Skip to content

Batch information on every product pageTHC < 0.3%Shipped from France10% off when you sign up

From the body

HEADihomo-gamma-linolenoylethanolamide

A 20:3 congener of anandamide described in brain in 1993, a modest-affinity CB1 and CB2 ligand.

Endogenous
Level of detail

C₂₂H₃₉NO₂

CAS 150314-34-4

Family
Endocannabinoid or related mediatorPutative
Molar mass
349.60 g/mol

Updated on

In plain terms

Dihomo-gamma-linolenoylethanolamide is a small fatty molecule that the body makes itself; it does not exist in hemp. It closely resembles anandamide and binds the same CB1 and CB2 receptors, but more weakly on human receptors in cell culture. Its role in the body is not known.

Receptors and activity

Target network

CB1AgonistKi = 857 nM · human[3H]CP 55,940 displacement, recombinant human CB1; cAMP inhibition
  • Activates

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

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. CB1AgonistKi = 857 nM · human34 out of 100

    Felder et al. 1995, Mol Pharmacol (new tab) · [3H]CP 55,940 displacement, recombinant human CB1; cAMP inhibition

  2. CB2AgonistKi = 598 nM · human37 out of 100

    Felder et al. 1995, Mol Pharmacol (new tab) · [3H]CP 55,940 displacement, recombinant human CB2; cAMP inhibition

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

A congener of anandamide whose fatty chain carries three double bonds instead of four (20:3 n-6), dihomo-gamma-linolenoylethanolamide was described in brain in 1993 by Raphael Mechoulam's group, together with docosatetraenoylethanolamide, as a fatty acid ethanolamide that binds the cannabinoid receptor (Hanuš 1993). On recombinant human receptors it binds CB1 (Ki 857 nM) and CB2 (Ki 598 nM) with similar affinity and inhibits cAMP accumulation through both subtypes (Felder 1995). Structure-activity analysis of the 20:x n-6 series places it at the threshold of activity: three or four double bonds are required for CB1 binding, two abolish it (Sheskin 1997). It is measured in human cerebrospinal fluid (Kantae 2017), but its physiological role is not established; the classification places it among putative endocannabinoids, anandamide and 2-AG remaining the only two established ones.

Key sources.

History

Source
An endogenous mammalian molecule, absent from cannabis. Described in the brain (Hanuš 1993), it has been measured in the cerebrospinal fluid of healthy volunteers by nano liquid chromatography coupled with tandem mass spectrometry (Kantae 2017).

Biosynthetic pathway

In vivo

Its biosynthesis has not been studied specifically. N-acylethanolamines are formed from N-acyl-phosphatidylethanolamines (NAPEs), produced by a calcium-dependent N-acyltransferase and then hydrolysed by NAPE-PLD; further enzymes of this pathway have been identified more recently (Tsuboi 2018).

Classification

Family, origin and source verification

Family

Endocannabinoid or related mediator › Putative

Verification

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

Wikipedia (English)

No dedicated article.

References

  1. Hanuš, Gopher, Almog & Mechoulam 1993, J Med Chem: two new unsaturated fatty acid ethanolamides in brain (new tab)PMID 8411021
  2. Felder et al. 1995, Mol Pharmacol: pharmacology of human CB1 and CB2 (Ki 857 and 598 nM) (new tab)PMID 7565624
  3. Sheskin et al. 1997, J Med Chem: structural requirements for CB1 binding (new tab)PMID 9057852
  4. Reggio 2010, Curr Med Chem: endocannabinoid binding to the cannabinoid receptors (review) (new tab)PMID 20166921
  5. Kantae et al. 2017, J Lipid Res: profile of N-acylethanolamines in human CSF (new tab)PMID 27999147
  6. Tsuboi et al. 2018, Inflamm Regen: metabolism of endocannabinoids and N-acylethanolamines (review) (new tab)PMID 30288203
  7. LIPID MAPS LMFA08040011, Dihomo-γ-linolenoyl ethanolamide (new tab)
  8. PubChem CID 5282272, (8Z,11Z,14Z)-N-(2-hydroxyethyl)-8,11,14-eicosatrienamide (new tab)

Identifiers

Names

Common name
Dihomo-gamma-linolenoylethanolamide
IUPAC name
(8Z,11Z,14Z)-N-(2-hydroxyethyl)icosa-8,11,14-trienamide
Other names
DGLEA · Dihomo-gamma-linolenoyl ethanolamide · Homo-gamma-linolenoylethanolamide · N-(8Z,11Z,14Z-eicosatrienoyl)-ethanolamine · Dihomo-gamma-linolenoyl-EA

Identifiers

Formula
C₂₂H₃₉NO₂
CAS
150314-34-4
PubChem CID
5282272(new tab)
ChEBI
CHEBI:34488(new tab)
InChIKey
ULQWKETUACYZLI-QNEBEIHSSA-N
SMILES
CCCCC/C=C\C/C=C\C/C=C\CCCCCCC(=O)NCCO

Machine-readable entry (JSON)

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