Molecular Formula | C25H30N2O2 |
Molar Mass | 390.52 |
Density | 1.100±0.06 g/cm3(Predicted) |
Melting Point | 126 °C |
Boling Point | 590.6±50.0 °C(Predicted) |
Solubility | Soluble in DMSO. |
Appearance | powder |
Color | white to beige |
pKa | 10.30±0.36(Predicted) |
Storage Condition | -20°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 3 months. |
In vitro study | SU1498 stimulates accumulation of phosphorylated ERKs in human umbilical vein endothelial cells and in human aortic endothelial cells in a manner that is dependent on the functioning of the upstream components of the MAPK pathway, B-Raf, and MEK kinases. The enhanced accumulation of phospho-ERKs is observed only in cells that have been stimulated with sphingosine 1-phosphate or protein growth factors; SU1498 by itself is ineffective. SU1498 blocks signal transduction from VEGFR2 in MS1 VEGF cells.In the presence of SU1498, levels of Ets-1 are decreased, suggesting that VEGF-VEGFR-2 interactions contributed to baseline levels of Ets-1 expression, and interruption of this autocrine interaction with SU1498 led to decreased expression of Ets-1. SU1498 treatment significantly impacts U87 cell proliferation and apoptosis. SU1498 induces a marked increase in lipids and a decrease in glycerophosphocholine. Accordingly, accumulation of lipid droplets is seen in the cytoplasm of SU1498-treated U87 cells. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.561 ml | 12.803 ml | 25.607 ml |
5 mM | 0.512 ml | 2.561 ml | 5.121 ml |
10 mM | 0.256 ml | 1.28 ml | 2.561 ml |
5 mM | 0.051 ml | 0.256 ml | 0.512 ml |
biological activity | SU1498 is a KDR inhibitor with an IC50 of 0.7 μM, which can stimulate the accumulation of phosphorylated ERK1/2 in endothelial cells. |
target | TargetValue KDR () |
Target | Value |
in vitro study | SU1498 stimulates accumulation of phosphorylated ERKs in human umbilical vein endothelial cells and in human aortic endothelial cells in a manner that is dependent on the functioning of the upstream components of the MAPK pathway, B- Raf, and MEK kinases. The enhanced accumulation of phospho-ERKs is observed only in cells that have been stimulated with sphingosine 1-phosphate or protein growth factors; SU1498 by self is ineffective. SU1498 blocks signal transduction from VEGFR2 in MS1 VEGF cells.In the presence of SU1498, levels of Ets-1 are decreased, suggesting that VEGF-VEGFR-2 interactions contributed to baseline levels of Ets-1 expression, and interruption of this autocrine interaction with SU1498 led to decreased expression of Ets-1. SU1498 treatment significantly impacts U87 cell proliferation and apoptosis. SU1498 induces a marked increase in lipds and a decrease in glycerophosphocholine. Accordingly, accumulation of lipid droplets is seen in the cytoplasm of SU1498-treated U87 cells. |