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Potent and selective NUAK1/2 inhibitor (IC50 values are 20 and 100 nM respectively). Exhibits no significant inhibition against a panel of 139 kinases, including ten AMPK family members. Inhibits NUAK1-mediated MYPT1 phosphorylation. Also inhibits cell proliferation in U2OS cells.
External Portal Information
Chemicalprobes.org is a portal that offers independent guidance on the selection and/or application of small molecules for research. The use of WZ 4003 is reviewed on the chemical probes website.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|DMSO||9.94||20 with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 496.99. 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|
|0.5 mM||4.02 mL||20.12 mL||40.24 mL|
|2.5 mM||0.8 mL||4.02 mL||8.05 mL|
|5 mM||0.4 mL||2.01 mL||4.02 mL|
|25 mM||0.08 mL||0.4 mL||0.8 mL|
References are publications that support the biological activity of the product.
Zhou et al (2009) Novel mutant-selective EGFR kinase inhibitors against EGFR T790M. Nature 462 1070 PMID: 20033049
Banerjee et al (2014) Interplay between Polo kinase, LKB1-activated NUAK1 kinase, PP1βMYPT1 phosphatase complex and the SCFβTrCP E3 ubiquitin ligase. Biochem.J. 461 233 PMID: 24785407
Banerjee et al (2014) Characterization of WZ4003 and HTH-01-015 as selective inhibitors of the LKB1-tumour-suppressor-activated NUAK kinases. Biochem.J. 457 215 PMID: 24171924
If you know of a relevant reference for WZ 4003, please let us know.
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.