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(S)-Crizotinib is a 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
(S)-Crizotinib is also offered as part of the Tocriscreen 2.0 Max. Find out more about compound libraries available from Tocris.
|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|
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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Keywords: (S)-Crizotinib, (S)-Crizotinib supplier, potent, MTH1, inhibitors, inhibits, ras, transformation, anticancer, hydrolases, g, proteins, mutT, homologue, NUDT1, nucleotide, pool, homeostasis, DNA, damage, MutT, homolog-1, (MTH1), 6025, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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This poster summarizes the main metabolic pathways in cancer cells and highlights potential targets for cancer therapeutics. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways providing potential cancer therapeutic targets.
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.