| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 100mg | 电议 |
Cell lines | MDA-MB-468, MDA-MB-231, MCF-7 and MDA-MB-435 cells |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
Reaction Conditions | 1 μM, 48 hours |
Applications | Effects on cell morphology were observed at a concentration of 1 μM SKI-606 for all cell lines examined, and morphological changes were apparent at concentrations as low as 0.25 μM. SKI-606 caused the cells to adhere to each other, forming dense clusters as compared to vehicle control (DMSO) treated cells, which showed spreading over larger areas. |
Animal models | Female athymic nude mice bearing human pancreas xenografts (P281 or P420) |
Dosage form | Oral administration, 100 mg/Kg/d, for 28 days |
Applications | Two xenografts, one sensitive (P281) and one resistant (P420), were chosen to assess pharmacodynamic changes by Western blot after treatment with bosutinib. Four different samples were analyzed from P281and P420, and optical scanning was done. The sensitive xenograft P281showed decreased posttreatment Src, STAT-5, p-STAT-5, p-Akt, MAPK, and EGFR. Bosutinib-treated P281showed a marked increase in cleaved PARP. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | Bosutinib (SKI-606) is a potent inhibitor of Src and Abl kinases with IC50 of 1.2 nM and 1 nM [1]. In chronic myelogenous leukemia (CML) cells, SKI-606 inhibited phosphorylation of Bcr-Abl, Src and Stat5. It also ablated the expression of v-Abl in fibroblasts and blocked proliferation of CML cells [2]. In colorectal cancer cells, SKI-606 inhibited Src autophosphorylation with an IC50 of ~ 0.25 μM, and simultaneity suppressed Tyr (925) phosphorylation of a Src substrate [3]. SKI-606 blocked beta-catenin function by inhibiting its binding to the TCF4 transcription factor and dose-dependently suppressed cyclin D1. SKI-606 increased its binding affinity of beta-catenin to E-cadherin and adhesion, with ensuing reduced motility in a wound healing assay [4]. Oral administration of SKI-606 at 100 mg/kg for 5 days causes complete regression of large K562 xenografts in nude mice [2]. [1]. Boschelli DH, Ye F, Wang YD, Dutia M, Johnson SL, Wu B, Miller K, Powell DW, Yaczko D, Young M, Tischler M, Arndt K, Discafani C, Etienne C, Gibbons J, Grod J, Lucas J, Weber JM, Boschelli F. Optimization of 4-phenylamino-3-quinolinecarbonitriles as potent inhibitors of Src kinase activity. J Med Chem. 2001 Nov 8;44(23):3965-77. References: |
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