Potent MTH1 inhibitor (IC50 = 72 nM). Induces DNA damage and disrupts nucleotide pool homeostasis in cancer cells. Also attenuates colony formation of KRAS-mutated PANC1 cells in vitro. Suppresses tumor growth ~50% in a colon cancer carcinoma xenograft model.
Sold for research purposes under agreement from Pfizer Inc
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|1eq. HCl||9.01||20mM with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 450.34. Batch specific molecular weights may vary from batch to batch due to solvent 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||2.22 mL||11.1 mL||22.21 mL|
|5 mM||0.44 mL||2.22 mL||4.44 mL|
|10 mM||0.22 mL||1.11 mL||2.22 mL|
|50 mM||0.04 mL||0.22 mL||0.44 mL|
References are publications that support the products' biological activity.
Huber et al (2014) Stereospecific targeting of MTH1 by (S)-crizotinib as an anticancer strategy. Nature 508 222 PMID: 24695225
If you know of a relevant reference for (S)-Crizotinib, please let us know.
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Keywords: (S)-Crizotinib, supplier, potent, MTH1, inhibitors, inhibits, ras, transformation, anticancer, hydrolases, g, proteins, mutT, homologue, NUDT1, nucleotide, pool, homeostasis, DNA, damage, G, Proteins, (Small), MutT, homolog-1, (MTH1), MutT, homolog-1, (MTH1), Tocris Bioscience
Citations for (S)-Crizotinib
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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* or download your copy today!
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Cancer Metabolism Poster
Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the main targets for cancer metabolism researchers. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways. These distinct metabolic circuits could provide viable cancer therapeutic targets.
Epigenetics in Cancer Poster
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.