Potent EP4 receptor antagonist (IC50 = 59 nM). Suppresses EP4-mediated Th1 differentiation, Th17 cell expansion, and IL-23 secretion by activated dendritic cells. Inhibits Th1 and Th17 cytokine production, suppresses collagen- and GPI-induced arthritis in mice. Attenuates CFA-induced inflammatory pain in rats. Analgesic. Orally bioavailable.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|ethanol||2.45||5mM with gentle warming|
|DMSO||0.98||2mM with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 489.65. Batch specific molecular weights may vary from batch to batch due to solvent 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||2.04 mL||10.21 mL||20.42 mL|
|5 mM||0.41 mL||2.04 mL||4.08 mL|
|10 mM||0.2 mL||1.02 mL||2.04 mL|
|50 mM||0.04 mL||0.2 mL||0.41 mL|
References are publications that support the products' biological activity.
Chen et al (2010) A novel antagonist of the prostaglandin E2 EP4 receptor inhibits Th1 differentiation and Th17 expansion and is orally active in arthritis models. Br.J.Pharmacol. 160 292 PMID: 20423341
Jones et al (2016) Role of EP2 and EP4 receptors in airway microvascular leak induced by prostaglandin E2. Br.J.Pharmacol. 173 992 PMID: 26639895
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Literature in this Area
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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.