Skip to content

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

Research tools

KML29

A highly selective covalent MAGL inhibitor, a research probe.

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.

C₂₄H₂₁F₆NO₇

CAS 1380424-42-9

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
549.40 g/mol

Updated on

In plain terms

KML29 is not a hemp molecule: it is a compound created in the laboratory. It blocks MAGL, the enzyme that normally destroys 2-AG, a cannabinoid the body makes itself, which raises its level in the mouse brain. It is used as a research tool in animals; it is not a consumer product.

Receptors and activity

Target network

MAGLInhibitorIC50 = 5.9 nM · humanlysates of HEK293T cells transfected with human MAGL, competitive activity-based protein profiling
  • Blocks or inhibits

The lower the cited value, the closer the target sits to KML29: 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 KML29.

Brain, side view
Body, front view
Blood

MAGLMAGL found in 5 regions of the body

  1. CortexdenseHighest PET signal in the cerebral cortex1
  2. Basal gangliapresentModerate levels in the putamen1
  3. HippocampuspresentAxon terminals in the hippocampus2
  4. Adipose tissuepresentPresent in subcutaneous adipose tissue3
  5. Immune cellspresentRNA enhanced in blood monocytes4

Map sources

  1. Takahata K et al. First-in-human in vivo imaging and quantification of monoacylglycerol lipase in the brain: a PET study with (18)F-T-401. Eur J Nucl Med Mol Imaging, 2022 (new tab)
  2. Ludányi A et al. Complementary synaptic distribution of enzymes responsible for synthesis and inactivation of the endocannabinoid 2-arachidonoylglycerol in the human hippocampus. Neuroscience, 2011 (new tab)
  3. Spoto B et al. Human adipose tissue binds and metabolizes the endocannabinoids anandamide and 2-arachidonoylglycerol. Biochimie, 2006 (new tab)
  4. Human Protein Atlas. MGLL expression summary (new tab)

Cited values

  1. MAGLInhibitorIC50 = 5.9 nM · human70 out of 100

    Chang et al., Chem Biol 2012 (new tab) · lysates of HEK293T cells transfected with human MAGL, competitive activity-based protein profiling

  2. MAGLInhibitorIC50 = 15 nM · mouse64 out of 100

    Chang et al., Chem Biol 2012 (new tab) · mouse brain membranes, competitive activity-based protein profiling

  3. MAGLInhibitorIC50 = 43 nM · rat56 out of 100

    Chang et al., Chem Biol 2012 (new tab) · rat brain membranes, competitive activity-based protein profiling

  4. ABHD6InhibitorIC50 = 4.9 µM · mouse22 out of 100

    Chang et al., Chem Biol 2012 (new tab) · mouse brain membranes, competitive activity-based protein profiling; 1.6 µM in the rat

  5. FAAHInhibitorno measured value cited
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

KML29 is a hexafluoroisopropyl carbamate that covalently inhibits monoacylglycerol lipase (MAGL), the enzyme that hydrolyses 2-arachidonoylglycerol (2-AG) (Chang et al. 2012). Its IC50 values are 5.9 nM on human MAGL, 15 nM in mice and 43 nM in rats, with no detectable cross-reactivity with FAAH and inhibition of ABHD6 at 4.87 µM in mice. In mice, it attenuated carrageenan-induced paw oedema and reversed mechanical allodynia, partially reversed allodynia in a sciatic nerve injury model and prevented diclofenac-induced gastric haemorrhages, without catalepsy, hypothermia or hypomotility (Ignatowska-Jankowska et al. 2014); at 10 mg/kg, Pasquarelli et al. (2015) observed hypothermia, analgesia and hypomotility without catalepsy. The antiallodynic effect underwent tolerance after repeated administration of a high dose, with CB1 desensitisation (Ignatowska-Jankowska et al. 2014). Combined with gabapentin, it additively reduced mechanical allodynia and synergistically reduced cold allodynia in a nerve injury model (Crowe et al. 2017). In the SOD1G93A mouse model of amyotrophic lateral sclerosis, oral administration delayed disease onset, progression and survival (Pasquarelli et al. 2017); in a rat model of cerebral ischaemia followed by PET, it eased the decline in accumulation of a MAGL tracer (Yamasaki et al. 2021). In rat cortical cultures, it increased the risk of neuronal death in the absence of glial cells, but not in mixed cultures (Rojo-Bustamante et al. 2020). All these data are preclinical.

Key sources.

History

Source
A synthetic molecule of the hexafluoroisopropyl carbamate class, absent from hemp and from any living organism. A preclinical research probe of the endocannabinoid system.

Origin

Research tool

No biosynthetic pathway: a synthetic molecule, a hexafluoroisopropyl carbamate carried by a piperidine.

Classification

Family, origin and source verification

Family

ECS pharmacological tool › Enzyme 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. Chang JW et al., Highly selective inhibitors of monoacylglycerol lipase bearing a reactive group that is bioisosteric with endocannabinoid substrates, Chem Biol 2012 (new tab)PMID 22542104
  2. Ignatowska-Jankowska BM et al., In vivo characterization of the highly selective monoacylglycerol lipase inhibitor KML29: antinociceptive activity without cannabimimetic side effects, Br J Pharmacol 2014 (new tab)PMID 23848221
  3. Pasquarelli N et al., Comparative biochemical characterization of the monoacylglycerol lipase inhibitor KML29 in brain, spinal cord, liver, spleen, fat and muscle tissue, Neuropharmacology 2015 (new tab)PMID 25497453
  4. Pasquarelli N et al., Evaluation of monoacylglycerol lipase as a therapeutic target in a transgenic mouse model of ALS, Neuropharmacology 2017 (new tab)PMID 28373073
  5. Crowe MS et al., The monoacylglycerol lipase inhibitor KML29 with gabapentin synergistically produces analgesia in mice, Br J Pharmacol 2017 (new tab)PMID 28963716
  6. Rojo-Bustamante E et al., CB2 Receptors and Neuron-Glia Interactions Modulate Neurotoxicity Generated by MAGL Inhibition, Biomolecules 2020 (new tab)PMID 32824740
  7. Yamasaki T et al., Neuroprotective effects of minocycline and KML29, a potent inhibitor of monoacylglycerol lipase, in an experimental stroke model: a small-animal positron emission tomography study, Theranostics 2021 (new tab)PMID 34646382
  8. ANSM, Consolidated list of substances classified as narcotics, updated 16 February 2026, annex IV (new tab)
  9. PubChem, compound CID 71656212 (KML29) (new tab)

Identifiers

Names

IUPAC name
1,1,1,3,3,3-hexafluoropropan-2-yl 4-[bis(1,3-benzodioxol-5-yl)-hydroxymethyl]piperidine-1-carboxylate
Other names
KML-29 · KML 29

Identifiers

Formula
C₂₄H₂₁F₆NO₇
CAS
1380424-42-9
PubChem CID
71656212(new tab)
InChIKey
SXHQLPHDBLTFPM-UHFFFAOYSA-N
SMILES
C1CN(CCC1C(C2=CC3=C(C=C2)OCO3)(C4=CC5=C(C=C4)OCO5)O)C(=O)OC(C(F)(F)F)C(F)(F)F

Machine-readable entry (JSON)

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