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SU-1498 is a selective inhibitor of the VEGFR2, which inhibits Flk-1 with an IC50 value of 700 nM.
In vitro: 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. SU 1498 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. SU-1498 induces a marked increase in lipids and a decrease in glycerophosphocholine.
| Cell Experiment | |
|---|---|
| Cell lines | U87 cells |
| Preparation method | For cell proliferation assay, SU1498 is prepared as a stock solution of 30 mM in DMSO, then diluted with culture medium to working concentrations before use. U87 cells are seeded in 24-well plates (30,000 cells/well) and allowed to attach overnight. Cells are then treated for 24 or 72 h with different concentrations of Bevacizumab (from 10 ng/mL to 250 µg/mL) or SU1498 (from 1 µM to 30 µM) in triplicate wells. The cell viability is then assessed with the MTT assay. |
| Concentrations | From 1 µM to 30 µM |
| Incubation time | 24 or 72 h |
| Animal Experiment | |
|---|---|
| Animal models | |
| Formulation | |
| Dosages | |
| Administration | |
| Molecular Weight | 390.52 |
| Formula | C25H30N2O2 |
| CAS Number | 168835-82-3 |
| Solubility (25°C) | DMSO: 100 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
[1] Mesti T, et al. PLoS One. Metabolic impact of anti-angiogenic agents on U87 glioma cells.
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| (Z)-Orantinib
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| (Rac)-SAR131675
(Rac)-SAR131675 is the racemate of SAR131675. |
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