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Informacje o tej pozycji
Wzór empiryczny (zapis Hilla):
C17H15BrN2O
Numer CAS:
Masa cząsteczkowa:
343.22
UNSPSC Code:
12352200
Pomoc techniczna
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Pozwól nam pomócassay
≥95% (HPLC)
form
solid
potency
70 nM IC50
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
brown
solubility
DMSO: 5 mg/mL
shipped in
ambient
storage temp.
−20°C
General description
A cell-permeable and reversible indolin-2-one class of receptor tyrosine kinase (RTK) inhibitor [IC50 = 70 nM for VEGF-R2 (KDR/Flk-1), 920 nM for PDGF-Rβ, 4.92 µM for p60c-src, and 13.3 µM for FGF-R1]. The inhibition is suggested to be competitive with respective to ATP. Also inhibits VEGF-induced (IC50 = 110 nM) and PDGF-induced (IC50 = 2.01 µM) cell proliferation in umbilical vein endothelial cells (HUVEC). Does not exhibit any inhibitory effect on EGF-R kinase activity (IC50 >100 µM).
A membrane permeant and reversible indolin-2-one class of receptor tyrosine kinase (RTK) inhibitor [IC50 = 70 nM for VEGF-R2 (KDR/Flk-1), 920 nM for PDGF-Rβ, 4.92 µM for p60c-src, and 13.3 µM for FGF-R1]. The inhibition is suggested to be competitive with respect to ATP. Does not inhibit EGF-R kinase activity (IC50 >100 µM).
Biochem/physiol Actions
Cell permeable: yes
Primary Target
VEGF-R2 (KDR/Flk-1)
VEGF-R2 (KDR/Flk-1)
Product competes with ATP.
Reversible: yes
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Other Notes
Sun, L., et al. 2000. J. Med. Chem.43, 2655.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Standard Handling (A)
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Klasa składowania
11 - Combustible Solids
wgk
WGK 1
Certyfikaty analizy (CoA)
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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.
Oisun Jung et al.
Journal of cell science, 132(20) (2019-09-29)
When targeted by the tumor-promoting enzyme heparanase, cleaved and shed syndecan-1 (Sdc1) then couples VEGFR2 (also known as KDR) to VLA-4, activating VEGFR2 and the directed migration of myeloma cells. But how VEGFR2 activates VLA-4-mediated motility has remained unknown. We now