Skip to content

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

Synthetic

ACPAArachidonylcyclopropylamide

Anandamide analogue, CB1 agonist (Ki 2.2 nM), with about 300-fold lower affinity for CB2.

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.

C₂₃H₃₇NO

CAS 229021-64-1

Family
Synthetic CB receptor agonistResearch ligand or medicine
Molar mass
343.50 g/mol

Updated on

In plain terms

ACPA is a laboratory-made molecule copied from anandamide, a cannabinoid the brain makes itself. Described in 1999, it mainly activates one of the two cannabinoid receptors, CB1, which lets researchers tell which receptor does what. It does not exist in hemp and is used only in animals and in cells; no study in humans was found.

Receptors and activity

Target network

CB1AgonistKi = 2.2 nMbinding assay; species and preparation not specified in the abstract; agonist: inhibits forskolin-induced cAMP in CHO cells expressing human CB1; Ki 2.2 ± 0.4 nM
  • Activates
  • Binds or modulates

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

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 = 2.2 nM78 out of 100

    Hillard et al., J Pharmacol Exp Ther 1999 (new tab) · binding assay; species and preparation not specified in the abstract; agonist: inhibits forskolin-induced cAMP in CHO cells expressing human CB1; Ki 2.2 ± 0.4 nM

  2. CB2Binding (function not established)Ki = 700 nM36 out of 100

    Hillard et al., J Pharmacol Exp Ther 1999 (new tab) · binding assay; species and preparation not specified in the abstract; low affinity (0.7 ± 0.01 µM), no functional effect measured at CB2

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

ACPA is a synthetic analogue of anandamide: the same twenty-carbon arachidonoyl chain with four cis double bonds, but a cyclopropylamide head in place of the ethanolamide group. Hillard and colleagues described it in 1999 with ACEA, at a time when most cannabinoid agonists bound CB1 and CB2 with similar affinities: it binds CB1 with a Ki of 2.2 nM and CB2 with a Ki of 0.7 µM. Its status as a CB1 agonist rests on three functional measurements (inhibition of cAMP in cells expressing human CB1, activation of G-protein coupling in cerebellar membranes, inhibition of mouse vas deferens contractions) and on hypothermia in mice, inhibited by SR141716A; the abstract does not quantify relative efficacy. Since then it has served as a pharmacological probe in rodents. In mice, intraperitoneal ACPA produced anxiolytic-like behaviour in the elevated plus maze and a conditioned place preference, both inhibited by AM251 injected into the basolateral amygdala (Tokutake et al. 2022); stopping repeated administration increased rearing, decreased rubbing and reduced total sleep time during the light phase, which the authors present as a mouse model of cannabis withdrawal (Asano et al. 2023). In rats given streptozotocin intracerebroventricularly, chronic ACPA microinjections (10 ng/0.5 µl) into the hippocampus (CA1), central amygdala or medial prefrontal cortex attenuated the passive-avoidance retention deficit; given alone, microinjection into CA1 or the central amygdala did not change retention, and in the medial prefrontal cortex it impaired memory formation (Hosseininia et al. 2023). In a mouse xenograft model of non-small cell lung cancer, a nanoparticle formulation of ACPA reduced Ki-67 proliferation scores and raised apoptosis (TUNEL) scores on days 7 to 21 (Boyacıoğlu et al. 2025). These results are preclinical; no study in humans was found.

Key sources.

History

Source
An entirely synthetic molecule, designed as an analogue of anandamide (Hillard et al. 1999). No natural occurrence, human use or circulation as a consumer product was found in the sources consulted: it is known as a research reagent.

Origin

Laboratory synthesis

No known biosynthetic pathway: ACPA is a synthetic compound, the amide of arachidonic acid and cyclopropylamine, produced by no described organism.

Classification

Family, origin and source verification

Family

Synthetic CB receptor agonist › Research ligand or medicine

Class

eicosanoid

Verification

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

Wikipedia (English)

Arachidonylcyclopropylamide (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. Hillard CJ et al. Synthesis and characterization of potent and selective agonists of the neuronal cannabinoid receptor (CB1). J Pharmacol Exp Ther, 1999 (new tab)PMID 10336536
  2. Tokutake T et al. Cannabinoid Type 1 Receptors in the Basolateral Amygdala Regulate ACPA-Induced Place Preference and Anxiolytic-Like Behaviors. Neurochem Res, 2022 (new tab)PMID 35984590
  3. Asano T et al. Sleep disturbance after cessation of cannabis administration in mice. Neuropsychopharmacol Rep, 2023 (new tab)PMID 36905178
  4. Hosseininia M et al. Memory impairment was ameliorated by corticolimbic microinjections of arachidonylcyclopropylamide (ACPA) and miRNA-regulated lentiviral particles in a streptozotocin-induced Alzheimer's rat model. Exp Neurol, 2023 (new tab)PMID 37783412
  5. Boyacıoğlu Ö et al. A novel injectable nanotherapeutic platform increasing the bioavailability and anti-tumor efficacy of Arachidonylcyclopropylamide on an ectopic non-small cell lung cancer xenograft model. Int J Pharm, 2025 (new tab)PMID 39746587
  6. PubChem, arachidonylcyclopropylamide, CID 5311007 (identifiers and properties) (new tab)

Identifiers

Names

Common name
Arachidonylcyclopropylamide
IUPAC name
(5Z,8Z,11Z,14Z)-N-cyclopropylicosa-5,8,11,14-tetraenamide
Other names
Arachidonoylcyclopropylamide · N-cyclopropylarachidonamide · N-cyclopropyl arachidonoylamide · (5Z,8Z,11Z,14Z)-N-cyclopropylicosa-5,8,11,14-tetraenamide

Identifiers

Formula
C₂₃H₃₇NO
CAS
229021-64-1
PubChem CID
5311007(new tab)
InChIKey
GLGAUBPACOBAMV-DOFZRALJSA-N
SMILES
CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(=O)NC1CC1

Machine-readable entry (JSON)

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