AM-3102
Synthetic analogue of oleoylethanolamide, a PPAR-alpha agonist resistant to amidases.
C₂₁H₄₁NO₂
CID 10569111
- Family
- ECS pharmacological toolOther target
- Molar mass
- 339.60 g/mol
Updated on
In plain terms
AM-3102 is a laboratory molecule, a stabilised copy of a lipid the body makes itself, oleoylethanolamide. It exists neither in hemp nor in the human body and is not sold as a consumer product. In rodents, it delayed the return to eating in laboratory experiments; 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 AM-3102: 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 AM-3102.
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
- PPARαAgonistEC50 = 100 nM · not specified in the abstract50 out of 100
Astarita et al., J Pharmacol Exp Ther 2006 (new tab) · PPARα transcriptional activity in cells (n = 11); anorexiant ED50 of 2.4 ± 1.8 mg/kg i.p. in the rat
- CB1Binding (function not established)Ki = 33 µM · rat8 out of 100
Lin et al., J Med Chem 1998 (values from ChEMBL, document CHEMBL1131442) (new tab) · [3H]CP 55,940 binding, rat forebrain membranes, without PMSF (19 µM with PMSF); negligible affinity
- CB2Binding (function not established)Ki = 26 µM · mouse10 out of 100
Lin et al., J Med Chem 1998 (values from ChEMBL, document CHEMBL1131442) (new tab) · [3H]CP 55,940 binding, mouse spleen membranes; negligible affinity
Measured effects
Not characterised. No placebo-controlled human trial has measured the effects of AM-3102, so no level is shown.
Levels computed from placebo-controlled human trials: difference from placebo on 100, at the dose and route stated. Read the method
Pharmacology
AM-3102, also published under the code KDS-5104, is an alpha-methylated analogue of oleoylethanolamide (OEA). The methyl carried by the ethanolamide head makes the molecule resistant to hydrolysis by FAAH and by N-acylethanolamine-hydrolysing acid amidase (NAAA), the two enzymes that end the action of OEA. Its main target is PPARα, which it activates in a cell assay with an EC50 of 100 ± 21 nM. In rats, intraperitoneal administration prolonged feeding latency and the post-meal interval (50% effective dose 2.4 ± 1.8 mg/kg), with higher and longer-lasting tissue exposure than OEA; oral administration also produced tissue exposure and a reduction in food intake in freely fed rats (Astarita et al. 2006). In mice fed a high-fat diet, 100 mg/kg orally decreased fat pad mass by 20% after 5 weeks, like OEA (Thabuis et al. 2011); in a mouse model of Alzheimer's disease (5xFAD mice), chronic treatment with KDS-5104 restored dysregulated lipid profiles and reduced reactive gliosis and amyloid pathology (Comerota et al. 2023). Affinity for CB1 and CB2 is micromolar, hence negligible. No study in humans was found.
Key sources.
- Astarita G et al. Pharmacological characterization of hydrolysis-resistant analogs of oleoylethanolamide with potent anorexiant properties. J Pharmacol Exp Ther, 2006 (new tab)PMID 16702440
- Thabuis C et al. Lipid transport function is the main target of oral oleoylethanolamide to reduce adiposity in high-fat-fed mice. J Lipid Res, 2011 (new tab)PMID 21515921
- Comerota MM et al. Oleoylethanolamide facilitates PPARα and TFEB signaling and attenuates Aβ pathology in a mouse model of Alzheimer's disease. Mol Neurodegener, 2023 (new tab)PMID 37580742
- Lin S et al. Novel analogues of arachidonylethanolamide (anandamide): affinities for the CB1 and CB2 cannabinoid receptors and metabolic stability. J Med Chem, 1998 (new tab)PMID 9876105
- ChEMBL, compound CHEMBL151084 (AM-3102 / KDS-5104), activities from document CHEMBL1131442 (Lin et al. 1998) (new tab)
- PubChem, AM-3102, CID 10569111 (identifiers and properties) (new tab)
History
- Source
- An entirely synthetic compound. It is found neither in cannabis nor in humans; only its natural congener, oleoylethanolamide, is an endogenous lipid mediator. AM-3102 is known only as a research compound (Astarita et al. 2006).
Origin
Research tool
No known biological pathway: AM-3102 is a synthetic compound, an amide of oleic acid and (R)-2-aminopropan-1-ol, which comes from no plant or animal enzyme.
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: AM-3102, a fatty acid amide, is not on the ANSM consolidated list of narcotics (updated 16/02/2026) and its structure falls within none of the generic families of that list. No marketing authorisation was found.
Sources: EUR-Lex, UNODC, CND, ANSM, IUPHAR/BPS, ChEBI, EUDA. Our method.
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)
No dedicated article.
References
- Astarita G et al. Pharmacological characterization of hydrolysis-resistant analogs of oleoylethanolamide with potent anorexiant properties. J Pharmacol Exp Ther, 2006 (new tab)PMID 16702440
- Thabuis C et al. Lipid transport function is the main target of oral oleoylethanolamide to reduce adiposity in high-fat-fed mice. J Lipid Res, 2011 (new tab)PMID 21515921
- Comerota MM et al. Oleoylethanolamide facilitates PPARα and TFEB signaling and attenuates Aβ pathology in a mouse model of Alzheimer's disease. Mol Neurodegener, 2023 (new tab)PMID 37580742
- Lin S et al. Novel analogues of arachidonylethanolamide (anandamide): affinities for the CB1 and CB2 cannabinoid receptors and metabolic stability. J Med Chem, 1998 (new tab)PMID 9876105
- ChEMBL, compound CHEMBL151084 (AM-3102 / KDS-5104), activities from document CHEMBL1131442 (Lin et al. 1998) (new tab)
- PubChem, AM-3102, CID 10569111 (identifiers and properties) (new tab)
Identifiers
Names
- IUPAC name
- (Z)-N-[(2R)-1-hydroxypropan-2-yl]octadec-9-enamide
- Other names
- KDS-5104 · AM3102 · Methyl oleoylethanolamide · (Z)-(R)-N-((2-Hydroxy-1-methyl)ethyl)-9-octadecenamide · 9-Octadecenamide, N-((1R)-2-hydroxy-1-methylethyl)-, (9Z)-
Identifiers
- Formula
- C₂₁H₄₁NO₂
- PubChem CID
- 10569111(new tab)
- InChIKey
- IPVYNYWIRWMRHH-JPMGXVIASA-N
- SMILES
- CCCCCCCC/C=
C\CCCCCCCC(= O) N[C@H] (C) CO
LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.