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NSC 146109 hydrochloride
Cell-permeable, genotype-selective antitumor agent that activates p53-dependent transcription. Increases levels of endogenous p53 in tumor cells and protects p53 from Mdm2-mediated degradation. Displays some selectivity for tumor cells vs. normal cells in an MTT cell viability assay.
|Storage||Desiccate 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|
Preparing Stock Solutions
The following data is based on the product molecular weight 316.85. 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|
|1 mM||3.16 mL||15.78 mL||31.56 mL|
|5 mM||0.63 mL||3.16 mL||6.31 mL|
|10 mM||0.32 mL||1.58 mL||3.16 mL|
|50 mM||0.06 mL||0.32 mL||0.63 mL|
References are publications that support the biological activity of the product.
Dolma et al (2003) Identification of genotype-selective antitumor agents using synthetic lethal chemical screening in engineered human tumor cells. Cancer Cell 3 285 PMID: 12676586
Berkson et al (2005) Pilot screening programme for small molecule activators of p53. Int.J.Cancer 115 701 PMID: 15729694
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1 Citation for NSC 146109 hydrochloride
Citations are publications that use Tocris products. Selected citations for NSC 146109 hydrochloride include:
Calo et al (2018) Tissue-selective effects of nucleolar stress and rDNA damage in developmental disorders. Nature 554 112 PMID: 29364875
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Literature in this Area
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.