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Plate 283 of 545Verified

Cannabigerol

Also known asCannabigerol (CBG) · CBG · geranylolivetol · Cannabigerol [WHO-DD]

2-[(2E)-3,7-dimethylocta-2,6-dienyl]-5-pentylbenzene-1,3-diol

PubChem CID
5315659
Measurements
17
InChIKey
QXACEHWTBCFNSA-SFQUDFHCSA-N

I · Summary

What is known

Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.

What it is

  • Cannabigerol is a member of the class of resorcinols that is resorcinol which is substituted by a (2E)-3,7-dimethylocta-2,6-dien-1-yl group at position 2 and by a pentyl group at position 5. It is a natural product found in Cannabis sativa and Helichrysum species. It has a role as an antioxidant, an antibacterial agent, an appetite enhancer, a neuroprotective agent, a cannabinoid receptor agonist, an anti-inflammatory agent and a plant metabolite. It is a member of resorcinols and a phytocannabinoid.
  • A natural product found in Cannabis sativa and Helichrysum species.
  • cannabigerol has been reported in Helichrysum umbraculigerum and Cannabis sativa with data available.
  • 1,3-Benzenediol, 2-(3,7-dimethyl-2,6-octadienyl)-5-pentyl-, (E)- has been reported in Helichrysum umbraculigerum and Cannabis sativa with data available.

History, discovery and cultural use

— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when Cannabigerol was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.

Histories of this field

Scholarship on psychedelics generally, not on Cannabigerol specifically. Whether any of these treats this compound is a question for the book, not for this page.

  • Mescaline: A Global History of the First Psychedelic

    Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.

    Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.

  • Expanding Mindscapes: A Global History of Psychedelicsopen access

    Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.

    Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.

  • Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers

    Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.

    Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.

  • Psychonauts: Drugs and the Making of the Modern Mind

    The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.

    Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.

  • Ancient Psychoactive Substances

    Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.

    Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.

  • History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders

    A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.

    Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.

    Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.

  • Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions

    Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.

    Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.

Institutional archives

  • Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
  • Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.

The rest of this dossier

  • Affinity — 17 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for Cannabigerol. An absent record is an absence of study, not evidence of safety.
  • Legal — no DEA record is held here — which is not a finding that this compound is uncontrolled.
  • Systems — where this compound’s targets are transcribed, by brain region and tissue.

Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Cannabigerol is the history note, which says so on its face and carries a reference for every claim in it.

II · Identity

Structure and descriptors

Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.

2D structural depiction of Cannabigerol
Depiction served by PubChem for CID 5315659. Not redrawn here, so the picture and the identity come from the same record.
Formula
C21H32O2R
Molecular weight
316.49g/molR
Exact mass
316.2402DaR
cLogP
6.07R
TPSA
40.5ŲR
H-bond donors
2R
H-bond acceptors
2R
Rotatable bonds
9R
Aromatic rings
1R
Heavy atoms
23R
Fraction sp³
0.524R
Formal charge
0R

Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.

III · Behavior

Behavioral summary

Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.

Classification

MeSH indexes no pharmacological class for this compound.

Duration of acute subjective effects

—

No controlled human trial reporting a duration for this compound is cited here. The archive holds no other record of one either. A duration is not inferred from a chemical relative.

Plasma elimination half-life

How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.

No half-life is published for this compound in the sources this site reads.

Primary pharmacological drivers

ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.

Nothing about this compound’s pharmacology is published with a citation in the sources this site reads. The measured binding data below is what the archive can show.

IV · Clinical

Clinical description

Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.

No diagnostic chapter is shown for this compound. Either PubChem records no MeSH pharmacological class for it, or the class it records is not one of the substance classes ICD-11 gives a chapter to. Inferring a chapter from the compound’s name or its binding profile would be a diagnosis this archive is in no position to make.

How much has been written about each domain

The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.

None of the 0 records this archive holds for this compound uses a term from any of the clinical domains. That is a statement about the literature recorded here, not about the compound.

V · Systems

Systems physiology

Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.

022 nTPM

Square-root ramp · shared scale across both plates

Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.

Brain regions

Regions where this compound's measured targets are transcribed. Linked from the plate above.

  1. cerebral cortex

    18.6 nTPM
    • CB1CNR16.4 pX18.6
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX5.8
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.4
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.1
  2. cerebellum

    18.3 nTPM
    • CB1CNR16.4 pX18.3
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX12.1
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.1
  3. pituitary gland

    17.3 nTPM
    • CB1CNR16.4 pX17.3
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX5.0
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX1.8
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.3
  4. basal ganglia

    15.1 nTPM
    • CB1CNR16.4 pX15.1
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX5.6
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.3
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.1
  5. amygdala

    13.3 nTPM
    • CB1CNR16.4 pX13.3
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX5.8
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.1
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.1
  6. hippocampal formation

    13.2 nTPM
    • CB1CNR16.4 pX13.2
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX6.3
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.2
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.2
  7. retina

    12.0 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX12.0
    • CB1CNR16.4 pX1.1
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.2
    • CB2CNR27.0 pX0.1
  8. hypothalamus

    9.0 nTPM
    • CB1CNR16.4 pX9.0
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX5.6
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.1
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.1
  9. midbrain

    6.6 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX6.6
    • CB1CNR16.4 pX2.1
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.2
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.1
  10. spinal cord

    6.4 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX6.4
    • CB1CNR16.4 pX1.7
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.2
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.2

Peripheral & autonomic

Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.

  1. liver

    21.8 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX21.8
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX7.7
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.5
    • CB2CNR27.0 pX0.1
    • CB1CNR16.4 pX0.1
  2. salivary gland

    18.1 nTPM
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX18.1
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX3.7
    • CB1CNR16.4 pX1.8
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.2
    • CB2CNR27.0 pX0.1
  3. kidney

    13.0 nTPM
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX13.0
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX7.2
    • CB1CNR16.4 pX0.6
  4. colon

    10.0 nTPM
    • CB1CNR16.4 pX10.0
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX5.1
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.8
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.4
    • CB2CNR27.0 pX0.2
  5. spleen

    8.4 nTPM
    • CB2CNR27.0 pX8.4
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX3.9
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX2.5
    • CB1CNR16.4 pX1.4
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.2
  6. small intestine

    8.1 nTPM
    • CB1CNR16.4 pX8.1
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX7.7
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX4.9
    • CB2CNR27.0 pX3.1
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.3
  7. duodenum

    6.9 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX6.9
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX1.9
    • CB1CNR16.4 pX0.6
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.6
    • CB2CNR27.0 pX0.1
  8. heart muscle

    6.8 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX6.8
    • CB1CNR16.4 pX0.8
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.7
  9. pancreas

    6.7 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX6.7
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX3.9
    • CB1CNR16.4 pX1.2
  10. skeletal muscle

    6.0 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX6.0
    • CB1CNR16.4 pX1.8
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX1.7
    • CB2CNR27.0 pX1.5
  11. stomach 1

    5.2 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX5.2
    • CB1CNR16.4 pX3.4
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.9
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.6
    • CB2CNR27.0 pX0.4
  12. urinary bladder

    4.6 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX4.6
    • CB1CNR16.4 pX3.4
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX1.6
    • CB2CNR27.0 pX0.3
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.2
  13. adrenal gland

    4.6 nTPM
    • CB1CNR16.4 pX4.6
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX4.4
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.7
  14. thyroid gland

    4.1 nTPM
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX4.1
    • CB1CNR16.4 pX3.9
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.8
    • CB2CNR27.0 pX0.2
  15. lung

    2.8 nTPM
    • CB1CNR16.4 pX2.8
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX2.8
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX1.9
    • CB2CNR27.0 pX0.1
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.1
  16. smooth muscle

    2.3 nTPM
    • CB1CNR16.4 pX2.3
    • Transient receptor potential cation channel subfamily V member 1TRPV15.9 pX1.5
    • Transient receptor potential cation channel subfamily V member 4TRPV45.9 pX0.7
    • Transient receptor potential cation channel subfamily V member 3TRPV36.0 pX0.1

Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.

3 of this compound’s targets could not be resolved to a gene and are absent from both columns: Transient receptor potential cation channel subfamily A member 1, Transient receptor potential cation channel subfamily M member 8, Transient receptor potential cation channel subfamily V member 2.

Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.

VI · Profile

Affinity rosette

The strongest measurement at each of 8 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

CB2 — Ki 7.00 pXCB1 — Ki 6.40 pXTransient receptor potential cation channel subfamily M member 8 — IC50 6.80 pXTransient receptor potential cation channel subfamily A member 1 — EC50 6.15 pXTransient receptor potential cation channel subfamily V member 3 — EC50 6.00 pXTransient receptor potential cation channel subfamily V member 1 — EC50 5.89 pXTransient receptor potential cation channel subfamily V member 4 — IC50 5.89 pXTransient receptor potential cation channel subfamily V member 2 — IC50 5.82 pXCB2CB1Transient recept…Transient recept…Transient recept…Transient recept…Transient recept…Transient recept…579
Fig. Radius is pX = −log₁₀(value in M), that is 9 − log₁₀(value in nM), computed from the normalized measurement. Hatched wedges are equilibrium binding constants (Ki, Kd); dashed outlines are functional readouts (IC₅₀, EC₅₀, AC₅₀, potency), which answer a different question and are not pooled with them. Rings mark whole pX units from 5 to 10, labeled every second ring in the gutter at the top. Where a target carries several measurements, the strongest is drawn.

VII · Toxicology

Toxicological profile

What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.

Measured in this archive

Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.

No hERG, cytochrome, cytotoxicity or transport measurement exists for Cannabigerol in this archive.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Cannabigerol. They index compounds that have been studied for decades, so most of this archive has no entry. An absent record is an absence of study, not evidence of safety.

Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.

VIII · Evidence

Every measurement

One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.

Equilibrium binding constants 3

Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.

TargetClassTypeValue (nM)pXOrganismAssay
CB2Cannabinoid receptorsKi1007.00Homo sapiensCHEMBL6083333
CB1Cannabinoid receptorsKi4006.40Homo sapiensCHEMBL6083332
UncheckedUnclassifiedKi1,1005.96— organism not recordedCHEMBL5096676

Functional readouts 14

IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.

TargetClassTypeValue (nM)pXOrganismAssay
Transient receptor potential cation channel subfamily M member 8Ion channelsIC501606.80Homo sapiensCHEMBL5096642
Transient receptor potential cation channel subfamily M member 8Ion channelsIC501606.80Homo sapiensCHEMBL5253448
Transient receptor potential cation channel subfamily A member 1Ion channelsEC507006.15Homo sapiensCHEMBL5096636
Transient receptor potential cation channel subfamily V member 3Ion channelsEC501,0006.00Homo sapiensCHEMBL5096629
Transient receptor potential cation channel subfamily V member 1Ion channelsEC501,3005.89Homo sapiensCHEMBL5096623
Transient receptor potential cation channel subfamily V member 4Ion channelsIC501,3005.89Homo sapiensCHEMBL5096634
Transient receptor potential cation channel subfamily V member 2Ion channelsIC501,5005.82Homo sapiensCHEMBL5096628
Transient receptor potential cation channel subfamily V member 2Ion channelsEC501,7005.77Homo sapiensCHEMBL5096626
Transient receptor potential cation channel subfamily V member 1Ion channelsIC502,6005.59Homo sapiensCHEMBL5096625
Transient receptor potential cation channel subfamily V member 4Ion channelsEC505,1005.29Homo sapiensCHEMBL5096632
Inhibin alpha chainUnclassifiedIC505,2005.28Homo sapiensCHEMBL5096678
UncheckedUnclassifiedIC508,8005.06— organism not recordedCHEMBL6080257
Transient receptor potential cation channel subfamily A member 1Ion channelsIC5013,0004.89Homo sapiensCHEMBL5096638
Transient receptor potential cation channel subfamily V member 3Ion channelsIC5066,0004.18Homo sapiensCHEMBL5096631
P
PubChem
C
ChEMBL
R
Computed here with RDKit
D
Derived here from the stored measurement

IX · Trials

Registered clinical trials

Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.

9T

Registered studies

5T

Open or ongoing

9T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Early phase 11
  • Phase 13
  • Phase 22
  • Not applicable4

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed4
  • Recruiting2
  • Active, not recruiting2
  • Not yet recruiting1

Every matched study

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT07577999Not yet recruiting · Early phase 1

    The Effects of Cannabis on Post Operative Recovery After Radical Cystectomy

    Enrollment
    20Testimated
    Started
    2027-07
    Sponsor
    Stanford University

    Conditions Non-metastatic Bladder Cancer

    Matched “Cannabigerol” in the study’s intervention “Cannabigerol”

  • NCT07592390Recruiting · Phase 1 / Phase 2

    Cannabigerol Oil for Adolescents With ADHD (CAN-ADHD)

    Enrollment
    60Testimated
    Started
    2026-05-01
    Sponsor
    Universidade do Sul de Santa Catarina

    Conditions Attention-Deficit/Hyperactivity Disorder (ADHD)

    Matched “CBG” in the study’s intervention “Experimental: Full-spectrum CBG oil 30 mg/mL”

  • NCT06115603Recruiting · Phase 2

    The Effects of Cannabigerol on Attention-Deficit/Hyperactivity Disorder

    Enrollment
    76Testimated
    Started
    2024-12-14
    Sponsor
    University of Arkansas, Fayetteville

    Conditions Attention-Deficit/Hyperactivity Disorder

    Matched “Cannabigerol” in the study’s intervention “Cannabigerol”

  • NCT06638996Completed · Not applicable

    Acute Psychological and Physiological Effects of Cannabigerol

    Enrollment
    100Tactual
    Started
    2024-10-28
    Sponsor
    Washington State University

    Conditions No Disease or Condition is Being Studied

    Matched “CBG” in the study’s intervention “CBG Intervention”

  • NCT06513507Active, not recruiting · Not applicable

    A Clinical Study to Assess the Efficacy of Cannabigerol in Patients with Active Rheumatoid Arthritis.

    Enrollment
    12Tactual
    Started
    2024-06-03
    Sponsor
    Raphael Pharma

    Conditions Rheumatoid Arthritis · Inflammatory Disease

    Matched “Cannabigerol (CBG)” in the study’s intervention “Cannabigerol (CBG)”

  • NCT04859296Active, not recruiting · Phase 1

    AnalgeSiC and appEtite-stimulating Effects of caNnabigerol and THC (ASCENT)

    Enrollment
    20Testimated
    Started
    2023-02-15
    Sponsor
    University of California, Los Angeles

    Conditions Pain · Appetite Loss · Abuse, Drug

    Matched “CBG” in the study’s intervention “Low CBG”

  • NCT05743985Completed · Not applicable

    Efficacy and Safety of Hemp-derived, Full Spectrum Cannabigerol (CBG) in Adults

    Enrollment
    69Tactual
    Started
    2022-08-01
    Sponsor
    Formula30A LLC

    Conditions Health, Subjective · Inflammatory Response · Adverse Effect · Side Effect

    Matched “Cannabigerol” in the study’s intervention “Cannabigerol”

  • NCT05257044Completed · Phase 1

    Acute Effects of Cannabigerol

    Enrollment
    38Tactual
    Started
    2022-03-24
    Sponsor
    Washington State University

    Conditions Focus: To Examine Acute Effects of CBG on Anxiety, Stress, and Cognition

    Matched “Cannabigerol” in the study’s intervention “Cannabigerol”

  • NCT05088018Completed · Not applicable

    Swallowable Cannabigerol Tablets for Sleep Quality In Veterans (Veterans Exploring Cannabigerol for Sleep)

    Enrollment
    68Tactual
    Started
    2021-10-11
    Sponsor
    Chris Emerson

    Conditions Sleep

    Matched “Cannabigerol” in the study’s intervention “Cannabigerol”

Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.

Searched as Cannabigerol · Cannabigerol (CBG) · geranylolivetol. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Cannabigerol worked.

XI · Literature

Sources behind this dossier

The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.

No reference is recorded against any value for this compound. Its measurements come from ChEMBL assay records that carry an assay identifier but no publication, so there is no paper to cite here — an absence in the upstream record, not a judgment about the evidence. The assay identifiers in Every measurement resolve to the records the values were read from.