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BAY 1816032 is a potent and selective inhibitor of BUB1 kinase, a mitotic checkpoint serine/threonine kinase (IC50 = 6.1 nM). BAY 1816032 shows 17-fold selectivity over a panel of 403 other human kinases. In vivo, BAY 1816032 decreases tumor size in tumor xenograft models. BAY 181603 is orally bioavailable.
BAY 1816032 is also offered as part of the Tocriscreen Kinase Inhibitor Library. Find out more about compound libraries available from Tocris.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
The following data is based on the product molecular weight 534.52. 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||3.74 mL||18.71 mL||37.42 mL|
|2.5 mM||0.75 mL||3.74 mL||7.48 mL|
|5 mM||0.37 mL||1.87 mL||3.74 mL|
|25 mM||0.07 mL||0.37 mL||0.75 mL|
References are publications that support the biological activity of the product.
Siemeister et al (2019) Inhibition of BUB1 kinase by BAY 1816032 sensitizes tumor cells toward taxanes, ATR, and PARP inhibitors in vitro and in vivo. Clin.Cancer Res. 25 1404 PMID: 30429199
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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 product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
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.