generation run 2026-05-12
60 min completedmodel pipeline-v5plan not recordedrun/0c3ee751…Selection
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28 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | cannabigerol | 1 | 1 | Primary chemical identity data for CBG |
| 2 | PubMed | cannabigerol safety toxicity adverse effects | 3 | 3 | Safety and toxicity data for CBG including in vivo chronic exposure |
| 3 | PubMed | cannabigerol pharmacology receptor binding | 15 | 5 | Selected articles directly addressing CBG receptor pharmacology, binding affinity data, and TRP channel activity |
| 4 | ClinicalTrials.gov | cannabigerol CBG | 14 | 10 | Selected trials specifically focused on CBG or with significant CBG arms |
| 5 | OpenAlex | cannabigerol CBG pharmacology | 10 | 3 | Selected landmark papers with substantial CBG pharmacology data |
| 6 | PubMed | cannabigerol CB1 CB2 receptor binding affinity Ki | 2 | 2 | Direct Ki measurement data for CBG at cannabinoid receptors |
| 7 | PubMed | cannabigerol neuroprotection neuroinflammation | 10 | 5 | Key neuroprotection and neuroinflammation studies with CBG |
| 8 | PubMed | cannabigerol antibacterial antimicrobial MRSA | 7 | 5 | Key papers on CBG antibacterial mechanism and potency |
| 9 | PubMed | cannabigerol human study acute effects anxiety cognition | 1 | 1 | Only published human RCT for CBG; critical for subjective effects and safety |
| 10 | PubMed | cannabigerol glaucoma intraocular pressure | 1 | 1 | Only published study on CBG and glaucoma; establishes IOP-lowering mechanism |
| 11 | WebSearch | cannabigerol CBG discovery history isolation 1964 Gaoni Mechoulam | 10 | 2 | Confirms 1964 discovery by Gaoni and Mechoulam; precursor biosynthetic role |
| 12 | WebSearch | cannabigerol CBG legal status scheduling United States UK EU Canada Australia | 10 | 3 | Comprehensive legal status information for major jurisdictions |
| 13 | PubMed | cannabigerol pain analgesic anti-nociceptive | 1 | 1 | Comprehensive in vitro/in vivo pharmacology including anti-nociceptive effects |
| 14 | PubMed | cannabigerol antidepressant mice forced swim | 1 | 1 | Key negative finding: CBG lacks antidepressant activity in FST contrary to popular claims |
| 15 | PubMed | cannabigerol antioxidant oxidative stress | 6 | 4 | CBG antioxidant mechanisms and skin applications including first clinical skin study |
| 16 | PubMed | cannabigerol VCE-003 quinone neuroprotection PPAR | 6 | 6 | CBG derivative VCE-003.2 neuroprotection via PPAR-gamma in PD, ALS, Huntington models |
| 17 | PubMed | cannabigerol safety toxicity adverse effects | 3 | 3 | Primary safety/toxicity data for CBG |
| 18 | PubMed | cannabigerol appetite feeding | 1 | 1 | Key study on CBG appetite-stimulating properties as non-psychoactive alternative |
| 19 | ClinicalTrials.gov | cannabigerol CBG | 14 | 9 | Selected CBG-specific or CBG-primary trials |
| 20 | PubMed | cannabigerol colitis inflammatory bowel disease | 8 | 7 | All directly address CBG anti-inflammatory effects in IBD/colitis models |
| 21 | PubMed | PMID 39003387 Cuttler 2024 CBG anxiety RCT | 1 | 1 | Only published human RCT for CBG effects; critical evidence |
| 22 | WebSearch | cannabigerol CBG legal status scheduling US UK EU | 10 | 2 | Legal status across major jurisdictions |
| 23 | PubMed | Valdeolivas cannabigerol Huntington disease neuroprotective 2015 | 1 | 1 | Key neuroprotection paper for CBG in Huntington's disease |
| 24 | PubMed | cannabigerol pharmacokinetics bioavailability | 1 | 1 | Only PK study for CBG; note this is equine, not human |
| 25 | OpenAlex | cannabigerol antitumor anticancer antiproliferative cancer cells | 5 | 1 | Only review-level evidence for CBG anticancer; no CBG-alone primary study found |
| 26 | PubChem | CID 5315659 cannabigerol | 1 | 1 | Chemical identity verification for seed data correction |
| 27 | PubMed | cannabigerol Borrelli colitis colon 2013 | 1 | 1 | Landmark IBD/colitis paper for CBG, highly relevant |
| 28 | Multiple sources | CBG pharmacological targets comparison | 8 | 7 | Cross-reference to build comprehensive pharmacological target profile |
81 claims by section — every cited sentence, checked against its source
pharmacology16 · 9 ok
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Direct radioligand competitive binding using [³H]CP-55,940 confirmed measurable but substantially lower affinity than THC or CBN at both human CB1 and CB2 receptorssupported
Ki values for CBG at human CB1 and CB2 receptors measured. j.ntt.2014.09.003
Claim in pharmacology — inconclusiveinconclusiveworking →
CBG also exhibits activity at CB1/CB2 heteromeric receptor complexes.supported
Mode of action of cannabigerol (CBG)...at CB1, CB2 and CB1/CB2 heteromer receptors. j.phrs.2020.104940
In the landmark study by De Petrocellis and colleagues, CBG stimulated and subsequently desensitized human TRPV1 and rat TRPV2 channels, while acting as one of the most potent TRPM8 antagonists among cannabinoids testedsupported
CBD, CBG, CBGV and THCV stimulated and desensitized human TRPV1. CBG-BDS and THCV-BDS were the most potent rat TRPM8 antagonists. All non-acid cannabinoids, except CBC and CBN, potently activated and desensitized rat TRPV2. j.1476-5381.2010.01166.x
Subsequent work identified TRPA1 as the principal TRP family target for CBG in rheumatoid arthritis synovial fibroblasts, where TRPA1 activation mediates intracellular calcium increases, drug uptake facilitation, and downstream anti-inflammatory effects.supported
CBG binds TRPA1 as main target among TRP family; increases intracellular calcium in TNF-stimulated rheumatoid synovial fibroblasts; reduces RASF cell viability, IL-6 and IL-8 production. ijms24010855
Molecular docking and molecular dynamics simulations predict that CBG binds at the orthosteric site of the human 5-HT₁A receptor and functions as a partial agonistsupported
Molecular docking and MD simulations: CBG (neutral) prefers binding at orthosteric site of 5-HT1A receptor as potential partial agonist. j.jmgm.2025.109186
Claim in pharmacology — not_supportednot supportedworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
PPAR-γ: Quinone derivatives of CBG (VCE-003, VCE-003.2) are established PPAR-γ agonists with demonstrated neuroprotective activity. Direct PPAR-γ activity of CBG itself is less well-characterized, though modest upregulation of PPAR-γ gene expression was observed in Huntington's disease mice after CBG treatment.supported
Improved BDNF, IGF-1, PPAR-gamma gene expression. s13311-014-0304-z
PPAR-γ: Quinone derivatives of CBG (VCE-003, VCE-003.2) are established PPAR-γ agonists with demonstrated neuroprotective activity. Direct PPAR-γ activity of CBG itself is less well-characterized, though modest upregulation of PPAR-γ gene expression was observed in Huntington's disease mice after CBG treatment.supported
Improved BDNF, IGF-1, PPAR-gamma gene expression. s13311-014-0304-z
GPR55: Identified as a likely non-canonical cannabinoid target in meta-analysis, but no CBG-specific binding or functional data have been published.supported
Non-psychotropic phytocannabinoids primarily act through non-canonical targets such as GPR55, TRPV1, and TRPM8. bs.pbr.2025.07.006
Claim in pharmacology — inconclusiveinconclusiveworking →
Endocannabinoid system modulation: In human keratinocytes, CBG increases CB1/CB2 receptor expression, stimulates TRPV1, and modulates FAAH/MAGL activity.supported
CBG modulates gene and protein expression of ECS elements in human keratinocytes; all compounds increased CB1/2 binding, TRPV1 channel stimulation and FAAH and MAGL catalytic activity in skin cells. ijms23105430
Claim in pharmacology — inconclusiveinconclusiveworking →
clinical-evidence14 · 5 ok
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Farha and colleagues subsequently established the mechanism: CBG targets the cytoplasmic membrane of Gram-positive bacteria, disrupting membrane integrity, with MIC values of 0.5–8 µg/mL and first in vivo efficacy in a murine MRSA modelsupported
Mechanism of action is through targeting the cytoplasmic membrane of Gram-positive bacteria. In vivo efficacy demonstrated in a murine systemic MRSA infection model. acsinfecdis.9b00419
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
The Cuttler human RCT found reduced anxiety and stress — not depression — at 20 mg oral.supported
20mg hemp-derived CBG tincture significantly reduced anxiety and stress, enhanced verbal memory relative to placebo. s41598-024-66879-0
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Borrelli and colleagues published the landmark study in murine DNBS-induced colitis: CBG reduced colon weight/length ratio, myeloperoxidase activity, and iNOS expression while increasing SOD activity and normalizing IL-1β, IL-10, and IFN-γ levels, with effects modulated by CB2 receptor activationsupported
CBG reduced colon weight/colon length ratio, myeloperoxidase activity, iNOS expression, increased SOD activity, normalized IL-1b, IL-10, IFN-gamma. Reduced NO production in macrophages (CB2-modulated). j.bcp.2013.01.017
CBG also inhibits MRSA biofilm formation, eradicates mature biofilms, and kills persister cellssupported
CBG inhibits MRSA biofilm formation, eradicates mature biofilms, rapidly eliminates MRSA persister cells. pharmaceutics15071889
In Huntington's disease, CBG was extremely active in 3-nitropropionate-lesioned mice (motor improvement, striatal neuroprotection, anti-microgliosis, antioxidant defense improvement) with more modest recovery in R6/2 transgenic mice; BDNF, IGF-1, and PPAR-γ gene expression were partially normalized, and mutant huntingtin aggregation was reducedsupported
CBG extremely active neuroprotectant in 3NP-lesioned mice (improved motor deficits, preserved striatal neurons, attenuated microgliosis, improved antioxidant defenses). In R6/2 mice: modest but significant recovery in rotarod performance. Reduced mutant huntingtin aggregation. s13311-014-0304-z
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
safety12 · 8 ok
Claim in safety — inconclusiveinconclusiveworking →
The single human RCT (20 mg oral, n = 34) reported no adverse eventssupported
No evidence of subjective drug effects or motor/cognitive impairment. s41598-024-66879-0
Claim in safety — inconclusiveinconclusiveworking →
Orally administered CBG at 0.66 and 1.33 mg/kg/day produced hepatotoxic manifestations including regressive histopathological changes, disrupted white cell counts, altered ALT activity, and changes in creatinine and ionized calciumsupported
CBG (0.66-1.33 mg/kg/day) produced hepatotoxic manifestations, oxidative stress, disrupted white cell count, altered ALT activity, creatinine and ionized calcium. j.tox.2023.153460
The geranyl (dimethyloctadienyl) moiety was proposed as the structural determinant responsible for the redox disruption and hepatic effects.supported
The dimethyloctadienyl structural pattern in CBG is likely responsible for redox disruption and hepatic effects. j.tox.2023.153460
A seemingly contradictory finding emerges from human iPSC-derived hepatocyte data: transcriptomic analysis ranked CBG as the least potent hepatotoxic agent among tested cannabinoids, with the potency order CBN > CBD > CBC > CBG based on benchmark concentration analysissupported
Transcriptomic analysis of hemp cannabinoids in human iPSC-derived hepatocytes. CBG has lowest transcriptional activity among cannabinoids tested (CBN > CBD > CBC > CBG). j.tox.2024.153885
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Cytotoxic properties were also noted in murine mesencephalic primary cell cultures and N18TG2 neuroblastoma cells, suggesting a non-receptor-mediated cytotoxic mechanism at high concentrations.supported
Cytotoxic properties found for CBN, CBDV and CBG in neural cell cultures despite receptor affinity data. Effects not linked to receptor binding affinity, pointing to non-receptor mechanism. j.ntt.2014.09.003
The Cuttler RCT found that 20 mg oral CBG produced no subjective drug effects, intoxication, or altered consciousnesssupported
No evidence of subjective drug effects or motor/cognitive impairment. s41598-024-66879-0
The human RCT (n = 34, single-dose design) found no evidence of reinforcing or psychoactive effects at 20 mg oral, suggesting low abuse potential based on pharmacological profile, but formal abuse liability assessment has not been conducted.supported
No evidence of subjective drug effects or motor/cognitive impairment. s41598-024-66879-0
Hepatic impairment: The 90-day rat study demonstrating hepatotoxic signals at 0.66 mg/kg/day warrants caution in individuals with pre-existing liver disease, elevated transaminases, or concurrent hepatotoxic medication use until human safety data are available.supported
90-day rat study: CBG (0.66-1.33 mg/kg/day) produced hepatotoxic manifestations, oxidative stress, disrupted white cell count, altered ALT activity, creatinine and ionized calcium. j.tox.2023.153460
summary9 · 6 ok
Cannabigerol (CBG) is a non-psychotomimetic phytocannabinoid of the terpenophenol structural class, distinguished from THC by its markedly lower affinity at CB1 and CB2 receptors (10–100× lower Ki) and correspondingly absent intoxicating effectssupported
CBG, CBC, and CBD exhibited 10-100 times lower affinities than THC at CB1/CB2. bs.pbr.2025.07.006
Claim in summary — inconclusiveinconclusiveworking →
As of 2026, fourteen clinical trials are registered on ClinicalTrials.gov, with published results from one completed randomized controlled trial examining acute anxiolytic and cognitive effects at 20 mg oral.partially supported
Double-blind, placebo-controlled crossover trial (n=34). 20mg hemp-derived CBG tincture significantly reduced anxiety and stress, enhanced verbal memory relative to placebo. s41598-024-66879-0
Claim in summary — inconclusiveinconclusiveworking →
Its primary pharmacological actions include TRPV1 and TRPV2 agonism with subsequent desensitization, potent TRPM8 antagonism, TRPA1 activation, anandamide reuptake inhibition, and predicted 5-HT₁A partial agonismsupported
Molecular docking and MD simulations: CBG (neutral) prefers binding at orthosteric site of 5-HT1A receptor as potential partial agonist. j.jmgm.2025.109186
Claim in summary — inconclusiveinconclusiveworking →
In the single published human trial (n = 34, double-blind crossover), 20 mg oral CBG significantly reduced anxiety and stress while enhancing verbal memory, with no detectable subjective drug effects, intoxication, or motor impairmentsupported
Double-blind, placebo-controlled crossover trial (n=34). 20mg hemp-derived CBG tincture significantly reduced anxiety and stress, enhanced verbal memory relative to placebo. No evidence of subjective drug effects or motor/cognitive impairment. s41598-024-66879-0
A 90-day rat study identified hepatotoxic signals at doses as low as 0.66 mg/kg/day, though human iPSC-derived hepatocyte data ranked CBG as the least hepatotoxic among tested cannabinoidssupported
90-day rat study: CBG (0.66-1.33 mg/kg/day) produced hepatotoxic manifestations, oxidative stress, disrupted white cell count, altered ALT activity, creatinine and ionized calcium. j.tox.2023.153460
A 90-day rat study identified hepatotoxic signals at doses as low as 0.66 mg/kg/day, though human iPSC-derived hepatocyte data ranked CBG as the least hepatotoxic among tested cannabinoidssupported
CBG has lowest transcriptional activity among cannabinoids tested (CBN > CBD > CBC > CBG). j.tox.2024.153885
receptor-pharmacology8 · 5 ok
TRPV1: Agonist with subsequent desensitization (human receptor)supported
CBD, CBG, CBGV and THCV stimulated and desensitized human TRPV1. j.1476-5381.2010.01166.x
TRPM8: Potent antagonist — CBG-BDS (botanical drug substance) ranked among the most potent TRPM8 antagonists of all cannabinoids testedsupported
CBG-BDS and THCV-BDS were the most potent rat TRPM8 antagonists. j.1476-5381.2010.01166.x
Meta-analysis of published radioligand binding data confirms CBG binds CB1 and CB2 receptors with 10–100× lower affinity than THCsupported
CBG, CBC, and CBD exhibited 10-100 times lower affinities than THC at CB1/CB2. bs.pbr.2025.07.006
Direct competitive binding using [³H]CP-55,940 in human receptor preparations established measurable but weak displacement at both receptor subtypessupported
Ki values for CBG at human CB1 and CB2 receptors measured. j.ntt.2014.09.003
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Computational modeling predicts CBG as a partial agonist at the 5-HT₁A receptor orthosteric sitesupported
CBG (neutral) prefers binding at orthosteric site of 5-HT1A receptor as potential partial agonist. j.jmgm.2025.109186
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
comparative-pharmacology7 · 3 ok
Hepatotoxicity: In human iPSC-derived hepatocytes, CBG was the least potent hepatotoxic agent among tested cannabinoids (potency order: CBN > CBD > CBC > CBG). In rats, however, CBG at 0.66 mg/kg/day produced hepatotoxic histopathological changes and elevated oxidative stress, whereas CBD showed antioxidant effects at comparable doses.supported
CBG has lowest transcriptional activity among cannabinoids tested (CBN > CBD > CBC > CBG). j.tox.2024.153885
Hepatotoxicity: In human iPSC-derived hepatocytes, CBG was the least potent hepatotoxic agent among tested cannabinoids (potency order: CBN > CBD > CBC > CBG). In rats, however, CBG at 0.66 mg/kg/day produced hepatotoxic histopathological changes and elevated oxidative stress, whereas CBD showed antioxidant effects at comparable doses.partially supported
90-day rat study: CBG (0.66-1.33 mg/kg/day) produced hepatotoxic manifestations, oxidative stress, disrupted white cell count, altered ALT activity, creatinine and ionized calcium. j.tox.2023.153460
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
CBG binds CB1 with 10–100× lower affinity and insufficient efficacy to generate psychoactive effects at any tested dosesupported
CBG, CBC, and CBD exhibited 10-100 times lower affinities than THC at CB1/CB2. bs.pbr.2025.07.006
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
neuroscience5 · 2 ok
The Cuttler human RCT found enhanced verbal memory following 20 mg oral CBG versus placebosupported
enhanced verbal memory relative to placebo. s41598-024-66879-0
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
In experimental autoimmune encephalomyelitis (a multiple sclerosis model), CBG attenuated microglial NO and TNF-α production and restored neuronal losssupported
CBG attenuated microglial nitric oxide production in BV2 and primary glial cells; reduced TNF-α and iNOS expression; attenuated clinical scores in EAE mouse model of MS and restored neuronal loss in lumbar sections. biom13020376
Claim in neuroscience — inconclusiveinconclusiveworking →
history4 · 0 ok
chemistry3 · 2 ok
CBG's retention of the linear geranyl chain defines its distinct pharmacological profile — the open terpene moiety modulates lipid membrane interactions relevant to both antibacterial activity and hepatic redox effects.supported
Activity tolerant to nature of prenyl moiety, suggesting prenyl serves as lipid affinity modulator for the olivetol antibacterial pharmacophore. np8002673
CBG's retention of the linear geranyl chain defines its distinct pharmacological profile — the open terpene moiety modulates lipid membrane interactions relevant to both antibacterial activity and hepatic redox effects.supported
The dimethyloctadienyl structural pattern in CBG is likely responsible for redox disruption and hepatic effects. j.tox.2023.153460
Claim in chemistry — inconclusiveinconclusiveworking →
pharmacokinetic-detail2 · 0 ok
effects-overview1 · 1 ok
At the single dose tested in humans (20 mg oral), the compound reduces anxiety and stress while preserving or mildly enhancing cognitive function — effects that are sub-perceptual in the sense that subjects cannot reliably distinguish active drug from placebo on standard subjective-effects measuressupported
significantly reduced anxiety and stress, enhanced verbal memory relative to placebo. No evidence of subjective drug effects or motor/cognitive impairment. s41598-024-66879-0