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Biological Activity for BAY-u 3405
BAY-u 3405 is a potent dual antagonist of TP/DP2 (CRTH2) prostanoid receptors (Ki values are 4.3, 4.5 and > 10000 nM for hDP2, hTP and hDP1 receptors respectively). Suppresses PGD2-induced migration of human eosinophils (IC50 = 170 nM).
Technical Data for BAY-u 3405
|Storage||Desiccate 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.
Solubility Data for BAY-u 3405
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for BAY-u 3405
The following data is based on the product molecular weight 416.47. 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||2.4 mL||12.01 mL||24.01 mL|
|5 mM||0.48 mL||2.4 mL||4.8 mL|
|10 mM||0.24 mL||1.2 mL||2.4 mL|
|50 mM||0.05 mL||0.24 mL||0.48 mL|
References for BAY-u 3405
References are publications that support the biological activity of the product.
Sundstrom et al (2003) Interactions among three classes of mediators explain antigen-induced bronchoconstriction in the isolated perfused and ventilated guinea pig lung. J.Pharmacol.Exp.Ther. 307 408 PMID: 12954791
Ishizuka et al (2004) Ramatroban (BAY u3405): a novel dual antagonist of TXA2 receptor and CRTh2, a newly identified prostaglandin D2 receptor. Cardiovasc.Drug Rev. 22 71 PMID: 15179446
Ulven and Kostenis (2005) Minor structural modifications convert the dual TP/CRTH2 antagonist ramatroban into a highly selective and potent CRTH2 antagonist. J.Med.Chem. 48 897 PMID: 15715457
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Keywords: BAY-u 3405, BAY-u 3405 supplier, Dual, TP/DP2, CRTH2, receptors, antagonists, Prostanoid, prostaglandins, prostacyclins, eicosanoids, BAY-u3405, Ramatroban, Receptors, 2732, Tocris Bioscience
Citations for BAY-u 3405
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Reviews for BAY-u 3405
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HL-1 cardiomyocytes were pre-incubated with BAY-u 3405 (2 µM, 30 min) followed by treatment with 15d-PGJ2 (15 µM, 30 min) to follow p38 activation using Western blot analysis. BAY-u 3405 completely abolished 15d-PGJ2-induced p38 phosphorylation.
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.