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From the plant

CBGCannabigerol

The neutral form of CBGA, the acid from which THCA, CBDA and CBCA derive; a very potent α2-adrenergic agonist in vitro.

Hemp exemption
Level of detail

C₂₁H₃₂O₂

CAS 25654-31-3

Family
PhytocannabinoidPrincipal
Origin
Decarboxylation
First described
1964
Molar mass
316.48 g/mol

Updated on

In plain terms

CBG is the neutral form of CBGA, the acid the plant then turns into THCA, CBDA and CBCA. It does not make you 'high': in a controlled trial, 20 mg produced no felt intoxication. In the laboratory it acts mainly on α2-adrenergic receptors.

Receptors and activity

Target network

5-HT1AAntagonistno measured value
  • Activates
  • Blocks or inhibits

The lower the cited value, the closer the target sits to CBG: one ring per factor of 100. A target with no measured value stays on the edge.

Where these targets live

Where each target has been found in humans, according to the cited studies. The map shows the target, not an effect of CBG.

Brain, side view
Body, front view
Blood

5-HT1A5-HT1A found in 6 regions of the body

  1. HippocampusdenseVery dense in the hippocampal CA1 field1
  2. BrainstemdenseHigh density in the raphe nuclei1
  3. CortexdenseDense in cortical layers I and II1
  4. AmygdaladenseHigh density in some amygdala nuclei1
  5. HypothalamuspresentIntermediate density, posterior hypothalamus1
  6. Spinal cordpresentPresent in the cervical spinal cord1

Map sources

  1. Pazos A et al. Serotonin receptors in the human brain--III. Autoradiographic mapping of serotonin-1 receptors. Neuroscience, 1987 (new tab)

Cited values

  1. α2-adrenergicAgonistEC50 = 0.2 nM · mouse95 out of 100

    Cascio et al. 2010, Br J Pharmacol: α2 and 5-HT1A (new tab) · [35S]GTPγS, MF1 mouse whole-brain membranes; 72.8 nM on isolated vas deferens

  2. 5-HT1AAntagonistno measured value cited
  3. CB1AntagonistKi = 381 nM · mouse40 out of 100

    Cascio et al. 2010, Br J Pharmacol: α2 and 5-HT1A (new tab) · [3H]CP55940 displacement, mouse brain membranes; competitive antagonism at 10 µM

  4. CB2Partial agonistKi = 2.6 µM · human26 out of 100

    Navarro et al. 2018, Front Pharmacol: CB1/CB2 (new tab) · [3H]CP55940 displacement, CHO-hCB2 (Cascio 2010); 152 nM in homogeneous assay, partial agonism (Navarro 2018)

  5. TRPM8AntagonistIC50 = 160 nM · rat47 out of 100

    De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab) · inhibition of the icilin response, Ca2+ (fluorescence), HEK-293 rat TRPM8

  6. TRPV1AgonistEC50 = 1.3 µM · human31 out of 100

    De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab) · intracellular Ca2+ (fluorescence), HEK-293 hTRPV1

  7. TRPV2AgonistEC50 = 1.7 µM · rat29 out of 100

    De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab) · intracellular Ca2+ (fluorescence), HEK-293 rat TRPV2

  8. TRPA1AgonistEC50 = 700 nM · rat36 out of 100

    De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab) · intracellular Ca2+ (fluorescence), HEK-293 rat TRPA1

Bar length follows the measured value (Ki, Kd, EC50 or IC50), on one scale shared by every entry, from 100 µM to 0.1 nM. A target with no cited value has no bar.

Measured effects

Psychoactive intensityIntensity of the felt effect (« feel drug effect », « high ») on a validated scale, compared with placebo.

Not distinct from placeboModerate confidence

up to 200 mg orally · Wolinsky 2026

Measured anxietyAnxiety measured on a validated scale, often during a laboratory stressor; it can fall or rise depending on the dose.

Varies with doseLow confidence

20–100 mg orally · Cuttler 2024, Wolinsky 2026

Cognitive impairmentLower performance on attention, memory or speed tests, compared with placebo.

Effect reported, size not measured · decreaseVery low confidence

20 mg orally · Cuttler 2024

SleepinessReported sleepiness or measured sedation, compared with placebo.

Not distinct from placeboVery low confidence

up to 20 mg orally · Cuttler 2024

Reported hungerReported hunger or measured food intake, compared with placebo.

Effect reported, size not measured · increaseVery low confidence

200 mg orally · Wolinsky 2026

Levels computed from placebo-controlled human trials: difference from placebo on 100, at the dose and route stated. Read the method

Pharmacology

CBG was isolated from cannabis resin in 1964 by Gaoni and Mechoulam, who confirmed its structure by synthesis (Radwan et al., 2021). Its acid form, CBGA, is the first cannabinoid of the biosynthetic pathway: a membrane prenyltransferase assembles it from olivetolic acid and geranyl pyrophosphate (Luo et al., 2019), then the THCA, CBDA and CBCA synthases convert it; so it is CBGA, not CBG, that precedes the other cannabinoids. Hanuš et al. (2016) and Maioli et al. (2022) count CBG among the four major cannabinoids; Walsh et al. (2021) class it as minor. In vitro, Cascio et al. (2010) described it as a very potent agonist at α2-adrenergic receptors (EC50 0.2 nM in mouse brain membranes; 72.8 nM in the isolated mouse vas deferens) and a moderately potent 5-HT1A antagonist (apparent KB 51.9 nM). Its affinity is lower for CB1 (Ki 381 nM, mouse brain) and variable for CB2 (Ki 2.6 µM according to Cascio et al., 2010; 152 nM in a homogeneous assay according to Navarro et al., 2018), where it acts as a partial agonist. It activates human TRPV1 (EC50 1.3 µM), rat TRPV2 (1.72 µM) and TRPA1 (0.7 µM), and blocks rat TRPM8 (IC50 0.16 µM; De Petrocellis et al., 2011). In humans, a single placebo-controlled crossover trial (34 adults; Cuttler et al., 2024) tested 20 mg of CBG: self-reported anxiety decreased relative to placebo, with no subjective intoxication; it is a single, industry-funded trial. No CBG-based medicine has been approved by the FDA.

Key sources.

History

Source
Cannabis: neutral form arising from decarboxylation of CBGA (heat, light, ageing)

Biosynthetic pathway

Non-enzymatic: decarboxylation of CBGA. CBGA, assembled by a membrane prenyltransferase from olivetolic acid and geranyl pyrophosphate (Luo et al., 2019), is the substrate of the THCA, CBDA and CBCA synthases; neutral CBG is not itself a precursor.

Classification

Family, origin and source verification

Family

Phytocannabinoid › Principal

Presence in the plant

Neutral form: decarboxylation of a plant acid

Chemistry

Type CBG · C5 side chain · neutral form

Verification

Every fact on this entry was checked against its primary sources on 20 October 2026.

Wikipedia (English)

Cannabigerol (new tab)

Article paired by the molecule's structure (InChIKey), revision read on 19 October 2026. Read as a second opinion, never cited as a source.

References

  1. Radwan et al. 2021, Molecules: isolation of CBG in 1964 (new tab)PMID 34066753
  2. Luo et al. 2019, Nature: CBGA biosynthesis (new tab)PMID 30814733
  3. Cascio et al. 2010, Br J Pharmacol: α2 and 5-HT1A (new tab)PMID 20002104
  4. Navarro et al. 2018, Front Pharmacol: CB1/CB2 (new tab)PMID 29977202
  5. De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab)PMID 21175579
  6. Cuttler et al. 2024, Sci Rep: 20 mg controlled trial (new tab)PMID 39003387

Identifiers

Names

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

Identifiers

Formula
C₂₁H₃₂O₂
CAS
25654-31-3
PubChem CID
5315659(new tab)
ChEBI
69477(new tab)
InChIKey
QXACEHWTBCFNSA-SFQUDFHCSA-N
SMILES
CCCCCC1=CC(=C(C(=C1)O)C/C=C(\C)/CCC=C(C)C)O

Machine-readable entry (JSON)

LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.

In the Journal