psychoactive — it produces no intoxication, no altered perception, and no measurable subjective effect on consciousness.[4][23] All documented pharmacological effects derive from animal and cell models. Whether CBC produces any perceptible human experience at any dose remains an open empirical question.
Where THC works through cannabinoid receptors to produce intoxication, and CBD modulates anxiety and seizure threshold through serotonin pathways, CBC acts primarily on pain nerve fibers and inhibitory brain signaling. This predicts a profile weighted toward peripheral pain suppression — not consciousness alteration.
CBC was first isolated in 1966 by two independent research groups analyzing cannabis plant material.[3] Early studies identified it as the second most abundant cannabinoid in drug-type cannabis, with anti-inflammatory potency exceeding standard pharmaceuticals.[4] Despite renewed preclinical interest since the 2010s, no completed human clinical trial exists — the sole registered Phase 1 study is currently suspended.
CBC does not produce psychoactive or intoxicating effects — it exhibits negligible CB1 affinity and fails to generate THC-like responses in animal discrimination models.[5][6] Its documented pharmacological actions — analgesia, anti-inflammatory activity, and anti-seizure effects — derive exclusively from cell and animal models with no human experiential data. Whether CBC produces any perceptible subjective response in humans at any dose remains an open question.
No dependence, tolerance, or withdrawal has been documented, consistent with CBC's negligible CB1 activity. CBC potentiates sedation from CNS depressants through a direct pharmacological mechanism rather than metabolic inhibition,[7] making co-administration with sedatives the primary identified risk. The evidence base rests entirely on preclinical research — no human pharmacokinetic, dose-response, or safety data exist for isolated CBC.
History[edit]
Discovery
Cannabichromene was isolated and structurally characterized in 1966 by two independent groups working concurrently. Yechiel Gaoni and Raphael Mechoulam identified it in Egyptian hashish at the Weizmann Institute,[3] extending Mechoulam's landmark 1964 elucidation of THC to a second major cannabinoid class. Simultaneously, Ulrich Claussen, Friedrich Von Spulak, and Friedrich Korte extracted CBC from hemp — the convergent discovery establishing it as the third recognized phytocannabinoid alongside THC and CBD.
Scientific significance
The first systematic biological study, conducted by Turner and ElSohly in 1981, established three foundational findings: CBC was the second most abundant cannabinoid in drug-type cannabis, its anti-inflammatory activity exceeded the NSAID phenylbutazone, and it possessed strong antibacterial properties.[4] These results positioned CBC as pharmacologically significant despite its lack of psychoactivity — a profile that would take decades to fully investigate.
Modern research
Pharmacological interest revived in the 2010s when De Petrocellis and colleagues established CBC as a potent TRPA1 agonist and NAAA inhibitor,[1] redirecting research away from CB1/CB2 paradigms toward non-canonical cannabinoid pathways. Subsequent work identified GABA_A positive allosteric modulation as a second major mechanism,[2] and anti-inflammatory, analgesic, and anti-seizure properties were demonstrated in rodent models. As of 2026, CBC remains one of the most pharmacologically characterized phytocannabinoids to lack any completed human clinical data.
The name "cannabichromene" combines "cannabis" with "chromene," the latter referring to the benzopyran ring system that defines its chemical structure and distinguishes it from the cyclohexane scaffold of THC. CBC occupies an unusual position in cannabis culture: historically the second most abundant cannabinoid yet almost entirely unknown outside pharmacological research, it has no street names, no recreational identity, and no cultural narrative beyond its role as a component of the entourage effect.
Chemistry[edit]
Structural class
CBC belongs to the chromene (benzopyran) subclass of phytocannabinoids. It shares the C₂₁ terpenophenolic scaffold common to all major cannabinoids derived from cannabigerolic acid, but its final biosynthetic cyclization produces a chromene ring rather than THC's cyclohexane system.[8] This structural divergence is the basis for CBC's non-psychoactive profile.
The pentyl side chain and chromene ring are critical pharmacophores for antibacterial activity, particularly against methicillin-resistant Staphylococcus aureus (MRSA).[9]
| Molecular formula | C₂₁H₃₀O₂ |
| Molecular weight | 314.46 g/mol |
Molecular structure
The molecule features a resorcinol ring bearing a pentyl side chain at C-7, fused to a pyran ring with a 4-methylpent-3-enyl substituent and geminal methyl group at C-2. The chromene double bond between C-3 and C-4 distinguishes CBC from cannabicyclol (CBL), its photoisomerization product formed when this bond undergoes intramolecular [2+2] cycloaddition.
Stereochemistry
CBC occurs in cannabis as a scalemate — a non-racemic mixture of enantiomers whose ratio varies by strain. The enantiomeric composition is genetically determined, linked to differential expression of CBCA synthase isoforms.[10] The biological activity of individual CBC enantiomers has not been independently studied, representing a significant pharmacological gap.
Physical properties and stability
CBC is a viscous oil at room temperature with a boiling point of approximately 220°C at reduced pressure. Its lipophilic character and molecular planarity facilitate intestinal lymphatic transport during oral absorption.[11]
Stability is a practical concern: CBC converts to cannabicyclol under acidic conditions or prolonged UV exposure.[12] Storage in neutral, light-protected conditions prevents this degradation.
Natural occurrence
CBC occurs in Cannabis sativa as the decarboxylation product of cannabichromenic acid (CBCA). CBCA is the first cannabinoid to accumulate in seedlings after germination,[13] preceding both THCA and CBDA — a pattern suggesting a developmental or protective role in early plant growth.
In mature drug-type cannabis, CBC was historically the second most abundant cannabinoid,[4] though modern high-THC cultivars have shifted this ranking. The propyl homolog cannabichromevarin (CBCV) also occurs naturally, and CBC content varies across chemotypes consistent with independent allelic control of the CBCA synthase locus.[14]
Pharmacology[edit]
Mechanism of action
CBC's pharmacology operates almost entirely outside the classical CB1/CB2 cannabinoid receptor system — a distinguishing feature among major phytocannabinoids. It exhibits negligible CB1 affinity and does not produce intoxication or THC-like effects in animal models.[5][6]
The primary mechanism is TRPA1 agonism followed by channel desensitization. CBC activates TRPA1 channels on pain-sensing neurons, producing initial excitation followed by prolonged functional silencing.[1] This desensitization underlies CBC's analgesic and anti-inflammatory effects, including suppression of intestinal hypermotility.[15]
The second major mechanism is GABA_A positive allosteric modulation. CBC enhances GABA-mediated inhibitory currents by binding at a site on the β2 subunit (valine-436) distinct from the benzodiazepine pocket.[2] This novel action accounts for anti-seizure effects confirmed in drug-induced seizure models.[16]
CBC also elevates endocannabinoid tone through two routes: inhibition of the enzyme that degrades palmitoylethanolamide (NAAA) and blockade of anandamide cellular uptake.[1] Both actions amplify endogenous anti-inflammatory signaling without direct CB1 engagement. In mice, CBC inhibited MAO-A (MAO-A) at 20 mg/kg, contributing to antidepressant-like behavioral effects comparable to imipramine.[17]
Pharmacokinetics
No human pharmacokinetic studies for isolated CBC have been published. Bioavailability, peak plasma concentration, half-life, and volume of distribution in humans are entirely unknown. All data derive from rat models and laboratory preparations.
In rats, intestinal lymphatic transport plays a major role in oral CBC absorption, facilitated by the molecule's lipophilicity and planar structure.[11] Nanoemulsion formulation increased lymphatic bioavailability 3-fold and portal vein bioavailability 8-fold compared to oil.
Co-administration with CBD in rats increased the plasma levels of both compounds without altering time to peak,[18] consistent with competition at shared metabolic enzymes. The major human liver metabolite is 2'-hydroxycannabicitran, a novel oxidized structure with no significant activity at CB1 or CB2 receptors.[19]
Despite serving as a substrate for multiple liver enzymes, CBC does not appear to significantly inhibit their activity[7] — meaning it is unlikely to cause dangerous elevations of co-administered drug levels through metabolic interference.
Neuroscience[edit]
Where it acts
CBC's neural effects operate through two primary pathways outside the classical endocannabinoid system. TRPA1 channels on pain-sensing nerve fibers undergo activation followed by prolonged desensitization, functionally silencing nociceptive C-fibers.[1] In rats, CBC modulates descending pain control through the rostral ventromedial medulla and periaqueductal gray — key brain regions that gate pain signals traveling up from the body.[20]
At GABA_A receptors, CBC enhances inhibitory neurotransmission via a binding site on the β2 subunit distinct from both the benzodiazepine and neurosteroid sites.[2] This pharmacologically novel mechanism accounts for anti-seizure effects observed in animal models[16] and suggests a mode of cortical inhibition unlike existing GABAergic drugs.
Why it matters
CBC's activity maps onto the "endocannabinoidome" — an expanded framework encompassing TRP channels, lipid mediators, and receptors beyond classical CB1/CB2 signaling. Through NAAA inhibition and anandamide reuptake blockade,[1] CBC amplifies endogenous anti-inflammatory and analgesic signaling without engaging CB1 directly. This positions it as a modulator of broad lipid signaling tone rather than a single-target drug.
Direct experimental support for the entourage effect hypothesis — the idea that cannabinoids and terpenes act synergistically — comes from CBC's efficacy at subtherapeutic doses when combined with other cannabinoids[21] and its synergy with β-caryophyllene.[22][23]
Whether CBC crosses the blood-brain barrier in humans is unknown — all CNS effects have been demonstrated only in rodents, and no human brain imaging or cerebrospinal fluid sampling data exist. The contribution of individual CBC enantiomers to neural activity is entirely unstudied.[10]
Subjective Effects[edit]
CBC is non-psychoactive and non-intoxicating — it produces none of the subjective alterations in consciousness, perception, or mood characteristic of THC.[6][24] All documented pharmacological effects — analgesia, anti-inflammatory activity, anti-seizure action, and antidepressant-like behavioral changes — derive exclusively from cell and animal models. Whether CBC produces any perceptible subjective response in humans at any dose is an open empirical question, and route of administration, formulation, and co-administered cannabinoids or terpenes may substantially alter its profile through entourage interactions.
CBC occupies a fundamentally different pharmacological niche than THC or CBD. Where THC produces intoxication via CB1 agonism and CBD modulates anxiety and seizure threshold through serotonin and TRPV1 activity, CBC's primary targets — TRPA1 desensitization and GABA_A allosteric modulation — predict a profile dominated by peripheral analgesia and subtle inhibitory effects rather than any centrally mediated alteration of consciousness.
Effect Grid
Common-range doses (25-75 mg oral) correspond to the pharmacological activity range suggested by animal model scaling. Mouse studies used 10-20 mg/kg for anti-inflammatory, analgesic, and antidepressant effects — roughly equivalent to this human dose range by simple body-weight scaling (without allometric correction).
Preclinical evidence predicts pain suppression via TRPA1 desensitization of nociceptors, potential anti-inflammatory activity, and modest sedation via GABAA allosteric modulation. No subjective psychoactive effects are expected. CBC does not produce intoxication, euphoria, or altered perception at any studied dose.
No human pharmacodynamic or subjective-effect data exist to confirm these predictions. Entourage effects with co-administered cannabinoids may substantially alter the pharmacological profile.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Timeline
Pharmacological activity onset. CBC is non-psychoactive — no subjective perceptual or cognitive changes occur. TRPA1 engagement and GABAA modulation begin as intestinal lymphatic absorption delivers CBC to target tissues.
Period of maximum pharmacological activity based on predicted Tmax from cannabinoid absorption kinetics. Peripheral analgesic and anti-inflammatory effects at maximum. No intoxication, altered perception, or cognitive changes occur.
Hepatic CYP-mediated clearance (CYP1A2, 2C19, 2D6, 3A4) reduces plasma concentrations. Pharmacological activity diminishes. No residual impairment expected from CBC alone.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- none
- Tolerance reset
- —
- Physical
- None
- Psychological
- None
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- —
Toxicity
No lethal dose has been established for CBC in any species. No human adverse event reports exist for isolated CBC.
Acute toxicity
Controlled toxicity studies do not exist. The longest published dosing regimen — 10–20 mg/kg daily for 21 days in mice — found no adverse effects on movement or behavior,[16] but this was an antidepressant study, not a safety assessment.
Cell toxicity
In human skin cells, CBC was well tolerated up to 10 μM. Concentrations at or above 50 μM triggered cell death[24] — levels far beyond anything achievable in the body.
Reproductive safety
CBC suppressed hormone-stimulated ovarian cell function in laboratory studies — an effect shared across the cannabinoid class.[25] This has not been studied in living organisms for CBC specifically. Clinical significance for human reproduction is unknown. safety citation needed
Immune effects
Historical data showed CBC suppressed immune cell activity, but only at concentrations far above those achievable at anticipated doses.[26] This is a class-wide effect and is unlikely to be clinically relevant.
Sedation potentiation
CBC amplifies the sedating effects of barbiturates and other CNS depressants in mice through direct pharmacological action — not by slowing the metabolism of those drugs.[7] This is likely related to CBC's enhancement of GABA signaling. safety citation needed
Psychological risks
CBC produces no psychoactive effects and does not generate cannabis-like responses in trained animals at doses up to 30 mg/kg.[23][4] No psychiatric adverse events or cognitive impairment have been reported in any study.
CBC's GABA activity raises a theoretical concern about sedation or cognitive blunting at high doses, analogous to other agents that enhance inhibitory signaling. This has not been investigated.
Tolerance and dependence
No published studies on CBC tolerance, dependence, or withdrawal exist. This is consistent with CBC's negligible CB1 activity — CB1 receptor adaptation is the primary driver of cannabinoid tolerance.
CBC did not alter the interoceptive effects of THC in trained animals[23] and showed no cannabimimetic properties,[4] suggesting minimal abuse potential.
Drug Interactions
CBC is metabolized by multiple liver enzymes.[27] Drugs that inhibit these pathways could raise CBC levels; inducers (e.g., rifampin) could lower them. CBC does not significantly block liver enzymes itself,[7] making it less likely than CBD to raise levels of co-administered medications. Co-administration with CBD raises mutual plasma levels in rats[17] — not yet confirmed in humans. safety citation needed
CBC amplifies sedation from CNS depressants through direct pharmacological action.[7] Given its GABA activity,[2] additive sedation with alcohol, benzodiazepines, barbiturates, and opioids is plausible. safety citation needed CBC also achieves stronger effects at lower doses combined with CBD, CBDV, CBG,[19][21] and β-caryophyllene[20] — meaning effects in full-spectrum products may differ substantially from isolated CBC.
Contraindications
5 knownNo substance-specific contraindication data exist for CBC. The following are inferred from mechanism and class effects:
Absolute (inferred):
- Cannabinoid hypersensitivity: Those with known allergic reactions to cannabis-derived compounds should avoid CBC.
Relative (inferred):
- Concurrent CNS depressant use: CBC pharmacologically amplifies sedation from benzodiazepines, barbiturates, opioids, and alcohol.[7][2] safety citation needed
- Drugs metabolized by shared liver enzymes: Competitive interactions may alter levels of both CBC and co-administered drugs.[27]
- Pregnancy and lactation: Antigonadal effects observed across the cannabinoid class.[25] No reproductive studies specific to CBC exist.
- Complex seizure disorders: CBC has anti-seizure effects via GABA modulation, but no human dosing or safety data exist. Interaction with existing anti-epileptic medications is unpredictable.
All contraindications are inferred from preclinical evidence. No human data support or refute any specific contraindication.
Harm Reduction[edit]
Forms & Identification
CBC products are sold as isolate oils, tinctures, and capsules in jurisdictions where hemp-derived cannabinoids are legal. Visual purity verification is impractical — CBC is a viscous oil, not a crystalline powder. Third-party certificates of analysis (COAs) with full cannabinoid profiles are the most reliable verification tool.
CBC does not cross-react with standard THC urine immunoassays. THC contamination in poorly tested products could still trigger a positive drug screen. Products without batch-specific COAs or from unverified manufacturers carry higher contamination risk.
Guidelines
- Obtain a certificate of analysis from an independent laboratory confirming cannabinoid profile and absence of THC above legal thresholds
- Start with low doses — no human dose-response data exist for isolated CBC, and individual responses are uncharacterized
- Avoid combining CBC with alcohol, benzodiazepines, barbiturates, or opioids until the sedation interaction is personally understood
- Store CBC products in cool, dark conditions to prevent degradation to cannabicyclol (CBL)
- Inform healthcare providers of CBC use, particularly if taking medications metabolized by common liver enzymes
Set & Setting
CBC produces no psychoactive effects, so set and setting are minimal concerns. The primary situational risk is sedation potentiation: anyone taking CBC alongside CNS depressants — including alcohol — should be in a safe environment and avoid driving or operating machinery until the interaction is personally understood.
Aftercare & integration. CBC does not produce psychoactive experiences requiring psychological integration. Aftercare considerations are primarily physical.
- If sedation occurred from CBC combined with other substances, allow full recovery before resuming normal activities or driving
- Note any unusual responses for future dosing decisions — individual reactions to CBC are poorly characterized in the absence of human clinical data
- If using CBC for a specific health concern, maintain a log of doses and responses to inform discussions with a healthcare provider
Recovery & Support
CBC has no documented abuse liability, and no withdrawal has been described. Individuals concerned about their use of any cannabis-derived product — including CBC as part of a broader cannabinoid regimen — can contact SAMHSA's National Helpline (1-800-662-4357) for confidential support and referral.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
CBC is non-intoxicating with no established acute toxicity at anticipated doses. Emergency situations involving CBC are most likely to arise from interaction with co-administered substances.
Recognizing an emergency:
- Excessive sedation, slurred speech, or difficulty breathing when CBC is combined with CNS depressants (alcohol, benzodiazepines, opioids)
- Allergic reaction: hives, swelling of face or throat, difficulty breathing
Immediate steps:
- Stop all substance administration
- If the person is excessively sedated or unresponsive, place them in the recovery position (on their side, airway clear)
- Call emergency services if breathing is slow, labored, or absent
- Do not induce vomiting
What to tell the dispatcher: Provide the substance name (cannabichromene / CBC), approximate amount taken, time of ingestion, any co-administered substances, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from legal consequences when seeking help.
Legal Status[edit]
CBC is not scheduled under any international drug control treaty and has not been restricted by any national drug authority.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not scheduled (federally legal if hemp-derived) | Legal under 2018 Farm Bill when source contains less than 0.3% Δ⁹-THC; not DEA-scheduled; FDA has not approved or restricted[28] |
| United Kingdom | Not controlled | Legal when derived from industrial hemp; finished products must contain no more than 1 mg of any controlled cannabinoid; not listed under Misuse of Drugs Act 1971 |
| European Union | Not controlled | Not classified as a controlled substance under EU law; individual member states may impose novel food regulations for CBC marketed as food supplements |
| Canada | Not specifically scheduled | CBC derived from licensed hemp cultivars is generally permitted under Canada's cannabis regulatory framework citation needed |
| Australia | Not specifically scheduled | Status under TGA regulatory framework not confirmed from primary regulatory sources citation needed |
| International (UN) | Not scheduled | Not listed in any UN drug control convention |
Legal status changes frequently and varies by jurisdiction. This information reflects available sources as of the article's last update and is not legal advice.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- none
- Tolerance reset
- —
- Physical
- None
- Psychological
- None
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- —
Toxicity
No lethal dose has been determined for CBC in any species. No human adverse event reports, overdose cases, or post-market safety signals for isolated CBC have been identified.
Acute toxicity
Controlled toxicity studies do not exist. The longest published dosing regimen — 10–20 mg/kg daily for 21 days in mice — reported no adverse effects on movement or general behavior,[17] but was designed as an antidepressant study, not a toxicology assessment.
Cell toxicity
In human sebocytes, CBC was well tolerated at concentrations up to 10 μM. Concentrations at or above 50 μM triggered cell death[25] — a threshold consistent with other cannabinoids at concentrations far exceeding those achievable in the body.
Reproductive safety
CBC inhibited hormone-stimulated ovarian cell function in laboratory studies — an antigonadal effect shared across the cannabinoid class.[26] This has not been studied in living organisms for CBC specifically, and clinical significance for human reproduction is unknown. safety citation needed
Immune effects
Historical data showed CBC inhibition of immune cell response at concentrations far above those achievable at anticipated therapeutic doses.[27] This is a class effect shared with other cannabinoids and unlikely to be clinically relevant.
Sedation potentiation
CBC potentiates sedation caused by barbiturates and other CNS depressants in mice through a direct pharmacological mechanism, not through metabolic interference.[7] This effect is likely related to CBC's GABA_A positive allosteric modulation. safety citation needed
Psychological risks
CBC does not produce psychoactive or intoxicating effects. It does not generate THC-like responses in trained animals at doses up to 30 mg/kg[24] and produces no cannabimimetic effects in drug discrimination assays.[6] No psychiatric adverse events, psychotomimetic effects, or cognitive impairment have been reported in any study.
CBC's GABA_A modulation raises a theoretical concern regarding sedation or cognitive blunting at high doses, analogous to other GABAergic agents. This has not been investigated.
Tolerance and dependence
No published studies on CBC tolerance, cross-tolerance, physical dependence, or withdrawal exist. This absence is consistent with CBC's negligible CB1 activity — CB1 receptor downregulation being the primary driver of cannabinoid tolerance.
CBC did not alter the interoceptive effects of THC in trained animals[24] and showed no cannabimimetic properties,[6] suggesting minimal abuse potential. No reinforcing properties, self-administration behavior, or conditioned place preference data have been published.
Drug Interactions
CBC is metabolized by multiple liver enzymes,[28] making it vulnerable to interactions from drugs that inhibit or accelerate those enzymes. Strong enzyme inhibitors (e.g., ketoconazole for CYP3A4, fluvoxamine for CYP1A2) could slow CBC clearance and raise its plasma levels. Strong inducers (e.g., rifampin) could accelerate its breakdown.
CBC does not significantly inhibit liver metabolic enzymes,[7] making it less likely than CBD to cause dangerous elevations of co-administered medication levels.
CBC + CBD co-administration in rats increased mutual plasma levels without altering time to peak,[18] consistent with competitive metabolism at shared enzymes. This interaction has not been confirmed in humans. safety citation needed
CBC potentiated CNS depressant-induced sedation in mice through a pharmacodynamic mechanism.[7] Given its GABA_A activity,[2] additive sedation with alcohol, benzodiazepines, barbiturates, and opioids is plausible. safety citation needed
CBC synergized with β-caryophyllene in cancer cell models[22] and achieved therapeutic effects at subtherapeutic doses only in combination with CBD, CBDV, and CBG.[21][23] These entourage interactions mean CBC's effects in full-spectrum cannabis products may differ substantially from isolated CBC.
Contraindications
5 knownNo substance-specific contraindication data exist for CBC. The following are inferred from mechanism of action and class effects:
Absolute (inferred):
- Cannabinoid hypersensitivity: Individuals with known allergic reactions to cannabis-derived compounds should avoid CBC.
Relative (inferred):
- Concurrent CNS depressant use: CBC's pharmacodynamic potentiation of sedatives[7] and GABA_A activity[2] suggest additive sedation risk with benzodiazepines, barbiturates, opioids, and alcohol. safety citation needed
- Drugs metabolized by shared liver enzymes: Competitive substrate interactions may alter levels of both CBC and co-administered drugs.[28]
- Pregnancy and lactation: Antigonadal effects observed across the cannabinoid class.[26] No reproductive studies specific to CBC exist.
- Complex seizure disorders: While CBC demonstrated anti-seizure effects via GABA_A modulation, no human dosing or safety data exist. Interaction with existing anti-epileptic medications is unpredictable.
All contraindications are inferred from preclinical evidence. No human clinical data support or refute any specific contraindication.
Harm Reduction[edit]
Forms & Identification
CBC products are sold primarily as isolate oils, tinctures, and capsules in jurisdictions where hemp-derived cannabinoids are legal. Because CBC is a viscous oil rather than a crystalline powder, visual identification of purity is impractical. The primary concern is Δ⁹-THC contamination above legal thresholds — third-party certificates of analysis (COAs) with full cannabinoid profiles are the most reliable verification tool.
CBC does not cross-react with standard THC urine immunoassays, but THC contamination in poorly tested products could trigger a positive drug screen. Products lacking batch-specific COAs or sourced from unverified manufacturers carry higher contamination risk.
Guidelines
- Obtain a certificate of analysis from an independent laboratory confirming cannabinoid profile and absence of THC above legal thresholds
- Start with low doses — no human dose-response data exist for isolated CBC, and individual responses are uncharacterized
- Avoid combining CBC with alcohol, benzodiazepines, barbiturates, or opioids until the sedation interaction is personally understood
- Store CBC products in cool, dark conditions to prevent degradation to cannabicyclol (CBL)
- Inform healthcare providers of CBC use, particularly if taking medications metabolized by common liver enzymes
Set & Setting
CBC does not produce psychoactive effects, so set and setting considerations are minimal compared to intoxicating cannabinoids. The primary situational concern is sedation potentiation: anyone taking CBC alongside CNS depressants — including alcohol — should be in a safe, stationary environment and avoid driving or operating machinery until the interaction is personally understood.
Aftercare & integration. CBC does not produce psychoactive experiences requiring psychological integration. Aftercare considerations relate primarily to physical monitoring.
- If sedation occurred from CBC combined with other substances, allow full recovery before resuming normal activities or driving
- Note any unusual responses for future dosing decisions — individual reactions to CBC are poorly characterized in the absence of human clinical data
- If using CBC for a specific health concern, maintain a log of doses and responses to inform discussions with a healthcare provider
Recovery & Support
CBC has no documented abuse liability, and no withdrawal has been described. Compulsive use patterns are not expected given its non-intoxicating profile. Individuals concerned about their use of any cannabis-derived product — including CBC as part of a broader cannabinoid regimen — can contact SAMHSA's National Helpline (1-800-662-4357) for confidential support and referral.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
CBC is non-intoxicating with no established acute toxicity at anticipated doses. Emergency situations involving CBC are most likely to arise from interaction with co-administered substances rather than CBC itself.
Recognizing an emergency:
- Excessive sedation, slurred speech, or difficulty breathing when CBC is combined with CNS depressants (alcohol, benzodiazepines, opioids)
- Allergic reaction: hives, swelling of face or throat, difficulty breathing
Immediate steps:
- Stop all substance administration
- If the person is excessively sedated or unresponsive, place them in the recovery position (on their side, airway clear)
- Call emergency services if breathing is slow, labored, or absent
- Do not induce vomiting
What to tell the dispatcher: Provide the substance name (cannabichromene / CBC), approximate amount taken, time of ingestion, any co-administered substances, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from legal consequences when seeking help.
Legal Status[edit]
CBC is not specifically scheduled under any major international drug control treaty. It is absent from the United Nations Single Convention on Narcotic Drugs (1961) and the Convention on Psychotropic Substances (1971). Its non-psychoactive, non-intoxicating profile has not triggered scheduling by any national drug control authority identified in the research literature.
In the United States, hemp-derived CBC is federally legal under the Agriculture Improvement Act of 2018 (2018 Farm Bill), provided the source plant material contains less than 0.3% Δ⁹-THC by dry weight.[29] CBC is not listed as a controlled substance by the Drug Enforcement Administration (DEA) and does not fall under Federal Analogue Act provisions due to its non-psychoactive nature.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not scheduled (federally legal if hemp-derived) | Legal under 2018 Farm Bill when source contains less than 0.3% Δ⁹-THC; not DEA-scheduled; FDA has not approved or restricted[29] |
| United Kingdom | Not controlled | Legal when derived from industrial hemp; finished products must contain no more than 1 mg of any controlled cannabinoid; not listed under Misuse of Drugs Act 1971 |
| European Union | Not controlled | Not classified as a controlled substance under EU law; individual member states may impose novel food regulations for CBC marketed as food supplements |
| Canada | Not specifically scheduled | CBC derived from licensed hemp cultivars is generally permitted under Canada's cannabis regulatory framework citation needed |
| Australia | Not specifically scheduled | Status under TGA regulatory framework not confirmed from primary regulatory sources citation needed |
| International (UN) | Not scheduled | Not listed in any UN drug control convention |
CBC products are commercially marketed in the United States and other jurisdictions where hemp-derived cannabinoids are legal. Product purity — particularly absence of Δ⁹-THC contamination above legal thresholds — is a regulatory compliance consideration. CBC does not produce cross-reactivity with standard THC urine drug screens due to its distinct metabolite profile.
Frequently asked questions
What is Cannabichromene?
Cannabichromene is a non-psychoactive phytocannabinoid of the chromene subclass, first isolated from cannabis in 1966. It acts primarily through TRPA1 agonism and GABAA positive allosteric modulation, with negligible CB1 receptor affinity.
How long does Cannabichromene last?
Total duration by route of administration — Oral: 4 – 8 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for Cannabichromene?
Psychedex publishes a dosage table for Cannabichromene on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with Cannabichromene?
The highest-severity documented interactions for Cannabichromene: GHB, Baclofen (Dangerous), GHB, GBL (Dangerous), Ibogaine (Dangerous), Ketamine, DXM, PCP (Dangerous), Local anesthetics (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is Cannabichromene addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for Cannabichromene: tolerance builds none. See the article's dependence and safety sections for recorded dependence data.
experience reports
No experience reports yet. Be the first to contribute.
First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abcdDe Petrocellis L, Ligresti A, Moriello AS, et al. (2011) Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes — British Journal of Pharmacology doi:10.1111/j.1476-5381.2010.01166.x
- [2]
- [3] ^abcQueiroz CM, de Oliveira Koren L, da Silva CRP, Ribeiro S, Silva SRB (2025) Chemical diversity, receptor binding affinity, and pharmacology of phytocannabinoids: Insights into neuronal mechanisms. — Progress in Brain Research doi:10.1016/bs.pbr.2025.07.006
- [4]
- [5] ^abGaoni Y, Mechoulam R (1966) Cannabichromene, a new active principle in hashish — Chemical Communications (London) doi:10.1039/c19660000020
- [6] ^abcTurner CE, Elsohly MA (1981) Biological activity of cannabichromene, its homologs and isomers — Journal of Clinical Pharmacology doi:10.1002/j.1552-4604.1981.tb02555.x
references
- [1]
- [2]
- [3] ^abGaoni Y, Mechoulam R (1966) Cannabichromene, a new active principle in hashish — Chemical Communications (London) doi:10.1039/c19660000020
- [4] ^abcTurner CE, Elsohly MA (1981) Biological activity of cannabichromene, its homologs and isomers — Journal of Clinical Pharmacology doi:10.1002/j.1552-4604.1981.tb02555.x
- [5] ^abQueiroz CM, de Oliveira Koren L, da Silva CRP, Ribeiro S, Silva SRB (2025) Chemical diversity, receptor binding affinity, and pharmacology of phytocannabinoids: Insights into neuronal mechanisms. — Progress in Brain Research doi:10.1016/bs.pbr.2025.07.006
- [6]