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Biological Activity for GW 441756
GW 441756 is a potent, selective inhibitor of the NGF receptor tyrosine kinase A (TrkA) (IC50 = 2 nM). Displays > 100-fold selectivity over a range of other kinases.
Sold for research purposes under agreement from GlaxoSmithKline.
Technical Data for GW 441756
|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.
Solubility Data for GW 441756
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for GW 441756
The following data is based on the product molecular weight 275.31. 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|
|0.15 mM||24.22 mL||121.08 mL||242.15 mL|
|0.75 mM||4.84 mL||24.22 mL||48.43 mL|
|1.5 mM||2.42 mL||12.11 mL||24.22 mL|
|7.5 mM||0.48 mL||2.42 mL||4.84 mL|
References for GW 441756
References are publications that support the biological activity of the product.
Wood et al (2004) Discovery and in vitro evaluation of potent TrkA kinase inhibitors: oxindole and aza-oxindoles. Bioorg.Med.Chem.Lett. 14 953 PMID: 15013000
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Keywords: GW 441756, GW 441756 supplier, Potent, selective, TrkA, inhibitors, inhibits, Neurotrophin, Receptors, Receptor, Tyrosine, Kinases, RTKs, GW441756, GlaxoSmithKline, GSK, Trk, 2238, Tocris Bioscience
5 Citations for GW 441756
Citations are publications that use Tocris products. Selected citations for GW 441756 include:
Lawn et al (2015) Neurotrophin signaling via TrkB and TrkC receptors promotes the growth of brain tumor-initiating cells. Nat Chem Biol 290 3814 PMID: 25538243
Edwards et al (2011) Effect of brain- and tumor-derived connective tissue growth factor on glioma invasion. J Natl Cancer Inst 103 1162 PMID: 21771732
Donatien et al (2018) Granulocyte-macrophage colony-stimulating factor receptor expression in clinical pain disorder tissues and role in neuronal sensitization. Pain Rep 3 e676 PMID: 30534627
Rees et al (2016) Correlating chemical sensitivity and basal gene expression reveals mechanism of action. Oncotarget 12 109 PMID: 26656090
Wang et al (2008) Cellular assays for high-throughput screening for modulators of Trk receptor tyrosine kinases. Curr Chem Genomics 1 27 PMID: 20161825
Do you know of a great paper that uses GW 441756 from Tocris? Please let us know.
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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.
Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
Huntington's Disease Poster
Huntington's disease (HD) is a monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the MSN intracellular signaling pathways implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
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.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.