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Potent and selective MAGL inhibitor. Blocks hydrolysis of the endocannabinoid 2-arachidonyl glycerol (2-AG) in vivo in the mouse brain (IC50 = 8 nM). Potentiates depolarization-induced suppression of excitability in cerebellar Purkinje neurons. Exhibits >300-fold selectivity for MAGL over FAAH in vitro. Attenuates nociception in neuropathic and inflammatory pain models. Also reduces free fatty acid levels in primary tumors.
Sold under license from The Scripps Research Institute.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 520.49. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.92 mL||9.61 mL||19.21 mL|
|5 mM||0.38 mL||1.92 mL||3.84 mL|
|10 mM||0.19 mL||0.96 mL||1.92 mL|
|50 mM||0.04 mL||0.19 mL||0.38 mL|
References are publications that support the biological activity of the product.
Long et al (2009) Selective blockade of 2-arachidonylglycerol hydrolysis produces cannabinoid behavioral effects. Nat.Chem.Biol. 5 37 PMID: 19029917
Pan et al (2009) Blockade of 2-arachidonylglycerol hydrolysis by selective monoacylglycerol lipase inhibitor 4-nitrophenyl 4-(dibenzo[d][1,3]dioxol-5-yl(hydroxy)methyl)piperidine-1-carboxylate (JZL184) enhances retrograde endocannabinoid signaling. J.Pharm.Exp.Ther. 331 591 PMID: 19666749
Kinsey et al (2013) Repeated low-dose administration of the monoacylglycerol lipase inhibitor JZL184 retains cannabinoid receptor type 1-mediated antinociceptive and gastroprotective effects. J.Pharmacol.Exp.Ther. 345 492 PMID: 23412396
Zhang et al (2012) Dysregulated lipid metabolism in cancer. World J.Biol.Chem. 3 167 PMID: 22937213
If you know of a relevant reference for JZL 184, please let us know.
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Keywords: JZL 184, JZL 184 supplier, JZL184, MAGL, inhibitor, MAG, lipase, monoacylglycerol, inhibitors, inhibits, MGL, 3836, Tocris Bioscience
7 Citations for JZL 184
Citations are publications that use Tocris products. Selected citations for JZL 184 include:
Argueta et al (2019) Cannabinoid CB1 Receptors Inhibit Gut-Brain Satiation Signaling in Diet-Induced Obesity. Front Physiol 10 704 PMID: 31281260
Bashashati et al (2015) Inhibiting endocannabinoid biosynthesis: a novel approach to the treatment of constipation. Br J Pharmacol 172 3099 PMID: 25684407
Hu et al (2019) Endocannabinoid Signaling Mediates Local Dendritic Coordination between Excitatory and Inhibitory Synapses. Cell Rep 27 666 PMID: 30995465
Sardinha et al (2014) Experimental cannabinoid 2 receptor-mediated immune modulation in sepsis. Front Cell Neurosci 2014 978678 PMID: 24803745
Martin et al (2015) Endocannabinoids Mediate Muscarinic Acetylcholine Receptor-Dependent Long-Term Depression in the Adult Medial Prefrontal Cortex. Stem Cells Dev 9 457 PMID: 26648844
Valdeolivas et al (2013) The inhibition of 2-arachidonoyl-glycerol (2-AG) biosynthesis, rather than enhancing striatal damage, protects striatal neurons from malonate-induced death: a potential role of cyclooxygenase-2-dependent metabolism of 2-AG. Cell Death Dis 4 e862 PMID: 24136226
Malenczyk et al (2013) CB1 cannabinoid receptors couple to focal adhesion kinase to control Ins release. J Biol Chem 288 32685 PMID: 24089517
Do you know of a great paper that uses JZL 184 from Tocris? Please let us know.
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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The key feature of drug addiction is the inability to stop using a drug despite clear evidence of harm. This poster describes the brain circuits associated with addiction, and provides an overview of the main classes of addictive drugs and the neurotransmitter systems that they target.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.