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Synthetic

AKB-48Also known as APINACA

An adamantyl synthetic cannabinoid, a full CB1 agonist, scheduled by name as a narcotic in France.

Narcotic: named in schedule
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.

C₂₃H₃₁N₃O

CAS 1345973-53-6

Family
Synthetic CB receptor agonistNew psychoactive substance
Molar mass
365.52 g/mol

Updated on

In plain terms

AKB-48 (APINACA) is a molecule made in the laboratory, absent from hemp. It has been found in smoking mixtures sold as legal products, and WHO reports its detection in about twenty countries. It acts on the same receptors as THC. It is classed as a narcotic in France.

Receptors and activity

Target network

CB1AgonistKi = 3.2 nM · humanradioligand displacement, CHO cells expressing human CB1
  • Activates

The lower the cited value, the closer the target sits to AKB-48: 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 AKB-48.

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 = 3.2 nM · human75 out of 100

    Canazza et al. 2016, Psychopharmacology (value reported by WHO, 42nd ECDD, 2019) (new tab) · radioligand displacement, CHO cells expressing human CB1

  2. CB2AgonistKi = 1.7 nM · human80 out of 100

    Canazza et al. 2016, Psychopharmacology (value reported by WHO, 42nd ECDD, 2019) (new tab) · radioligand displacement, CHO cells expressing human 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

APINACA is an adamantyl-substituted indazole carboxamide, a full agonist at CB1 and CB2 receptors. In CHO cells expressing the human receptors, the reported affinities are 3.24 nM at CB1 and 1.68 nM at CB2, with functional activation confirmed by inhibition of forskolin-stimulated cAMP (Canazza et al. 2016, as reported in the WHO report). In mice, it reproduces the cannabinoid tetrad (suppressed locomotor activity, antinociception, hypothermia, catalepsy), with neurological signs abolished by a CB1 antagonist, and stimulates dopamine release in the nucleus accumbens. The effects vary with sex and treatment duration, with tolerance at the third injection (Corli et al. 2024). Human pharmacology has not been studied: WHO notes the absence of formal surveys of adverse effects specific to this molecule and of data on the active dose. Metabolism is mainly by CYP3A4 and proceeds by multiple hydroxylations of the adamantane cage followed by conjugations.

Key sources.

History

Source
A wholly synthetic molecule, absent from hemp and from any living organism. According to the WHO report (2019), synthetic cannabinoids are mostly synthesised in chemical companies in China, with packaging done in the destination country; the presumed route of exposure is inhalation, after spraying on plant material or by vaping.

Origin

Laboratory synthesis

No biological pathway: this compound comes from no plant or animal metabolism. It is a synthetic molecule of the indazole-3-carboxamide class, described here by its chemical class only.

Classification

Family, origin and source verification

Family

Synthetic CB receptor agonist › New psychoactive substance

Class

indazole-3-carboxamide

Verification

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

Wikipedia (English)

APINACA (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. WHO, Expert Committee on Drug Dependence, 42nd meeting: critical review report on APINACA (AKB-48) (2019) (new tab)
  2. Canazza et al. · Psychopharmacology 2016 (new tab)PMID 27527584
  3. Gandhi et al. · AAPS J 2013 (new tab)PMID 23913126
  4. Kim et al. · Molecules 2019 (new tab)PMID 31430908
  5. Oztas et al. · Toxicol In Vitro 2019 (new tab)PMID 30550854
  6. Corli et al. · Br J Pharmacol 2024 (new tab)PMID 38148741
  7. Karinen et al. · Forensic Sci Int 2015 (new tab)PMID 25485949

Identifiers

Names

Common name
AKB-48 (APINACA)
IUPAC name
N-(1-adamantyl)-1-pentylindazole-3-carboxamide
Other names
APINACA · AKB48

Identifiers

Formula
C₂₃H₃₁N₃O
CAS
1345973-53-6
PubChem CID
57404063(new tab)
InChIKey
UCTCCIPCJZKWEZ-UHFFFAOYSA-N
SMILES
CCCCCN1C2=CC=CC=C2C(=N1)C(=O)NC34CC5CC(C3)CC(C5)C4

Machine-readable entry (JSON)

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