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Biological Activity for QWF
QWF is a 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.
Technical Data for QWF
(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 Data for QWF
|Solubility||Soluble to 10 mg/ml in DMSO|
References for QWF
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
1 Citation for QWF
Citations are publications that use Tocris products. Selected citations for QWF include:
Song and Shim et al (2021) Lithocholic Acid Activates Mas-Related G Protein-Coupled Receptors, Contributing to Itch in Mice Biomol Ther (Seoul) PMID: 34263729
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Protocols for QWF
The following protocol features additional information for the use of QWF (Cat. No. 6642).
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!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.