Skip to content

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

Research tools

MJN110

A covalent MAGL inhibitor, a research tool for 2-AG; no human data.

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.

C₂₂H₂₁Cl₂N₃O₄

CAS 1438416-21-7

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
462.30 g/mol

Updated on

In plain terms

MJN110 is not a hemp molecule: it is a laboratory compound created by American chemists and described in 2013. It blocks an enzyme in the body, MAGL, which normally destroys 2-AG, a cannabinoid the body makes itself. By slowing this enzyme, it lets this natural messenger build up in animals; no human study was found and it is in no consumer product.

Receptors and activity

Target network

MAGLInhibitorIC50 = 0.4 nM · humanrecombinant human MAGL, 2-AG hydrolysis; 2.1 nM in mouse brain homogenate
  • Blocks or inhibits

The lower the cited value, the closer the target sits to MJN110: 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 MJN110.

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 = 0.4 nM · human90 out of 100

    Niphakis et al., ACS Chem Neurosci 2013 (new tab) · recombinant human MAGL, 2-AG hydrolysis; 2.1 nM in mouse brain homogenate

  2. 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

MJN110 is a covalent inhibitor of monoacylglycerol lipase (MAGL), the enzyme responsible for hydrolysing the main brain endocannabinoid, 2-arachidonoylglycerol (2-AG). It belongs to the class of N-hydroxysuccinimide carbamates and acts by carbamylating the nucleophilic serine of the enzyme (Niphakis et al., ACS Chem Neurosci 2013, PMID 23731016). In mice it raises brain 2-AG 2-fold at 0.5 mg/kg by mouth and 10-fold at 5 mg/kg, without notable change in anandamide-type amides and with a fall in arachidonic acid; an oral dose of 1 mg/kg inhibits brain MAGL by about 70% from 1 hour, an effect maintained up to 12 hours and almost entirely gone at 72 hours (Niphakis 2013). MJN110 attenuated mechanical allodynia in a rat model of diabetic neuropathy (Niphakis 2013), had an opioid-sparing effect in a mouse model of neuropathic pain (Wilkerson et al. 2016) and suppressed neuroinflammation in a mouse model of repeated traumatic brain injury (Selvaraj et al. 2021). In mice it serves as a discriminative stimulus, an effect blocked by rimonabant (Owens et al. 2017), and repeated treatment produced partial tolerance in females and desensitisation of CB1 receptors (Diester et al. 2024). No clinical trial was found.

Key sources.

History

Source
A wholly synthetic molecule, absent from hemp and from every living organism. It has never been identified in a plant or in an animal tissue, and remains distributed exclusively as a reagent intended for preclinical research on the endocannabinoid system.

Origin

Research tool

No known biosynthetic pathway: MJN110 does not exist in nature and no organism produces it. It is a synthetic molecule of the class of N-hydroxysuccinimide carbamates carried by a piperazine.

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. Niphakis MJ et al., ACS Chem Neurosci 2013: N-hydroxysuccinimide carbamates, endocannabinoid hydrolase inhibitors (original MJN110 paper) (new tab)PMID 23731016
  2. Wilkerson JL et al., J Pharmacol Exp Ther 2016: opioid-sparing effects of MJN110 (new tab)PMID 26791602
  3. Owens RA et al., Neuropharmacology 2017: discriminative stimulus of MJN110 mediated by CB1 (new tab)PMID 28673548
  4. Selvaraj P et al., Cells 2021: MJN110 and neuroinflammation after repeated traumatic brain injury (new tab)PMID 34943962
  5. Diester CM et al., J Pharmacol Exp Ther 2024: repeated MJN110 treatment, tolerance and CB1 desensitisation (new tab)PMID 38262742
  6. PubChem, MJN110, CID 71722059 (identifiers and structural descriptors; CAS 1438416-21-7) (new tab)
  7. ANSM, consolidated list of substances classified as narcotics (updated 16/02/2026) (new tab)

Identifiers

Names

IUPAC name
(2,5-dioxopyrrolidin-1-yl) 4-[bis(4-chlorophenyl)methyl]piperazine-1-carboxylate
Other names
MJN-110

Identifiers

Formula
C₂₂H₂₁Cl₂N₃O₄
CAS
1438416-21-7
PubChem CID
71722059(new tab)
InChIKey
BEADRWVIFHOSGN-UHFFFAOYSA-N
SMILES
C1CC(=O)N(C1=O)OC(=O)N2CCN(CC2)C(C3=CC=C(C=C3)Cl)C4=CC=C(C=C4)Cl

Machine-readable entry (JSON)

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