AMG-36
Δ8-THC analogue with a 1-hexylcyclopentyl chain: high affinity for CB1 (Ki 0.45 nM) and CB2 (Ki 1.92 nM).
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.
C₂₇H₄₀O₂
CID 10982174
- Family
- Synthetic CB receptor agonistResearch ligand or medicine
- Molar mass
- 396.60 g/mol
Updated on
In plain terms
AMG-36 is a laboratory molecule made by synthesis: it exists in no plant and is in no consumer product. Chemists prepared it by modifying the side chain of a THC derivative to understand how its shape changes the way the molecule attaches to cannabinoid receptors. It binds them very strongly in membrane assays; no study in humans was found.
Receptors and activity
Target network
- Binds or modulates
The lower the cited value, the closer the target sits to AMG-36: 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 AMG-36.
CB1CB1 found in 7 regions of the body
- Basal gangliadenseMost dense in basal ganglia outflow nuclei1
- CerebellumdenseVery dense in the cerebellum1
- HippocampusdenseVery high concentrations in the hippocampus2
- AmygdaladenseHigh concentrations in the amygdala2
- CortexpresentPresent throughout the neocortex2
- Adipose tissuepresentExpressed in adipose tissue3
- GutpresentColonic epithelium, smooth muscle and plexus4
Map sources
- Herkenham M et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A, 1990 (new tab)
- 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)
- Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
- Wright K et al. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology, 2005 (new tab)
Cited values
- CB1Binding (function not established)Ki = 0.5 nM · rat89 out of 100
Papahatjis et al., J Med Chem 2003 (values read from ChEMBL, document CHEMBL1145850, and from table 2 of Bow and Rimoldi 2016) (new tab) · [3H]CP-55,940 displacement, rat brain membranes (0.45 ± 0.07 nM); functional efficacy not found
- CB2Binding (function not established)Ki = 1.9 nM · mouse79 out of 100
Papahatjis et al., J Med Chem 2003 (values read from ChEMBL, document CHEMBL1145850, and from table 2 of Bow and Rimoldi 2016) (new tab) · [3H]CP-55,940 displacement, mouse spleen membranes (1.92 ± 0.4 nM); functional efficacy not found
Pharmacology
AMG-36 is a synthetic classical cannabinoid: it keeps the tricyclic core of (−)-Δ8-tetrahydrocannabinol and differs only in its side chain, whose C1' carbon is part of a cyclopentane ring bearing a hexyl group. The modification was used to probe a subsite of the CB1 and CB2 binding domain corresponding to C1' substituents (Papahatjis et al. 2003). It gives sub-nanomolar affinity at both receptors: Ki 0.45 nM at rat brain CB1 and 1.92 nM at mouse spleen CB2, in [3H]CP-55,940 displacement. Affinity was measured; in the open sources, functional efficacy was not. No data on TRPV1, GPR55, PPARγ or 5-HT1A were found, nor any in vivo study, pharmacokinetics, toxicology or human data.
Key sources.
- Papahatjis DP et al. Pharmacophoric requirements for the cannabinoid side chain. Probing the cannabinoid receptor subsite at C1'. J Med Chem, 2003 (new tab)PMID 12852753
- Papahatjis DP et al. C1'-cycloalkyl side chain pharmacophore in tetrahydrocannabinols. J Med Chem, 2007 (new tab)PMID 17672444
- Bow EW, Rimoldi JM. The Structure-Function Relationships of Classical Cannabinoids: CB1/CB2 Modulation. Perspect Medicin Chem, 2016 (new tab)PMID 27398024
- PubChem, AMG-36, CID 10982174 (identifiers and properties) (new tab)
History
- Source
- An entirely synthetic molecule from a medicinal chemistry programme (Makriyannis laboratory, AM series); no natural occurrence was found in the sources consulted. It is known as a research compound: no medical use or circulation as a consumer product was found.
Origin
Laboratory synthesis
No known biosynthetic pathway: AMG-36 is a synthetic compound, an analogue of Δ8-tetrahydrocannabinol with a 1-hexylcyclopentyl side chain, not described in any living organism.
Legal framework
- European Union
The substance is not listed in the Annex to Council Framework Decision 2004/757/JHA (consolidated version of 12 January 2026), which lists the new psychoactive substances controlled at European Union level; control is a matter for national law. It is not listed in the schedules of the 1971 Convention on Psychotropic Substances (INCB Green List, 36th edition, 2025, text reviewed). No marketing authorisation was found.
- France
AMG-36 is not named in the ANSM consolidated list of narcotics (updated 16/02/2026). On a literal reading of the generic clause "any substance derived from the benzo[c]chromene nucleus" (annex IV, decisions of 22 May and 3 June 2024), it carries a hydroxyl at position 1, two methyls at position 6, a methyl at position 9 (ring A partly hydrogenated) and, at position 3, an alkyl chain bearing a ring (1-hexylcyclopentyl), motifs the text lists; the stated exclusions (CBN, CBNA, THCV, THCVA, THCA) do not concern it. This is a reading of the text, not a named ANSM decision. The entry "tetrahydrocannabinols, their esters, ethers, salts" (annex III since the decision of 6 February 2026) does not name analogues with a modified side chain. No marketing authorisation was found.
Sources: EUR-Lex, UNODC, CND, ANSM, IUPHAR/BPS, ChEBI, EUDA. Our method.
Classification
Family, origin and source verification
- Family
Synthetic CB receptor agonist › Research ligand or medicine
- Class
classical
- Verification
Classification, sources and binding values checked on 20 October 2026; text read against its sources and Wikipedia.
- Wikipedia (English)
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
- Papahatjis DP et al. Pharmacophoric requirements for the cannabinoid side chain. Probing the cannabinoid receptor subsite at C1'. J Med Chem, 2003 (new tab)PMID 12852753
- Papahatjis DP et al. C1'-cycloalkyl side chain pharmacophore in tetrahydrocannabinols. J Med Chem, 2007 (new tab)PMID 17672444
- Bow EW, Rimoldi JM. The Structure-Function Relationships of Classical Cannabinoids: CB1/CB2 Modulation. Perspect Medicin Chem, 2016 (new tab)PMID 27398024
- PubChem, AMG-36, CID 10982174 (identifiers and properties) (new tab)
Identifiers
Names
- IUPAC name
- (6aR,10aR)-3-(1-hexylcyclopentyl)-6,6,9-trimethyl-6a,7,10,10a-tetrahydrobenzo[c]chromen-1-ol
- Other names
- 3-(1-hexylcyclopentyl)-Δ8-THC · CHEMBL108868
Identifiers
- Formula
- C₂₇H₄₀O₂
- PubChem CID
- 10982174(new tab)
- InChIKey
- FONCHEGPDSYFCG-FGZHOGPDSA-N
- SMILES
- CCCCCCC1(CCCC1)
C2= CC3= C([C@@H] 4CC(= CC[C@H] 4C(O3) (C) C) C) C(= C2) O
LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.