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From the body

1-AG1-arachidonoylglycerol

Isomerisation product of 2-AG: a weaker CB1 agonist, a TRPV1 activator, with no human data.

Endogenous
Level of detail

C₂₃H₃₈O₄

CAS 35474-99-8

Family
Endocannabinoid or related mediatorEndocannabinoidome
Molar mass
378.50 g/mol

Updated on

In plain terms

1-AG is a small fatty molecule that appears when 2-AG, one of the body's own endocannabinoid messengers, rearranges by itself in water within minutes; the same rearrangement happens in laboratory tubes. It acts on the same targets as 2-AG, but more weakly at the CB1 receptor. It does not come from hemp.

Receptors and activity

Target network

CB1Agonistno measured value
  • Activates

The lower the cited value, the closer the target sits to 1-AG: 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 1-AG.

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
  2. TRPV1Agonistno 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

1-arachidonoylglycerol is the positional isomer of 2-AG. It forms without any enzyme, by migration of the arachidonoyl chain to an outer position of glycerol, a base-catalysed reaction that converts half of the 2-AG into 1(3)-AG in 2.3 to 10 minutes in culture medium (Rouzer 2002) and also occurs during sample extraction (Higuchi 2010): 1-AG is an isomerisation product, not an autonomous endocannabinoid. It is not inert, however. In transfected cells it activates the CB1 receptor at a concentration about threefold higher than 2-AG requires, and the ratio of the two isomers changes CB1 activation (Dócs 2017). In intact form it activates the TRPV1 channel of vascular sensory fibres, independently of its hydrolysis, and inhibiting monoacylglycerol lipase enhances the vasodilator response observed (Zygmunt 2013). Two limits: the molecule does not exist in hemp, and no human pharmacokinetic or safety data are published, the literature resting on transfected cells, homogenates and isolated rodent arteries.

Key sources.

History

Source
A lipid formed from 2-AG by non-enzymatic migration of the arachidonoyl group, in aqueous media under the conditions commonly used in biological assays (Rouzer 2002) as well as during sample extraction (Higuchi 2010). It is not an independent endocannabinoid but an isomerisation product of 2-AG, and the fraction genuinely present in tissues is hard to separate from a preparation artefact. Not reported in cannabis.

Biosynthetic pathway

In vivo

No dedicated biosynthetic enzyme is described: 1-AG arises from the isomerisation of 2-AG, a base-catalysed acyl migration. In RPMI culture medium at 37 °C the reaction follows first-order kinetics, the half-life of 2-AG being 10 minutes without serum and 2.3 minutes in the presence of 10% fetal calf serum (Rouzer 2002).

Classification

Family, origin and source verification

Family

Endocannabinoid or related mediator › Endocannabinoidome

Verification

Every fact on this entry was checked against its primary sources on 20 October 2026.

Wikipedia (English)

No dedicated article.

References

  1. Rouzer C.A., Ghebreselasie K., Marnett L.J., Chemical stability of 2-arachidonylglycerol under biological conditions, Chem Phys Lipids 2002 (new tab)PMID 12270674
  2. Higuchi S. et al., Reducing acyl migration during purification of 2-arachidonoylglycerol from biological samples before gas chromatography mass spectrometry analysis, Anal Sci 2010 (new tab)PMID 21079352
  3. Dócs K. et al., The Ratio of 2-AG to Its Isomer 1-AG as an Intrinsic Fine Tuning Mechanism of CB1 Receptor Activation, Front Cell Neurosci 2017 (new tab)PMID 28265242
  4. Zygmunt P.M. et al., Monoacylglycerols activate TRPV1 - a link between phospholipase C and TRPV1, PLoS One 2013 (new tab)PMID 24312564
  5. Navia-Paldanius D., Savinainen J.R., Laitinen J.T., Biochemical and pharmacological characterization of human alpha/beta-hydrolase domain containing 6 (ABHD6) and 12 (ABHD12), J Lipid Res 2012 (new tab)PMID 22969151
  6. ChEBI, 1-arachidonoylglycerol (CHEBI:75612) (new tab)
  7. PubChem CID 5282281, 1-Monoarachidin (new tab)

Identifiers

Names

Common name
1-arachidonoylglycerol
IUPAC name
2,3-dihydroxypropyl (5Z,8Z,11Z,14Z)-icosa-5,8,11,14-tetraenoate
Other names
1(3)-AG · 1-AG

Identifiers

Formula
C₂₃H₃₈O₄
CAS
35474-99-8
PubChem CID
5282281(new tab)
ChEBI
CHEBI:75612(new tab)
InChIKey
DCPCOKIYJYGMDN-DOFZRALJSA-N
SMILES
CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(=O)OCC(CO)O

Machine-readable entry (JSON)

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