Semi-synthetic cannabinoid

CBGQCannabigerol quinone

Oxidised form of CBG (VCE-003), a PPARγ activator studied in preclinical neuroinflammation.

Harm-reduction warning

No characterised human dose: animal / in vitro data only. Effect profile, safety margin and acute toxicity are not documented in human clinical practice. Extremely potent compound: severe effects, seizures and deaths reported in the literature.

Receptors and activity

PPARγAgonist60 out of 100
active l'activité transcriptionnelle de PPARγ (Granja et coll., 2012) ; aucune constante reprise ici

Bar length shows the relative strength of the interaction, as an indication.

Subjective signature

Calm: 6 out of 100; Relaxation of body and mind; reduced mental noise without marked drowsiness.
Clarity: 4 out of 100; Sustained attention and clear thinking; functional lucidity, not euphoria.
High: 2 out of 100; Euphoria and sensory intensity; altered perception of time and space.
Appetite: 4 out of 100; Stimulation of hunger and of taste appreciation (the “munchies” effect).
Sleep: 4 out of 100; Sedative effect: aids sleep onset and the continuity of deep sleep.

Editorial estimate, not clinical.

Pharmacology

Cannabigerol quinone (CBGQ, VCE-003) is the oxidation product of the resorcinol core of CBG. It was reported in 2012 by Granja and colleagues, who were studying the effect of this oxidation on affinities for CB1, CB2 and PPARγ. The compound activates PPARγ transcriptional activity, protects neurons from excitotoxicity and curbs the release of pro-inflammatory mediators by microglia. In the Theiler's virus mouse model of multiple sclerosis, it improved motor performance and reduced microglial reactivity. The quinone then served as the basis for derivatives, including VCE-003.2, evaluated in experimental models of Huntington's disease, Parkinson's disease and amyotrophic lateral sclerosis. No human data exist for VCE-003 itself.

Key sources.

History

Source: An oxidation product of cannabigerol: the resorcinol core of CBG is converted into a hydroxyquinone. It was studied under the code VCE-003 by Spanish and Italian teams and served as the starting point for non-thiophilic derivatives such as VCE-003.2.

Route of preparation (chemical process)

Route of preparation: cannabigerol quinone derives from CBG by oxidation of the resorcinol core. This is a chemical transformation of the oxidation class, not an enzymatic pathway described in the plant.

Legal framework

European Union: No control measure of its own at European Union level. The molecule appears in no schedule of the 1961 Convention on Narcotic Drugs or of the 1971 Convention on Psychotropic Substances. It holds no marketing authorisation and no novel food authorisation under Regulation (EU) 2015/2283: it circulates only as a chemical or reference standard intended for research.
France: Unscheduled substance. Cannabigerol quinone is named in no annex of the order of 22 February 1990 and falls under no generic clause: it is not a tetrahydrocannabinol and it lacks the benzo[c]chromene nucleus targeted by the ANSM decision of 22 May 2024. This absence of scheduling is not an authorisation: the molecule is neither an authorised medicine nor an ingredient permitted in food or cosmetics.

Sources: EUR-Lex, UNODC, CND, ANSM, IUPHAR/BPS, ChEBI, EUDA. Our method.

References

Structured data

SMILES: CCCCCC1=CC(=O)C(=C(C1=O)O)C/C=C(\C)/CCC=C(C)C
InChIKey: WQJZGZRGXVDCJN-FOWTUZBSSA-N

Machine-readable entry (JSON)

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