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 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|
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
|Solubility||DMSO: 100 mg/mL|
Metabolic impact of anti-angiogenic agents on U87 glioma cells.
Mesti T, et al. PLoS One. 2014 Jun 12;9(6):e99198. PMID: 24922514.
SU1498, an inhibitor of vascular endothelial growth factor receptor 2, causes accumulation of phosphorylated ERK kinases and inhibits their activity in vivo and in vitro.
Boguslawski G, et al. J Biol Chem. 2004 Feb 13;279(7):5716-24. PMID: 14625306.
Overexpression of VEGF 121 in immortalized endothelial cells causes conversion to slowly growing angiosarcoma and high level expression of the VEGF receptors VEGFR-1 and VEGFR-2 in vivo.
Arbiser JL, et al. Am J Pathol. 2000 Apr;156(4):1469-76. PMID: 10751370.
|Related VEGFR/PDGFR Products|
|EG00229 Trifluoroacetate salt
EG00229 Trifluoroacetate is the first small molecule inhibitor of the neuropilin-1 and VEGF-A interaction with an IC50 of inhibition of 8 uM (125I-VEGF binding to PAE/NRP1 cells).
Apatinib is a selective VEGFR2 inhibitor with IC50 of 1 nM.
JI-101 is an orally available multi-kinase inhibitor of VEGFR2，PDGFRβ and EphB4 with potential antiangiogenic and antineoplastic activities.
BAW2881 (NVP-BAW2881) is a potent and selective VEGFR2 inhibitor with activity to inhibit chronic and acute skin inflammation.
EG00229 is an antagonist of the VEGF-A receptor neuropilin 1 (NRP1), which decreases viability of A549 lung carcinoma cells.
Products are for research use only. Not for human use. We do not sell to patients.
© Copyright 2010-2017 AbMole BioScience. All Rights Reserved.