676484
VEGFR2 Kinase Inhibitor VI, Ki8751
The VEGFR2 Kinase Inhibitor VI, Ki8751, also referenced under CAS 228559-41-9, controls the biological activity of VEGFR2 Kinase. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
别名:
VEGFR2 Kinase Inhibitor VI, Ki8751, N-(2,4-Difluorophenyl)-Nʹ-(4-(6,7-dimethoxy-4-quinolyloxy)-2-fluorophenyl)urea, Vascular Endothelial Growth Factor Receptor 2 Kinase Inhibitor VI, VEGFR Tyrosine Kinase Inhibitor XXIV
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About This Item
推荐产品
品質等級
化驗
≥97% (HPLC)
形狀
solid
製造商/商標名
Calbiochem®
儲存條件
OK to freeze
protect from light
顏色
off-white
溶解度
DMSO: 50 mg/mL
運輸包裝
ambient
儲存溫度
2-8°C
InChI
1S/C24H18F3N3O4/c1-32-22-11-15-20(12-23(22)33-2)28-8-7-21(15)34-14-4-6-19(17(27)10-14)30-24(31)29-18-5-3-13(25)9-16(18)26/h3-12H,1-2H3,(H2,29,30,31)
InChI 密鑰
LFKQSJNCVRGFCC-UHFFFAOYSA-N
一般說明
A cell-permeable quinolyloxyphenyl-urea compound that acts as a VEGFR-2-selective inhibitior in both cell-based (IC50 = 0.9 nM in VEGF-induced receptor phosphorylation) and cell-free (IC50 = 4.0 nM in kinase reactions) assays. It inhibits c-Kit, PDGFRα, and FGFR-2 only at much higher concentrations (IC50 = 40, 67, and 170 nM, respectively, in cell-based assays), while exhibiting no effect against eight other commonly studied receptor and non-receptor kinases even at concentrations as high as 10 µM. Effectively blocks VEGF-dependent, but not VEGF-independent, cell proliferation in vitro and tumor growth in mice and rats (5 to 20 mg/kg, daily p.o.) in vivo.
包裝
Packaged under inert gas
警告
Toxicity: Regulatory Review (Z)
重構
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
其他說明
Kubo, K., et al. 2005. J. Med. Chem.48, 1359.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
儲存類別代碼
11 - Combustible Solids
水污染物質分類(WGK)
WGK 1
閃點(°F)
Not applicable
閃點(°C)
Not applicable
eNeuro, 8(4) (2021-06-18)
Intercellular adhesion molecule-1 (ICAM-1) promotes adhesion and transmigration of circulating leukocytes across the blood-brain barrier (BBB). Traumatic brain injury (TBI) causes transmigrated immunocompetent cells to release mediators [function-associated antigen (LFA)-1 and macrophage-1 antigen (Mac-1)] that stimulate glial and endothelial cells
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