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Research tools

JZL195

Dual FAAH/MAGL inhibitor, a research tool for the endocannabinoid system.

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.

C₂₄H₂₃N₃O₅

CAS 1210004-12-8

Family
ECS pharmacological toolEnzyme inhibitor
Molar mass
433.50 g/mol

Updated on

In plain terms

JZL195 is a laboratory molecule, obtained by chemical synthesis: it exists neither in hemp nor in any plant. It blocks the two enzymes that normally destroy anandamide and 2-AG, two cannabinoids the body makes. It is used for research in animals; the data cited are preclinical.

Receptors and activity

Target network

FAAHInhibitorIC50 = 2 nMsubstrate hydrolysis, recombinant enzyme expressed in COS7 cells or brain membranes; 13 nM by competitive activity-based protein profiling in mouse brain
  • Blocks or inhibits
  • Binds or modulates

The lower the cited value, the closer the target sits to JZL195: 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 JZL195.

Brain, side view
Body, front view
Blood

FAAHFAAH found in 7 regions of the body

  1. CortexpresentCortical pyramidal neurons1
  2. Basal gangliapresentStriatal neurons1
  3. HypothalamuspresentPresent in hypothalamic nuclei1
  4. CerebellumpresentPurkinje cells and cerebellar layers1
  5. BrainstempresentInferior olivary nuclei1
  6. Adipose tissuepresentExpressed in mature adipocytes2
  7. BonepresentPresent on osteoclasts3

Map sources

  1. Romero J et al. Fatty acid amide hydrolase localization in the human central nervous system: an immunohistochemical study. Brain Res Mol Brain Res, 2002 (new tab)
  2. Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
  3. Rossi F et al. The endovanilloid/endocannabinoid system in human osteoclasts: possible involvement in bone formation and resorption. Bone, 2009 (new tab)

Cited values

  1. FAAHInhibitorIC50 = 2 nM78 out of 100

    Long et al., PNAS 2009 (new tab) · substrate hydrolysis, recombinant enzyme expressed in COS7 cells or brain membranes; 13 nM by competitive activity-based protein profiling in mouse brain

  2. MAGLInhibitorIC50 = 4 nM73 out of 100

    Long et al., PNAS 2009 (new tab) · substrate hydrolysis, recombinant enzyme expressed in COS7 cells or brain membranes; 19 nM by competitive activity-based protein profiling in mouse brain

  3. ABHD6Inhibitorno measured value cited
  4. CB1Binding (function not established)no 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

JZL195 is an N-(3-phenoxybenzyl) piperazine carbamate that covalently inhibits two serine hydrolases of the endocannabinoid system: FAAH, which breaks down anandamide, and MAGL, which breaks down 2-arachidonoylglycerol. Its IC50 values are 2 nM on FAAH and 4 nM on MAGL in substrate hydrolysis assays, with no notable binding to CB1 or CB2 (IC50 above 20 µM). In mice, it produced broad activity in the tetrad test for CB1 agonism (analgesia, hypomotility, catalepsy). Comparison with specific FAAH and MAGL inhibitors distinguished processes regulated by a single pathway (hypomotility by the 2-AG/MAGL pathway) and others where inhibiting both enzymes had additive effects reversed by a CB1 antagonist; this is the case for drug discrimination, where dual blockade, but not inhibition of either enzyme alone, produced THC-like responses reversed by a CB1 antagonist (Long et al. 2009). In spontaneously hypertensive rats, a single administration produced weak, dose-dependent hypotensive and bradycardic responses, absent in normotensive rats, and chronic treatment prevented the progression of hypertension without tolerance (Toczek et al. 2023). All these data are preclinical.

Key sources.

History

Source
A synthetic molecule of the piperazine carbamate class, absent from hemp and from any living organism. A research reagent.

Origin

Research tool

No known biosynthetic pathway: JZL195 has no plant precursor or enzymatic origin; it is a synthetic piperazine carbamate.

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)

JZL195 (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. Long JZ, Nomura DK, Vann RE et al., Dual blockade of FAAH and MAGL identifies behavioral processes regulated by endocannabinoid crosstalk in vivo, PNAS 2009;106(48):20270-20275 (new tab)PMID 19918051
  2. Toczek M, Ryszkiewicz P, Remiszewski P et al., Weak Hypotensive Effect of Chronic Administration of the Dual FAAH/MAGL Inhibitor JZL195 in Spontaneously Hypertensive Rats as Revealed by Area under the Curve Analysis, Int J Mol Sci 2023;24(13):10942 (new tab)PMID 37446125
  3. ANSM, Consolidated list of substances classified as narcotics, updated 16 February 2026, annex IV (new tab)
  4. PubChem, JZL195 compound record (CID 46232606) (new tab)

Identifiers

Names

IUPAC name
(4-nitrophenyl) 4-[(3-phenoxyphenyl)methyl]piperazine-1-carboxylate
Other names
JZL-195

Identifiers

Formula
C₂₄H₂₃N₃O₅
CAS
1210004-12-8
PubChem CID
46232606(new tab)
InChIKey
QNYRAEKLMNDRFY-UHFFFAOYSA-N
SMILES
c1ccc(cc1)Oc2cccc(c2)CN3CCN(CC3)C(=O)Oc4ccc(cc4)[N+](=O)[O-]

Machine-readable entry (JSON)

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