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Tripeptide substance P (SP) antagonist (IC50 = 90 μM). Also inhibits binding of SP to Mas-related GPCR (MRGPR) X2. Inhibits SP-induced IgE-independent degranulation of mast cells in vitro. Inhibits compound 48/80-induced MRGPRX2 activation and scratching in mice in vivo.
(Modifications: Gln-1 = N-terminal Boc, Trp-2 = D-Trp (Formyl), Phe-3 = Phe-OBzl)
|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.
|Solubility||Soluble to 10 mg/ml in DMSO|
References are publications that support the biological activity of the product.
Hagiwara et al (1992) Studies on neurokinin antagonists. 1. The design of novel tripeptides possessing the glutaminyl-D-tryptophylphenylalanine sequence as substance P antagonists. J.Med.Chem. 35 2015 PMID: 1375965
Azimi et al (2016) Dual action of neurokinin-1 antagonists on Mas-related GPCRs. JCI Insight. 1 e89362 PMID: 27734033
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Keywords: QWF, QWF supplier, substance, P, antagonist, antagonism, NK1R, neurokinin, 1, mas-related, GPCR, X2, MRGPRX2, mast, cell, degranulation, SP, MRGX2, Mas-related, G, Protein-Coupled, Receptors, NK1, Receptor, 6642, Tocris Bioscience
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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.