generation run 2026-05-07
65 min completedmodel pipeline-v5plan not recordedrun/c5aa14d6…Selection
Verification
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- seen / partial
- working
The model's own caveats
- sparse_evidence
- sparse_evidence
Reproduce
- inputs
- 40 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
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- none — agent transcripts are persisted from 2026-09 onward
23 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | cannabinol CB1 CB2 receptor binding affinity Ki | 4 | 4 | Specific binding affinity data for CBN |
| 2 | PubMed | cannabinol pharmacokinetics metabolism CYP enzyme | 3 | 3 | CYP metabolism data for CBN |
| 3 | PubMed | cannabinol CBN pharmacology receptor binding | 12 | 5 | Core pharmacology papers with receptor binding data |
| 4 | ClinicalTrials.gov | cannabinol CBN | 10 | 3 | Directly relevant clinical trials of CBN |
| 5 | OpenAlex | cannabinol CBN pharmacology cannabinoid receptor | 10 | 5 | Landmark papers on cannabinoid pharmacology that include significant CBN data |
| 6 | PubChem | cannabinol | 1 | 1 | Primary chemical identity data for CBN verified |
| 7 | PubMed | cannabinol antibacterial antimicrobial MRSA | 4 | 3 | Antibacterial/antimicrobial data for CBN |
| 8 | PubMed | cannabinol CBN sedation sleep effects | 1 | 1 | Key systematic review directly addressing CBN sleep claims |
| 9 | WebSearch | cannabinol first isolation 1896 Wood Spivey Easterfield cannabis history | 10 | 0 | Historical discovery narrative not in PubMed |
| 10 | WebSearch | cannabinol CBN DEA Schedule I legal status United States 2026 | 10 | 0 | Critical legal status data not in academic databases |
| 11 | OpenAlex | cannabinol first isolation cannabis history Wood Spivey Easterfield | 8 | 2 | Key history and neuroprotection papers for CBN |
| 12 | PubMed | cannabinol immunomodulation cytokine T cell | 3 | 3 | CBN immunomodulatory mechanism papers |
| 13 | PubMed | cannabinol intraocular pressure glaucoma | 5 | 2 | Direct CBN glaucoma/IOP data |
| 14 | PubMed | cannabinol anticancer tumor apoptosis | 8 | 3 | CBN-specific anticancer data |
| 15 | PubMed | cannabinol CB1 partial agonist in vivo functional | 3 | 0 | No CBN-specific partial agonist functional papers found |
| 16 | PubMed | cannabinol SOD1 G93A transgenic mice symptom onset survival Weydt 2005 | 1 | 1 | Key CBN neuroprotection study in ALS mouse model |
| 17 | Multiple databases | CBN Ki CB1 CB2 receptor binding values | 4 | 0 | Cross-reference of binding affinity data across studies |
| 18 | WebSearch | cannabinol ALS neuroprotection Weydt 2005 motor neuron disease onset delayed | 10 | 0 | Historical ALS neuroprotection data contextualization |
| 19 | Crossref via verify_doi | 10.1080/14660820510030149 | 1 | 1 | DOI verification for Weydt ALS paper |
| 20 | PubMed | CUPID cannabinol sleep insomnia protocol | 1 | 1 | First published RCT protocol for CBN sleep study |
| 21 | WebSearch | cannabinol CBN psychoactive effects humans 1970s Hollister Perez-Reyes studies | 10 | 0 | Historical human studies - critical for psychoactivity section |
| 22 | PubMed | cannabinol pharmacokinetics plasma administration | 2 | 2 | Available pharmacokinetic data for CBN |
| 23 | WebSearch/WebFetch | INM-755 cannabinol epidermolysis bullosa Phase 2 trial results | 10 | 0 | Only available CBN dermatology clinical trial results |
76 claims by section — every cited sentence, checked against its source
pharmacology19 · 15 ok
Conversely, CBN inhibits AP-1 activity through suppression of c-fos/c-jun and inhibition of ERK MAP kinase, providing an immunosuppressive counterpartsupported
CBN inhibited binding to AP-1-containing sites from the IL-2 promoter, decreased nuclear expression of c-fos and c-jun, and inhibited ERK MAP kinases. pmid:10670588
At CB2, Showalter et al. (1996) reported Ki = 96.3 ± 14 nM against [³H]CP-55,940 at cloned human CB2, compared to Δ⁹-THC Ki = 36.4 ± 10 nM — placing CBN within roughly 3-fold of THC at this receptorsupported
The affinity of cannabinol for CB2 receptors (Ki = 96.3 +/- 14 nM) was confirmed to be in approximately the same range as that of delta 9-THC (Ki = 36.4 +/- 10 nM). pmid:8819477
At CB1, published Ki values range widely (approximately 100–500 nM depending on assay conditions), with a meta-analysis of 211 cannabinoid binding studies noting that methodological sensitivity analyses did not strongly validate some CBN CB1 Ki values in the literaturesupported
Pooled data from 211 studies measured ligand binding affinities at human or rat cannabinoid receptors CB1 and CB2. Sensitivity analyses did not support the numerical validity of cannabidiol, cannabinol... pmid:17641667
A 2025 systematic review confirmed that both THC and CBN show significantly higher CB1 affinity than CBD, CBG, and CBC.supported
A systematic review and meta-analysis of binding affinities (Ki) for CB1, CB2 confirmed that THC and CBN showed high affinities for CB1 and CB2, while CBG, CBC, and CBD exhibited 10-100 times lower affinities. bs.pbr.2025.07.006
Claim in pharmacology — inconclusiveinconclusiveworking →
CBN exhibits functional context-dependence at CB2: while binding assays show partial agonism, Walter et al. (2003) demonstrated that CBN acts as a CB2 receptor antagonist in the context of 2-AG-induced microglial cell migration, blocking migration triggered by pathological neuronal stimulationsupported
Cannabinol and cannabidiol, two nonpsychotropic ingredients present in the marijuana plant, prevent the 2-AG-induced cell migration by antagonizing the CB2 and abnormal-cannabidiol-sensitive receptors, respectively. jneurosci.23-04-01398.2003
TRPA1: Potent rat TRPA1 agonist and desensitizer, contributing to analgesic and anti-inflammatory potentialsupported
CBC, CBD and CBN were potent rat TRPA1 agonists and desensitizers. j.1476-5381.2010.01166.x
TRPV2: Weak agonist with EC₅₀ = 77.7 µM — substantially weaker than CBD at this target; physiological significance at typical cannabinoid concentrations is unclearsupported
All non-acid cannabinoids, except CBC and CBN, potently activated and desensitized rat TRPV2. CBN had EC50=77.7 µM at TRPV2. j.1476-5381.2010.01166.x
Claim in pharmacology — inconclusiveinconclusiveworking →
Pregnane X receptor (PXR/NR1I2): CBN is a human PXR agonist. At 10 µM, CBN activated hPXR 17-fold, rPXR 4-fold, and mPXR 3-fold in reporter gene assays. The minimum effective concentration for hPXR activation was 0.3 µM — within the pharmacological range — carrying significant drug interaction implications via CYP3A4 inductionsupported
CBN (10 µM) activated human PXR by 17-fold, rat PXR by 4-fold, and mouse PXR by 3-fold. Minimum effective concentration for hPXR activation by CBN was 0.3 µM. j.bbrc.2026.153250
GABA_A receptor: Anti-seizure effects observed in hemp extract studies with involvement of GABA_A receptor allosteric modulationsupported
CBN showed significant anti-seizure effects. Investigation of allosteric modulation on the GABAA receptor. j.fmre.2023.05.023
GABA_A receptor: Anti-seizure effects observed in hemp extract studies with involvement of GABA_A receptor allosteric modulationsupported
CBN was involved in the anti-seizure process. GABAA receptor seems to be the primary anti-epileptic target of full-spectrum hemp extract. j.fmre.2024.11.002
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
In vivo, CBN (50 mg/kg i.p.) significantly attenuated Th2 cytokines (IL-4, IL-5, IL-13) and reduced IgE levels and mucus overproduction in an ovalbumin-induced allergic airway mouse model.supported
CBN (50 mg/kg ip) significantly attenuated elevation of IL-2, IL-4, IL-5, IL-13 mRNA in lungs after ovalbumin challenge. Serum IgE elevation and mucus overproduction also attenuated. pmid:12668119
In one analytical study, CBN was not detected in plasma after oral administration of small doses of cannabis extract (detection limit approximately 1.1 ng/mL by GC-MS), suggesting extremely poor oral bioavailability when present only as a trace constituent.supported
CBN was not detected in plasma after oral administration of 10mg THC + 5.4mg CBD cannabis extract. GC-MS analytical method developed with CBN detection limit of 1.1 ng/mL. pmid:16356335
General cannabinoid pharmacokinetic principles apply: high lipophilicity drives extensive tissue distribution, high first-pass hepatic metabolism limits oral bioavailability, and elimination half-lives are prolonged by redistribution from adipose tissuesupported
High first-pass metabolism affects oral cannabinoids. Cannabinoids distributed particularly to fatty tissues. pmid:16237477
Havlasek et al. (2023) identified CYP1A2, CYP2C9, CYP2C19, and CYP2D6 as hepatic biotransformation pathways, with CBN being the most rapidly biotransformed among the phytocannabinoids testedsupported
CBN was most rapidly metabolized of the phytocannabinoids tested. CBN primarily metabolized by CYPs 1A2, 2C9, 2C19 and 2D6. j.taap.2023.116654
A systematic review also noted CYP2C9 and CYP3A4 involvementsupported
CYP-450 enzymes as potential significant contributors to the primary metabolism of CBN: CYPs 2C9, 3A4. 03602532.2013.849268
safety15 · 9 ok
Claim in safety — inconclusiveinconclusiveworking →
This cytotoxicity did not correlate with receptor binding affinity, suggesting a non-receptor-mediated mechanism at suprapharmacological concentrationssupported
Ki values of phytocannabinoids to human CB1 and CB2 receptors were detected... Cytotoxic properties of CBN, CBDV and CBG were found in N18TG2 neuroblastoma cells. j.ntt.2014.09.003
Claim in safety — inconclusiveinconclusiveworking →
Heal et al. (2024) assessed non-psychoactive cannabinoids broadly and concluded they do not produce intoxicating, cognitive, or rewarding properties in humanssupported
Non-psychoactive cannabinoids do not produce intoxicating, cognitive or rewarding properties in humans. fpsyt.2024.1322434
Claim in safety — inconclusiveinconclusiveworking →
Heal et al. (2024) assessed non-psychoactive cannabinoids and found no intoxicating or rewarding properties, consistent with very low dependence liabilitysupported
Non-psychoactive cannabinoids do not produce intoxicating, cognitive or rewarding properties in humans. fpsyt.2024.1322434
PXR/CYP3A4 induction: CBN activates the pregnane X receptor at concentrations as low as 0.3 µM, inducing CYP3A4 expressionsupported
Minimum effective concentration for hPXR activation by CBN was 0.3 µM. CBN is a human PXR agonist with preferential activation of hPXR over rodent PXR. j.bbrc.2026.153250
CYP2C9 competition: As a CYP2C9 substrate, CBN may competitively inhibit the metabolism of other CYP2C9 substrates, potentially increasing plasma levels of warfarin, phenytoin, and some NSAIDs.supported
CYP-450 enzymes as potential significant contributors to the primary metabolism of CBN: CYPs 2C9, 3A4. 03602532.2013.849268
CYP2C9 competition: As a CYP2C9 substrate, CBN may competitively inhibit the metabolism of other CYP2C9 substrates, potentially increasing plasma levels of warfarin, phenytoin, and some NSAIDs.supported
CBN primarily metabolized by CYPs 1A2, 2C9, 2C19 and 2D6. j.taap.2023.116654
CBN inhibits the ABCG2 (BCRP) multidrug efflux transporter, which could increase the bioavailability of anticancer drugs that are ABCG2 substrates (e.g., topotecan, mitoxantrone)supported
Cannabinoids including CBN, CBD, and THC interact with the related multidrug transporter ABCG2. CBN inhibits ABCG2 activity. pmid:17906686
Claim in safety — not_supportednot supportedworking →
Claim in safety — inconclusiveinconclusiveworking →
Competitive inhibition at CYP2C9 poses a relative contraindication for concurrent warfarin use, where even modest changes in metabolism can produce clinically significant alterations in INR.supported
CYP-450 enzymes as potential significant contributors to the primary metabolism of CBN: CYPs 2C9, 3A4. 03602532.2013.849268
Claim in safety — inconclusiveinconclusiveworking →
GC-MS confirmation testing differentiates CBN from THC metabolites (detection limit approximately 1.1 ng/mL for CBN in plasma).supported
GC-MS analytical method developed with CBN detection limit of 1.1 ng/mL. pmid:16356335
summary10 · 9 ok
It acts as a partial agonist at both CB1 and CB2 receptors with approximately 1/4 to 1/10 the potency of THC at CB1, and possesses a broader multi-target pharmacological profile encompassing TRP channels, the pregnane X receptor, and GABA_A allosteric modulationpartially supported
This study sought to evaluate select minor cannabinoids and terpenes for Δ9-THC-like psychoactivity in mouse Δ9-THC drug discrimination and determine their binding affinities at CB1 and CB2 receptors. j.pnpbp.2024.110984
Claim in summary — inconclusiveinconclusiveworking →
Structure elucidation by Adams and Todd in the early 1940s enabled the synthetic cannabinoid era, culminating in Mechoulam and Gaoni's identification of Δ⁹-THC in 1964supported
Research into the pharmacology of individual cannabinoids that began in the 1940s, several decades after the presence of a cannabinoid was first detected in cannabis, is concisely reviewed. pmid:16402100
Contemporary research interest centers on CBN's potential therapeutic applications in dermatology, neuroprotection, antimicrobial activity, and sleep — though for the last of these, a systematic review of all eligible human studies found insufficient evidence to support the widely marketed sleep-promoting claims.supported
Consequently, there is insufficient published evidence to support sleep-related claims. can.2021.0006
At the CB2 receptor, CBN binds with Ki = 96.3 ± 14 nM — within roughly 3-fold of THCsupported
The affinity of cannabinol for CB2 receptors (Ki = 96.3 +/- 14 nM) was confirmed to be in approximately the same range as that of delta 9-THC (Ki = 36.4 +/- 10 nM). pmid:8819477
CB1 affinity values range widely across studies (approximately 100–500 nM) due to methodological variability in radioligand binding assayssupported
Sensitivity analyses did not support the numerical validity of cannabidiol, cannabinol, 2-arachidonoyl glycerol and all ligands at RnCB2. pmid:17641667
Beyond cannabinoid receptors, CBN activates TRPA1 (contributing to analgesic potential), acts as a potent human pregnane X receptor agonist with a minimum effective concentration of 0.3 µM (carrying significant CYP3A4 induction and drug interaction implications), and demonstrates GABA_A receptor allosteric modulation linked to anti-seizure effects in preclinical models.supported
CBN (10 µM) activated human PXR by 17-fold, rat PXR by 4-fold, and mouse PXR by 3-fold. Minimum effective concentration for hPXR activation by CBN was 0.3 µM. j.bbrc.2026.153250
Beyond cannabinoid receptors, CBN activates TRPA1 (contributing to analgesic potential), acts as a potent human pregnane X receptor agonist with a minimum effective concentration of 0.3 µM (carrying significant CYP3A4 induction and drug interaction implications), and demonstrates GABA_A receptor allosteric modulation linked to anti-seizure effects in preclinical models.supported
CBN showed significant anti-seizure effects. Investigation of allosteric modulation on the GABAA receptor. j.fmre.2023.05.023
Preclinical safety data from subacute mouse exposure suggest an acceptable safety profile at therapeutic doses, and the largest human safety dataset — a Phase 2 topical trial in 19 epidermolysis bullosa patients — reported no serious drug-related adverse eventssupported
Physiological and behavioral effects of subacute exposure to therapeutic and low pharmacological levels of a water-soluble CBN nano-emulsion (CBNight) in male mice. s42238-022-00153-w
Dependence liability is considered very low based on the absence of intoxicating or rewarding properties at typical doses, though no direct self-administration or withdrawal characterization studies have been publishedsupported
Non-psychoactive cannabinoids do not produce intoxicating, cognitive or rewarding properties in humans. fpsyt.2024.1322434
clinical-evidence7 · 7 ok
Neuroprotection (ALS): Weydt et al. (2005) demonstrated that CBN (5 mg/kg/day subcutaneous) delayed disease onset by more than 2 weeks in SOD1(G93A) transgenic mice — an amyotrophic lateral sclerosis model. Survival was not affected. No human data exist.supported
CBN was delivered via subcutaneously implanted osmotic mini-pumps (5 mg/kg/day)... Treatment significantly delayed disease onset by more than two weeks while survival was not affected in SOD1 (G93A) mouse model of ALS. 14660820510030149
The CUPID study represents the first formal randomized controlled trial of CBN for insomnia.supported
Protocol for RCT testing CBN 30mg and 300mg vs placebo in insomnia disorder. bmjopen-2022-071148
Corroon (2021) identified a total of 8 eligible human studies across all endpoints and concluded the evidence base is insufficient to support either cannabis-like psychoactive effects or sleep-promoting effects.partially supported
Consequently, there is insufficient published evidence to support sleep-related claims. In addition, evidence demonstrating that CBN itself elicits cannabis-like effects in humans is mixed. can.2021.0006
Glaucoma (IOP reduction): Early data demonstrated CBN reduces intraocular pressure. Somvanshi et al. (2022) extended this with neuroprotective and IOP-lowering effects in glaucoma models.supported
Evaluates the role of cannabinol (CBN) on RGC protection, modulation of intraocular pressure (IOP), and effects on extracellular matrix proteins using in vitro and in vivo models of glaucoma. j.bbadis.2021.166325
Antimicrobial (MRSA): CBN demonstrates antibacterial activity against methicillin-resistant Staphylococcus aureus, with recent work confirming anti-biofilm activity.supported
All five major cannabinoids including cannabinol (5) showed potent activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance. np8002673
Anticancer: In vitro effects have been reported in acute myeloid leukemia cells (dose-dependent, p53 activation), ER+ breast cancer cells (most pronounced effects among minor cannabinoids tested), and MCF-7 breast cancer cells (cytoplasmic vacuolation in cannabinoid combinations). All anticancer data are from cell lines at concentrations (>5–40 µM) far above physiologically achievable plasma levels. No animal tumor model or clinical cancer data for CBN exist.supported
CBN inhibited cell growth and induced THP-1 (AML) cell apoptosis and cell cycle arrest in a dose- and time-dependent manner. Correlation between CBN doses >50 µM and p53 activation. molecules29245970
Anticancer: In vitro effects have been reported in acute myeloid leukemia cells (dose-dependent, p53 activation), ER+ breast cancer cells (most pronounced effects among minor cannabinoids tested), and MCF-7 breast cancer cells (cytoplasmic vacuolation in cannabinoid combinations). All anticancer data are from cell lines at concentrations (>5–40 µM) far above physiologically achievable plasma levels. No animal tumor model or clinical cancer data for CBN exist.supported
CBN caused the most pronounced anticancer effects in ER+ breast cancer models. j.bbalip.2025.159658
neuroscience6 · 4 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
CBN's CB2 antagonism in the context of microglial migration has neurological implicationssupported
Cannabinol and cannabidiol, two nonpsychotropic ingredients present in the marijuana plant, prevent the 2-AG-induced cell migration by antagonizing the CB2... Microglial cells express CB2 receptors at the leading edge of lamellipodia. jneurosci.23-04-01398.2003
CBN's anti-seizure effects in hemp extract studies implicate GABA_A receptor allosteric modulation — a mechanism distinct from CB1 partial agonismsupported
CBN showed significant anti-seizure effects. Investigation of allosteric modulation on the GABAA receptor. j.fmre.2023.05.023
CBN's anti-seizure effects in hemp extract studies implicate GABA_A receptor allosteric modulation — a mechanism distinct from CB1 partial agonismsupported
CBN was involved in the anti-seizure process. GABAA receptor seems to be the primary anti-epileptic target of full-spectrum hemp extract. j.fmre.2024.11.002
Does CBN's GABA_A modulation produce distinct EEG signatures (e.g., increased spindle density, altered slow-wave activity)? The CUPID trial includes sleep staging as a secondary endpoint and may address this.supported
Protocol for RCT testing CBN 30mg and 300mg vs placebo in insomnia disorder. Primary outcome: wake after sleep onset by polysomnography. bmjopen-2022-071148
receptor-pharmacology6 · 6 ok
CBN is a potent human pregnane X receptor (PXR/NR1I2) agonistsupported
CBN is a human PXR agonist with preferential activation of hPXR over rodent PXR. j.bbrc.2026.153250
McPartland et al. (2007) conducted sensitivity analyses across 211 cannabinoid binding studies and explicitly noted that some CBN Ki values in the literature should be interpreted with cautionsupported
Pooled data from 211 studies measured ligand binding affinities at human or rat cannabinoid receptors CB1 and CB2. Sensitivity analyses did not support the numerical validity of cannabidiol, cannabinol... pmid:17641667
A 2025 systematic meta-analysis confirmed that CBN shows high CB1 affinity — significantly higher than CBD, CBG, or CBC — but did not resolve the inter-study variability for CBN specifically.supported
THC and CBN showed high affinities for CB1 and CB2, while CBG, CBC, and CBD exhibited 10-100 times lower affinities. bs.pbr.2025.07.006
CBN blocked pathological neuronal stimulation-triggered microglial migration at concentrations consistent with its binding affinitysupported
Cannabinol and cannabidiol, two nonpsychotropic ingredients present in the marijuana plant, prevent the 2-AG-induced cell migration by antagonizing the CB2... receptors. jneurosci.23-04-01398.2003
CBN showed significant anti-seizure effects in hemp extract studies, with evidence pointing to GABA_A receptor allosteric modulation as a contributing mechanismsupported
CBN was involved in the anti-seizure process. GABAA receptor seems to be the primary anti-epileptic target of full-spectrum hemp extract. j.fmre.2024.11.002
CBN inhibits the ABCG2 (BCRP) multidrug efflux transporter, which is relevant in oncology settings where cancer drug resistance is mediated by ABCG2supported
CBN inhibits ABCG2 activity. pmid:17906686
history4 · 3 ok
The first formal randomized controlled trial specifically investigating CBN for insomnia — the CUPID study, testing 30 mg and 300 mg CBN versus placebo — has been protocolized but results remain unpublished as of 2026.supported
Protocol for RCT testing CBN 30mg and 300mg vs placebo in insomnia disorder. Primary outcome: wake after sleep onset by polysomnography. bmjopen-2022-071148
Claim in history — inconclusiveinconclusiveworking →
The complete structure was independently elucidated in the early 1940s by Roger Adams in the United States and by Alexander Todd (later a Nobel laureate) in the United Kingdomsupported
Contributions by Roger Adams and Alexander Todd. Includes structure elucidation of cannabinol. s12210-020-00956-0
Pharmacological research on CBN began in the 1940s with studies on individual cannabinoidssupported
Research into the pharmacology of individual cannabinoids that began in the 1940s, several decades after the presence of a cannabinoid was first detected in cannabis, is concisely reviewed. pmid:16402100
chemistry3 · 0 ok
pharmacokinetic-detail3 · 3 ok
Nadulski et al. (2005): CBN was not detected in plasma (LOD ~1.1 ng/mL by GC-MS) after oral administration of small doses of cannabis extract, despite being present in the administered extract. This suggests extremely poor oral bioavailability when CBN is present only as a trace component.supported
CBN was not detected in plasma after oral administration of 10mg THC + 5.4mg CBD cannabis extract. GC-MS analytical method developed with CBN detection limit of 1.1 ng/mL. pmid:16356335
In the absence of CBN-specific human PK data, general cannabinoid pharmacokinetic principles provide context:supported
Review focuses on THC pharmacokinetics but also includes known information for cannabinol and cannabidiol. pmid:16237477
Metabolism: CBN is metabolized by multiple hepatic CYP enzymes. Havlasek et al. (2023) identified CYP1A2, CYP2C9, CYP2C19, and CYP2D6 as biotransformation pathways, with CBN being the most rapidly biotransformed among the phytocannabinoids tested in their panel (which included CBD, CBG, CBC, and CBDV). A systematic review by Stout and Cimino (2014) additionally noted CYP2C9 and CYP3A4 involvement. The rapid biotransformation rate likely contributes to high first-pass metabolism.supported
CYP-450 enzymes as potential significant contributors to the primary metabolism of CBN: CYPs 2C9, 3A4. 03602532.2013.849268
botanical-overview2 · 0 ok
comparative-pharmacology1 · 0 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →