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Synthetic

AB-CHMINACA

An indazole-3-carboxamide, full agonist at CB1 and CB2; in Schedule II of the 1971 Convention since 2018, 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.

C₂₀H₂₈N₄O₂

CAS 1185887-21-1

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

Updated on

In plain terms

AB-CHMINACA is a molecule made in the laboratory, with no link to hemp. It acts on the same receptors as cannabis. In a series of 98 deaths around Munich (2014-2020), it is among the synthetic cannabinoids most frequently found. It is classed as a narcotic in France and is in Schedule II of the 1971 Convention.

Receptors and activity

Target network

CB1AgonistKi = 0.8 nM · human[3H]CP55,940 displacement, human CB1
  • Activates

The lower the cited value, the closer the target sits to AB-CHMINACA: 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 AB-CHMINACA.

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 = 0.8 nM · human85 out of 100

    Wiley et al. 2015, J Pharmacol Exp Ther (new tab) · [3H]CP55,940 displacement, human CB1

  2. CB2AgonistKi = 0.5 nM · human89 out of 100

    Wiley et al. 2015, J Pharmacol Exp Ther (new tab) · [3H]CP55,940 displacement, 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

AB-CHMINACA belongs to the synthetic cannabinoid receptor agonists, in the family of indazole-3-carboxamides with a valinamide residue. Wiley et al. (2015) describe it as a full agonist at CB1 and CB2 with nanomolar affinity (Ki = 0.78 nM at CB1 and 0.45 nM at CB2), whose efficacy exceeds that of most known full agonists at CB1; in mice, it substitutes for Δ9-THC in a discrimination test, with an ED50 of 0.34 µmol/kg against 5.7 µmol/kg for Δ9-THC. This maximal efficacy explains the gap with cannabis: Δ9-THC activates the receptor only partially. No controlled human administration study was found in the sources consulted; human data come from post-mortem case series, such as that of Groth et al. (2023): among 98 deaths around Munich between 2014 and 2020 involving 41 synthetic agonists, these substances played a causative role in 51% of cases, and AB-CHMINACA was the third most frequent, after 5F-ADB and 5F-MDMB-PICA. In mice, daily administration for four weeks produced histological changes in the liver and kidney, even at low doses (Mohammad et al. 2024).

Key sources.

History

Source
A wholly synthetic molecule, absent from hemp and from any living organism. It was reported in 2013 in several countries as a substance of abuse (Mohammad et al. 2024).

Origin

Laboratory synthesis

No known biosynthetic pathway: the molecule exists in no living organism and derives from no plant precursor. It is a synthetic molecule of the indazole-3-carboxamide class, described here by its chemical class only, with no relation to the cannabigerol pathway that produces hemp cannabinoids.

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)

AB-CHMINACA (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. Wiley et al. · J Pharmacol Exp Ther 2015 (new tab)PMID 26105953
  2. Longworth et al. · Forensic Toxicol 2016 (new tab)PMID 27547266
  3. Sommer et al. · Addiction 2026 (new tab)PMID 41423817
  4. Eccarius et al. · J Anal Toxicol 2026 (new tab)PMID 42226022
  5. Abdelgadir et al. · Med Sci Law 2026 (new tab)PMID 41642956
  6. Mohammad et al. · Forensic Toxicol 2024 (new tab)PMID 37573525
  7. Groth et al. · Int J Legal Med 2023 (new tab)PMID 37072496
  8. Santos et al. · Pharmaceuticals 2025 (new tab)PMID 40284016

Identifiers

Names

IUPAC name
N-[(2S)-1-amino-3-methyl-1-oxobutan-2-yl]-1-(cyclohexylmethyl)indazole-3-carboxamide

Identifiers

Formula
C₂₀H₂₈N₄O₂
CAS
1185887-21-1
PubChem CID
44206133(new tab)
InChIKey
KJNZIEGLNLCWTQ-KRWDZBQOSA-N
SMILES
CC(C)[C@@H](C(=O)N)NC(=O)C1=NN(C2=CC=CC=C21)CC3CCCCC3

Machine-readable entry (JSON)

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