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Research tools

O-1602

Agonist of GPR55 and GPR18 with no notable affinity for CB1 or CB2: a laboratory tool.

Unscheduled
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.

C₁₇H₂₂O₂

CAS 317321-41-8

Family
ECS pharmacological toolOther target
Molar mass
258.40 g/mol

Updated on

In plain terms

O-1602 is a laboratory-made molecule, close to cannabidiol in shape but absent from hemp and from any other plant. Researchers use it as a tool to study two still poorly known receptors, GPR55 and GPR18; it does not bind to any notable extent the usual cannabis receptors, CB1 and CB2. The data cited come from experiments on cells and animals; it is not a consumer product.

Receptors and activity

Target network

GPR55AgonistEC50 = 2 nM · humanrecombinant human GPR55, HEK293T cell membranes, GTPγS activity (value « about 2 nM »)
  • Activates
  • Binds or modulates

The lower the cited value, the closer the target sits to O-1602: 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 O-1602.

Brain, side view
Body, front view
Blood

GPR55GPR55 found in 4 regions of the body

  1. Basal gangliapresentmRNA found in the caudate nucleus and putamen1
  2. BonepresentOsteoclasts and osteoblasts2
  3. Adipose tissuepresentExpressed in visceral adipose tissue3
  4. LiverpresentExpressed in the liver3

Map sources

  1. Sawzdargo M et al. Identification and cloning of three novel human G protein-coupled receptor genes GPR52, PsiGPR53 and GPR55: GPR55 is extensively expressed in human brain. Brain Res Mol Brain Res, 1999 (new tab)
  2. Whyte LS et al. The putative cannabinoid receptor GPR55 affects osteoclast function in vitro and bone mass in vivo. Proc Natl Acad Sci U S A, 2009 (new tab)
  3. Moreno-Navarrete JM et al. The L-α-lysophosphatidylinositol/GPR55 system and its potential role in human obesity. Diabetes, 2012 (new tab)

Cited values

  1. GPR55AgonistEC50 = 2 nM · human78 out of 100

    Johns et al., Br J Pharmacol 2007 (new tab) · recombinant human GPR55, HEK293T cell membranes, GTPγS activity (value « about 2 nM »)

  2. GPR18AgonistEC50 = 65.3 nM53 out of 100

    McHugh et al., Br J Pharmacol 2012 (new tab) · HEK293 cells expressing GPR18, p44/42 MAPK phosphorylation, full agonist (Emax 102%); no β-arrestin recruitment (Console-Bram 2014)

  3. Human neutrophil migration (a site distinct from CB1/CB2)ModulatorIC50 = 33 nM · human58 out of 100

    McHugh et al., Mol Pharmacol 2008 (new tab) · inhibition of fMLP-induced migration

  4. Atypical endothelial target (unidentified)AgonistEC50 = 1.6 µM · rat30 out of 100

    Al Suleimani et al., Eur J Pharmacol 2015 (new tab) · vasorelaxation of the rat mesenteric artery (myography), pEC50 of 5.8 ± 0.3 converted to nM; partly endothelium-dependent

  5. CB1 / CB2Binding (function not established)no measured value cited
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

O-1602 is the methylated analogue of abnormal cannabidiol: its resorcinol ring is linked to the menthadienyl ring at position 4 and carries a methyl at position 5 where abnormal cannabidiol carries a pentyl chain. It does not bind CB1 or CB2 with high affinity (Ashton 2012) and acts on other targets: GPR55 (EC50 of about 2 nM in GTPγS; Johns et al. 2007), GPR18 (full agonist, EC50 of 65.3 nM; McHugh et al. 2012) and unidentified sites governing neutrophil migration (IC50 of 33 nM) and vasodilation. In mice, 5 mg/kg intraperitoneally reduced DSS- and TNBS-induced colitis scores, including in mice lacking CB1 and CB2 or GPR55 (Schicho et al. 2011), and 3 mg/kg (12 injections) reduced tumour area by 50% and incidence by 30% in a colitis-associated colon cancer model (Kargl et al. 2013). In rats, it reduced the firing of nociceptive C fibres in acute arthritis, an effect blocked by O-1918 (Schuelert and McDougall 2011), but it increased paw sensitisation in a chronic constriction injury model (Breen et al. 2012), stimulated food intake and increased adiposity independently of GPR55 (Díaz-Arteaga et al. 2012) and, given for 6 weeks at 5 mg/kg/day to obese rats, reduced body weight and fat mass but caused morphological changes in the liver and kidney (Simcocks et al. 2019). It also promoted hepatic steatosis in hepatocytes and in mice fed a high-fat diet, through a pathway involving GPR55, PI3 kinase, Akt and SREBP-1c (Kang et al. 2021). All these data are preclinical.

Key sources.

History

Source
A synthetic molecule, an analogue of abnormal cannabidiol (a methyl group in place of the pentyl chain), absent from cannabis and from any living organism. A research reagent.

Origin

Research tool

No biosynthetic pathway: a synthetic molecule, the 5-methyl analogue of abnormal cannabidiol.

Classification

Family, origin and source verification

Family

ECS pharmacological tool › Other target

Verification

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

Wikipedia (English)

O-1602 (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. Járai Z et al., Cannabinoid-induced mesenteric vasodilation through an endothelial site distinct from CB1 or CB2 receptors, PNAS 1999 (new tab)PMID 10570211
  2. Johns DG et al., The novel endocannabinoid receptor GPR55 is activated by atypical cannabinoids but does not mediate their vasodilator effects, Br J Pharmacol 2007 (new tab)PMID 17704827
  3. McHugh D et al., Δ9-Tetrahydrocannabinol and N-arachidonyl glycine are full agonists at GPR18 receptors and induce migration in human endometrial HEC-1B cells, Br J Pharmacol 2012 (new tab)PMID 21595653
  4. Console-Bram L et al., Activation of GPR18 by cannabinoid compounds: a tale of biased agonism, Br J Pharmacol 2014 (new tab)PMID 24762058
  5. McHugh D et al., Inhibition of human neutrophil chemotaxis by endogenous cannabinoids and phytocannabinoids: evidence for a site distinct from CB1 and CB2, Mol Pharmacol 2008 (new tab)PMID 17965195
  6. Al Suleimani YM et al., Mechanisms of vasorelaxation induced by the cannabidiol analogue compound O-1602 in the rat small mesenteric artery, Eur J Pharmacol 2015 (new tab)PMID 26297305
  7. Schicho R et al., The atypical cannabinoid O-1602 protects against experimental colitis and inhibits neutrophil recruitment, Inflamm Bowel Dis 2011 (new tab)PMID 21744421
  8. Kargl J et al., O-1602, an atypical cannabinoid, inhibits tumor growth in colitis-associated colon cancer through multiple mechanisms, J Mol Med 2013 (new tab)PMID 22965195
  9. Schuelert N, McDougall JJ, The abnormal cannabidiol analogue O-1602 reduces nociception in a rat model of acute arthritis via the putative cannabinoid receptor GPR55, Neurosci Lett 2011 (new tab)PMID 21683763
  10. Breen C et al., The atypical cannabinoid O-1602 increases hind paw sensitisation in the chronic constriction injury model of neuropathic pain, Neurosci Lett 2012 (new tab)PMID 22227298
  11. Díaz-Arteaga A et al., The atypical cannabinoid O-1602 stimulates food intake and adiposity in rats, Diabetes Obes Metab 2012 (new tab)PMID 21981246
  12. Kang S et al., O-1602 promotes hepatic steatosis through GPR55 and PI3 kinase/Akt/SREBP-1c signaling in mice, Int J Mol Sci 2021 (new tab)PMID 33803038
  13. Simcocks AC et al., Atypical cannabinoid ligands O-1602 and O-1918 administered chronically in diet-induced obesity, Endocr Connect 2019 (new tab)PMID 30707678
  14. Ashton JC, The atypical cannabinoid O-1602: targets, actions, and the central nervous system, Cent Nerv Syst Agents Med Chem 2012 (new tab)PMID 22831390
  15. ANSM, consolidated list of substances classified as narcotics, updated 16 February 2026, annex IV (benzo[c]chromene heading) (new tab)
  16. PubChem, compound CID 45073499 (O-1602) (new tab)

Identifiers

Names

IUPAC name
5-methyl-4-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]benzene-1,3-diol
Other names
O 1602 · O1602

Identifiers

Formula
C₁₇H₂₂O₂
CAS
317321-41-8
PubChem CID
45073499(new tab)
InChIKey
KDZOUSULXZNDJH-LSDHHAIUSA-N
SMILES
CC1=C[C@H]([C@@H](CC1)C(=C)C)C2=C(C=C(C=C2C)O)O

Machine-readable entry (JSON)

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