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Highly selective cannabinoid CB2 receptor inverse agonist. Binds with high affinity to rat, mouse and human CB2 receptors (Ki values are 0.38, 1.55 and 35.9 nM respectively). Produces anti-inflammatory effects in vivo.
|Storage||Store at RT|
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 438.48. 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||2.28 mL||11.4 mL||22.81 mL|
|5 mM||0.46 mL||2.28 mL||4.56 mL|
|10 mM||0.23 mL||1.14 mL||2.28 mL|
|50 mM||0.05 mL||0.23 mL||0.46 mL|
References are publications that support the biological activity of the product.
Iwamura et al (2001) In vitro and in vivo pharmacological characterization of JTE-907, a novel selective ligand for cannabinoid CB2 receptor. J.Pharmacol.Exp.Ther. 296 420 PMID: 11160626
Ueda et al (2005) Involvement of cannabinoid CB2 receptor-mediated response and efficacy of cannabinoid CB2 receptor inverse agonist, JTE 907, in cutaneous inflammation in mice. Eur.J.Pharmacol. 520 164 PMID: 16153638
Maekawa et al (2006) The cannabinoid CB2 receptor inverse agonist JTE-907 suppresses spontaneous itch-associated responses of NC mice, a model of atopic dermatitis. Eur.J.Pharmacol. 542 179 PMID: 16824511
If you know of a relevant reference for JTE 907, please let us know.
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Keywords: JTE 907, JTE 907 supplier, Selective, CB2, receptor, antagonists, inverse, agonists, cannabinoids, Receptors, JTE907, cb2r, 2479, Tocris Bioscience
9 Citations for JTE 907
Citations are publications that use Tocris products. Selected citations for JTE 907 include:
Wang et al (2016) Endothelial cation channel PIEZO1 controls blood pressure by mediating flow-induced ATP release. J Clin Invest 126 4527 PMID: 27797339
Sánchez-Blázquez et al (2013) Cannabinoid receptors couple to NMDA receptors to reduce the production of NO and the mobilization of zinc induced by glutamate. Antioxid Redox Signal 19 1766 PMID: 23600761
Marini et al (2013) Characterization of cannabinoid receptor ligands in tissues natively expressing cannabinoid CB2 receptors. Br J Pharmacol 169 887 PMID: 23711022
Vicente-Sánchez et al (2013) HINT1 protein cooperates with cannabinoid 1 receptor to negatively regulate glutamate NMDA receptor activity. Mol Brain 6 42 PMID: 24093505
Price et al (2009) WIN55,212-2, a cannabinoid receptor agonist, protects against nigrostriatal cell loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. Eur J Neurosci 29 2177 PMID: 19490092
Tan and Cao (2018) Cannabinoid WIN-55,212-2 mesylate inhibits tumor necrosis factor-α-induced expression of nitric oxide synthase in dorsal root ganglion neurons. Int J Mol Med 42 919 PMID: 29786105
Kong et al (2016) Cannabinoid WIN-55,212-2 mesylate inhibits ADAMTS-4 activity in human osteoarthritic articular chondrocytes by inhibiting expression of syndecan-1. Mol Cell Neurosci 13 4569 PMID: 27082728
Zhou et al (2015) Regional effects of endocannabinoid, BDNF and FGF receptor signalling on neuroblast motility and guidance along the rostral migratory stream. Br J Pharmacol 64 32 PMID: 25481343
Mair et al (2010) Interaction between anandamide and sphingosine-1-phosphate in mediating vasorelaxation in rat coronary artery. Br J Pharmacol 161 176 PMID: 20718749
Do you know of a great paper that uses JTE 907 from Tocris? Please let us know.
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Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.