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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.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|1eq. HCl||9.01||20 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 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||4.44 mL||22.21 mL||44.41 mL|
|2.5 mM||0.89 mL||4.44 mL||8.88 mL|
|5 mM||0.44 mL||2.22 mL||4.44 mL|
|25 mM||0.09 mL||0.44 mL||0.89 mL|
References are publications that support the biological activity of the product.
Huber et al (2014) Stereospecific targeting of MTH1 by (S)-crizotinib as an anticancer strategy. Nature 508 222 PMID: 24695225
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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* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.