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AM-1172Also known as N-arachidonyl-4-hydroxybenzamide

FAAH-resistant anandamide analogue, used in the laboratory to block its reuptake.

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.

C₂₇H₃₉NO₂

CID 10364179

Family
ECS pharmacological toolTransport inhibitor
Molar mass
409.60 g/mol

Updated on

In plain terms

AM-1172 is a molecule made in the laboratory, derived from anandamide, a cannabinoid the body makes itself. It does not come from hemp and is in no product sold to the public: researchers use it to stop cells from taking anandamide back up, and it also activates the CB1 receptor, at lower concentrations. No study in humans was found; work on cells shows it also damages healthy cells.

Receptors and activity

Target network

CB1Partial agonistEC50 = 86 nM · ratstimulation of [35S]GTPγS binding, rat cerebellar membranes (n = 2); binding IC50 of 271 nM
  • Activates
  • Blocks or inhibits
  • Binds or modulates

The lower the cited value, the closer the target sits to AM-1172: 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-1172.

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. Transport cellulaire de l'anandamideInhibitorIC50 = 2.1 µM · rat28 out of 100

    Fegley et al., PNAS 2004 (new tab) · [3H]anandamide internalisation, rat cortical neurons (2.5 µM in CCF-STTG1 human astrocytoma cells); also active in FAAH-/- mouse neurons; neither substrate nor inhibitor of FAAH

  2. CB1Partial agonistEC50 = 86 nM · rat51 out of 100

    Fegley et al., PNAS 2004 (new tab) · stimulation of [35S]GTPγS binding, rat cerebellar membranes (n = 2); binding IC50 of 271 nM

  3. CB2Binding (function not established)IC50 = 189 nM · not specified in the text consulted45 out of 100

    Fegley et al., PNAS 2004 (new tab) · radioligand displacement; functional activity not characterised

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

AM-1172 is a reversed-amide analogue of anandamide and of AM404: the arachidonyl chain is linked to 4-hydroxybenzoic acid by an amide bond oriented the opposite way to that of AM404. Its documented function is inhibition of the cellular transport of anandamide, with an IC50 of about 2 µM in human astrocytoma and in rat cortical neurons; because it is neither a FAAH substrate nor a FAAH inhibitor and keeps its effect in neurons from FAAH-deficient mice, it was used to show that anandamide reuptake is independent of FAAH (Fegley et al. 2004). The molecule is not silent at receptors: its binding IC50 is 271 nM at CB1 and 189 nM at CB2, and it partially activates CB1 (EC50 86 nM in [35S]GTPγS binding), so its biological effects may combine reuptake and direct receptor action. In mice, it raised the maximal electroshock seizure threshold, the doses raising the threshold by 20% and 50% being 2.48 and 6.29 mg/kg intraperitoneally (Tutka et al. 2018). In human cell lines, it reduced the viability of melanoma cells, but also of healthy melanocytes and keratinocytes, with more marked toxicity on healthy cells (Marzęda et al. 2024), and inhibited the proliferation of neuroblastoma and glioblastoma lines (IC50 2.29 to 17.21 µM; Załuska-Ogryzek et al. 2025). No pharmacokinetics, clinical trial or safety data in humans was found.

Key sources.

History

Source
An entirely synthetic molecule with no known natural occurrence: it is found neither in cannabis nor in any other plant, even though its fatty chain is that of anandamide. It is known only as a research compound (Fegley et al. 2004).

Origin

Research tool

No biosynthetic pathway: the molecule comes from no living organism. It belongs to the class of fatty amine and aromatic acid amides.

Classification

Family, origin and source verification

Family

ECS pharmacological tool › Transport inhibitor

Verification

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

Wikipedia (English)

No dedicated article.

References

  1. Fegley D et al. Anandamide transport is independent of fatty-acid amide hydrolase activity and is blocked by the hydrolysis-resistant inhibitor AM1172. PNAS, 2004 (new tab)PMID 15138300
  2. Tutka P et al. Arvanil, olvanil, AM 1172 and LY 2183240 (various cannabinoid CB1 receptor agonists) increase the threshold for maximal electroshock-induced seizures in mice. Pharmacol Rep, 2018 (new tab)PMID 29335158
  3. Marzęda P et al. AM1172 (a hydrolysis-resistant endocannabinoid analog that inhibits anandamide cellular uptake) reduces the viability of the various melanoma cells, but it exerts significant cytotoxic effects on healthy cells. Pharmacol Rep, 2024 (new tab)PMID 38019413
  4. Załuska-Ogryzek K et al. Isobolographic interactions of cannabidiol and AM 1172 with cisplatin in human neuroblastoma and glioblastoma cell lines. Chem Biol Interact, 2025 (new tab)PMID 39828184
  5. PubChem, AM-1172, CID 10364179 (identifiers and properties) (new tab)

Identifiers

Names

Common name
AM-1172 (N-arachidonyl-4-hydroxybenzamide)
IUPAC name
4-hydroxy-N-[(5Z,8Z,11Z,14Z)-icosa-5,8,11,14-tetraenyl]benzamide
Other names
AM1172 · AM 1172 · N-arachidonyl 4-hydroxybenzamide · N-(5Z,8Z,11Z,14Z)-5,8,11,14-eicosatetraen-1-yl-4-hydroxybenzamide · 4-hydroxy-N-[(5Z,8Z,11Z,14Z)-icosa-5,8,11,14-tetraenyl]benzamide

Identifiers

Formula
C₂₇H₃₉NO₂
PubChem CID
10364179(new tab)
InChIKey
XCWBOAHOJHPWLA-DOFZRALJSA-N
SMILES
CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCCNC(=O)C1=CC=C(C=C1)O

Machine-readable entry (JSON)

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