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Biological Activity for LY 2603618
LY 2603618 is a potent and selective Chk1 inhibitor (IC50 = 7 nM). Inhibits Chk1 autophosphorylation. Induces cell cycle arrest in the G2/M phase and induces the DNA damage response in lung cancer cells. Inhibits growth of NSCLC xenografts in mice when administered in combination with Pemetrexed (Cat.No. 6185).
Compound Libraries for LY 2603618
Technical Data for LY 2603618
|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.
Solubility Data for LY 2603618
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for LY 2603618
The following data is based on the product molecular weight 436.3. 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|
|0.2 mM||11.46 mL||57.3 mL||114.6 mL|
|1 mM||2.29 mL||11.46 mL||22.92 mL|
|2 mM||1.15 mL||5.73 mL||11.46 mL|
|10 mM||0.23 mL||1.15 mL||2.29 mL|
References for LY 2603618
References are publications that support the biological activity of the product.
Wang et al (2014) The checkpoint 1 kinase inhibitor LY2603618 induces cell cycle arrest, DNA damage response and autophagy in cancer cells. Apoptosis 19 1389 PMID: 24928205
Calvo et al (2014) Preclinical analyses and phase I evaluation of LY2603618 administered in combination with pemet. and cisp. in patients with advanced cancer. Invest.New Drugs 32 955 PMID: 24942404
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Citations for LY 2603618
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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.