AZ-11713908
A laboratory CB1 agonist designed to stay out of the brain. No human data.
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.
C₂₇H₃₂N₄O₃S₂
CAS 1309682-69-6
- Family
- Synthetic CB receptor agonistResearch ligand or medicine
- Molar mass
- 524.70 g/mol
Updated on
In plain terms
AZ-11713908 is a laboratory molecule developed by the pharmaceutical company AstraZeneca. It has nothing to do with hemp and is found in no plant: it was designed to activate the same receptors as THC while staying mostly outside the brain. It has been studied in rodents; no study in humans was found.
Receptors and activity
Target network
- Activates
- Binds or modulates
The lower the cited value, the closer the target sits to AZ-11713908: 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 AZ-11713908.
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
- CB1AgonistEC50 = 6 nM · human70 out of 100
Cheng et al., Bioorg Med Chem Lett 2012 (values from ChEMBL, document CHEMBL1949601) (new tab) · [35S]GTPγS binding, HEK293 EBNA cells expressing human CB1, maximal effect of 115% of that of WIN 55,212-2; Ki of 3.0 nM ([3H]CP 55,940 displacement, HEK293 cells)
- CB2Binding (function not established)Ki = 0.6 nM · human88 out of 100
Cheng et al., Bioorg Med Chem Lett 2012 (values from ChEMBL, document CHEMBL1949601) (new tab) · binding at human CB2; inverse agonist in the rat, partial agonist in the mouse (Yu et al. 2010)
Pharmacology
A cannabinoid receptor agonist from a pharmaceutical programme, AZ-11713908 binds human CB1 with a Ki of 3.0 nM and activates it with a maximal effect of 115% of that of WIN 55,212-2 (Cheng et al. 2012, from ChEMBL). Its affinity for human CB2 is higher (Ki 0.56 nM), but the direction of the effect changes with species: inverse agonism in the rat, partial agonism in the mouse (Yu et al. 2010). It enters the brain poorly (brain-to-plasma ratio of 0.07 in rats after 1 mg/kg subcutaneously), so that the analgesia seen in rodents in inflammatory and neuropathic pain models, comparable to that of WIN 55,212-2, goes through peripheral CB1 receptors: the effect disappeared in mice lacking CB1 and persisted in mice lacking CB2, in vivo electrophysiology places the site of action in the periphery, and local intraplantar application was enough to produce it (Yu et al. 2010). In an Irwin test in rats, it produced fewer central effects than WIN 55,212-2. No toxicology study and no study in humans was found.
Key sources.
- Yu XH et al. A peripherally restricted cannabinoid receptor agonist produces robust anti-nociceptive effects in rodent models of inflammatory and neuropathic pain. Pain, 2010 (new tab)PMID 20696525
- Cheng YX et al. γ-Carbolines: a novel class of cannabinoid agonists with high aqueous solubility and restricted CNS penetration. Bioorg Med Chem Lett, 2012 (new tab)PMID 22284817
- ChEMBL, activities of compound CHEMBL1950329 (AZ-11713908), document CHEMBL1949601 (Cheng et al. 2012) (new tab)
- Hossain MZ et al. Targeting peripherally restricted cannabinoid receptor 1, cannabinoid receptor 2, and endocannabinoid-degrading enzymes for the treatment of neuropathic pain including neuropathic orofacial pain. Int J Mol Sci, 2020 (new tab)PMID 32093166
- PubChem, AZ-11713908, CID 57390958 (identifiers and properties) (new tab)
History
- Source
- An entirely synthetic molecule. It exists in no plant or living organism and is not known in cannabis. It comes from an AstraZeneca pharmaceutical programme (Montréal site) on peripherally restricted cannabinoid agonists (Yu et al. 2010).
Origin
Laboratory synthesis
No biological pathway: the molecule is produced by no organism. It is a synthetic compound of the benzimidazole sulfonamide class.
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. No marketing authorisation was found: the compound is described only in the research literature.
- France
Not classified: AZ-11713908, a benzimidazole sulfonamide, is not on the ANSM consolidated list of narcotics (updated 16/02/2026); on a literal reading, its structure falls within none of the generic families of annex IV (indol-3-yl methanones, benzo[c]chromene ring, 2-benzyl-benzimidazol-1-yl ethanamine family…). 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
benzimidazole-sulfonamide
- 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
- Yu XH et al. A peripherally restricted cannabinoid receptor agonist produces robust anti-nociceptive effects in rodent models of inflammatory and neuropathic pain. Pain, 2010 (new tab)PMID 20696525
- Cheng YX et al. γ-Carbolines: a novel class of cannabinoid agonists with high aqueous solubility and restricted CNS penetration. Bioorg Med Chem Lett, 2012 (new tab)PMID 22284817
- ChEMBL, activities of compound CHEMBL1950329 (AZ-11713908), document CHEMBL1949601 (Cheng et al. 2012) (new tab)
- Hossain MZ et al. Targeting peripherally restricted cannabinoid receptor 1, cannabinoid receptor 2, and endocannabinoid-degrading enzymes for the treatment of neuropathic pain including neuropathic orofacial pain. Int J Mol Sci, 2020 (new tab)PMID 32093166
- PubChem, AZ-11713908, CID 57390958 (identifiers and properties) (new tab)
Identifiers
Names
- IUPAC name
- N-[1-(cyclohexylmethyl)-2-[(5-ethoxy-2-pyridinyl)methyl]benzimidazol-5-yl]-N-methylthiophene-2-sulfonamide
- Other names
- AZ11713908 · AZ 11713908
Identifiers
- Formula
- C₂₇H₃₂N₄O₃S₂
- CAS
- 1309682-69-6
- PubChem CID
- 57390958(new tab)
- InChIKey
- YIEVWZCZMDYKQH-UHFFFAOYSA-N
- SMILES
- CCOC1=
CN= C(C= C1) CC2= NC3= C(N2CC4CCCCC4) C= CC(= C3) N(C) S(= O) (= O) C5= CC= CS5
LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.