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Synthetic

Canbisol

A synthetic cannabinoid related to nabilone: active in animals, no human data.

FranceNarcotic: generic clauseInternationalUnscheduled
Level of detail

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.

C₂₄H₃₈O₃

CAS 56689-43-1

Family
Synthetic CB receptor agonistResearch ligand or medicine
Molar mass
374.60 g/mol

Updated on

In plain terms

Canbisol is a laboratory molecule made by chemical synthesis: it does not occur in hemp and no consumer product containing it has been found. It was studied in publications of 1980 and 1985 as a cousin of nabilone, a medicine derived from cannabis chemistry; no study in human beings has been found. The only experiments available are old and were carried out in animals, in which it proves more active than THC in some tests.

Receptors and activity

Target network

CB1AgonistNot measured for canbisol: agonist presumed from its cannabimimetic effects in vivo (Stark and Dews, 1980; Koe et al., 1985); the affinities of 100 pM (CB1) and 200 pM (CB2) often cited are those of 11-hydroxycannabinol-DMH (Rhee et al., 1997)
  • Activates

The lower the cited value, the closer the target sits to Canbisol: 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 Canbisol.

Brain, side view
Body, front view
Blood

CB1CB1 found in 7 regions of the body

  1. Basal gangliadenseMost dense in basal ganglia outflow nuclei1
  2. CerebellumdenseVery dense in the cerebellum1
  3. HippocampusdenseVery high concentrations in the hippocampus2
  4. AmygdaladenseHigh concentrations in the amygdala2
  5. CortexpresentPresent throughout the neocortex2
  6. Adipose tissuepresentExpressed in adipose tissue3
  7. GutpresentColonic epithelium, smooth muscle and plexus4

Map sources

  1. Herkenham M et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A, 1990 (new tab)
  2. Glass M et al. Cannabinoid receptors in the human brain: a detailed anatomical and quantitative autoradiographic study in the fetal, neonatal and adult human brain. Neuroscience, 1997 (new tab)
  3. Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
  4. Wright K et al. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology, 2005 (new tab)

Cited values

  1. CB1Agonistno measured value cited

    Not measured for canbisol: agonist presumed from its cannabimimetic effects in vivo (Stark and Dews, 1980; Koe et al., 1985); the affinities of 100 pM (CB1) and 200 pM (CB2) often cited are those of 11-hydroxycannabinol-DMH (Rhee et al., 1997)

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.

Pharmacology

Canbisol is a classical synthetic cannabinoid: the dibenzopyran skeleton of THC is fully hydrogenated on ring A, the methyl at position 9 is replaced by a hydroxyl and the pentyl chain by a 1,1-dimethylheptyl chain, a substitution that, in the cannabinol series studied by Rhee et al. (1997), makes the derivatives much more potent than their pentyl counterparts. Agonist action at CB1 is therefore presumed, and the in vivo observations point that way: in dogs, canbisol causes ataxia from 0.004 mg/kg intravenously, against 0.032 mg/kg for nabilone and 0.062 mg/kg for delta-9-THC; it slows intracranial self-stimulation and reduces food intake in rats; and, according to Koe et al. (1985), its potency for increasing [3H]flunitrazepam binding in vivo, correlated with analgesic efficacy, exceeds that of nabilone and of delta-9-THC. Stark and Dews nevertheless note that it resembles chlordiazepoxide in some tests and delta-9-THC in others. What is missing is essential: no affinity measurement, no functional assay and no human data concern canbisol itself, so that its efficacy at CB1 is not established and it is impossible to say whether it acts as a partial or a full agonist. The sub-nanomolar values sometimes copied across in connection with it belong to another molecule.

Key sources.

History

Source
A wholly synthetic compound, absent from Cannabis sativa and from any other plant. No consumer product containing it has been found. Its documented presence is confined to the animal pharmacology publications of 1980 and 1985 and to chemical databases, where it appears as a reference substance.

Origin

Laboratory synthesis

No biosynthetic pathway is known. Canbisol is produced by no living organism: it results from total synthesis, described here by chemical class only.

Classification

Family, origin and source verification

Family

Synthetic CB receptor agonist › Research ligand or medicine

Class

9-hydroxylated classical cannabinoid (hexahydrobenzo[c]chromene with a 1,1-dimethylheptyl chain, parent of nabilone)

Verification

Classification, sources and binding values checked on 20 October 2026; text read against its sources and Wikipedia.

Wikipedia (English)

Canbisol (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. Stark P, Dews PB. Cannabinoids. I. Behavioral effects. J Pharmacol Exp Ther. 1980;214(1):124-130. Behavioural study of canbisol and nabilone in the mouse, rat, dog and rhesus monkey. (new tab)PMID 6771386
  2. Koe BK, Milne GM, Weissman A, Johnson MR, Melvin LS. Enhancement of brain [3H]flunitrazepam binding and analgesic activity of synthetic cannabimimetics. Eur J Pharmacol. 1985;109(2):201-212. Canbisol is classed there as more potent than nabilone and delta-9-THC. (new tab)PMID 2986995
  3. Rhee MH, Vogel Z, Barg J, et al. Cannabinol derivatives: binding to cannabinoid receptors and inhibition of adenylylcyclase. J Med Chem. 1997;40(20):3228-3233. Source of the Ki values of 100 ± 50 pM (CB1) and 200 ± 40 pM (CB2) often wrongly attributed to canbisol: they concern 11-hydroxycannabinol-DMH, a distinct molecule. (new tab)PMID 9379442
  4. PubChem, Canbisol, CID 41969 (identifiers, synonyms, Lilly code 106990, name Nabidrox). (new tab)
  5. ChEMBL, molecule CHEMBL2105525: canbisol (international nonproprietary name; no biological activity measurement reported) (new tab)
  6. ANSM, consolidated list of substances classified as narcotics, updated 16 February 2026: generic benzo[c]chromene clause (decisions of 22 May and 3 June 2024), named entries nabilone, HU-210 and HU-243, canbisol absent; Annex III: tetrahydrocannabinols clause (decision of 6 February 2026). (new tab)
  7. ANSM, scheduling of hexahydrocannabinol (HHC) and of two of its derivatives on the narcotics list, decision of 12 June 2023, applicable from 13 June 2023. (new tab)
  8. INCB, Green List of psychotropic substances, 36th edition, 2025 (1971 Convention: HHC in Schedule II, canbisol absent) (new tab)

Identifiers

Names

IUPAC name
6,6-dimethyl-3-(2-methyloctan-2-yl)-6a,7,8,9,10,10a-hexahydrobenzo[c]chromene-1,9-diol
Other names
Nabidrox · Canbisolum · Lilly 106990 · 9-nor-9beta-hydroxyhexahydrocannabinol-DMH

Identifiers

Formula
C₂₄H₃₈O₃
CAS
56689-43-1
PubChem CID
41969(new tab)
InChIKey
UEKGZFCGRQYMRM-UHFFFAOYSA-N
SMILES
CCCCCCC(C)(C)C1=CC2=C(C3CC(CCC3C(O2)(C)C)O)C(=C1)O

Machine-readable entry (JSON)

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