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About This Item
Empirical Formula (Hill Notation):
C18H18N2O3
CAS Number:
Molecular Weight:
310.35
UNSPSC Code:
12352200
InChI key
NHFDRBXTEDBWCZ-ZROIWOOFSA-N
InChI
1S/C18H18N2O3/c1-10-12(7-8-17(21)22)11(2)19-16(10)9-14-13-5-3-4-6-15(13)20-18(14)23/h3-6,9,19H,7-8H2,1-2H3,(H,20,23)(H,21,22)/b14-9-
assay
≥97% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
dark yellow
solubility
DMSO: 100 mg/mL
shipped in
ambient
Quality Level
General description
A cell-permeable indolinone compound that acts as a potent ATP-competitive inhibitor against RTKs (receptor tyrosine kinases) Kit, PDGFRβ, VEGFR2 (Flk-1/KDR), FGFR1 activity in vitro (IC50 = 0.01, 0.1, 3.9, and 3.8 µM, respectively) and PDGF/VEGF/bFGF-mediated angiogenesis and tumor development in vivo. Although initially characterized as an RTK inhibitor, SU6668 is now also known to target ser/thr kinases Aurora A, Aurora B, TBK1 (NAK/T2K), and AMPK (IC50 = 0.85, 0.047, 1.4, and 1.8 µM, respectively), as well as non-receptor TKs Lyn and Yes (IC50 = 4.3 and 5.8 µM, respectively).
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
Other Notes
Godl, K., et al. 2005. Cancer Res.65, 6919.
Laird, A.D., et al. 2002. FASEB J.16, 681.
Krystal, G.W., et al. 2001. Cancer Res.61, 3660.
Smolich, B.D., et al. 2001. Blood97, 1413.
Laird, A.D., et al. 2000. Cancer Res.60, 4152.
Shaheen, R.M., et al. 1999. Cancer Res.59, 5412.
Sun, L. et al. 1999. J. Med. Chem.42, 5120.
Laird, A.D., et al. 2002. FASEB J.16, 681.
Krystal, G.W., et al. 2001. Cancer Res.61, 3660.
Smolich, B.D., et al. 2001. Blood97, 1413.
Laird, A.D., et al. 2000. Cancer Res.60, 4152.
Shaheen, R.M., et al. 1999. Cancer Res.59, 5412.
Sun, L. et al. 1999. J. Med. Chem.42, 5120.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Harmful (C)
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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SU6668 is a potent antiangiogenic and antitumor agent that induces regression of established tumors.
A D Laird et al.
Cancer research, 60(15), 4152-4160 (2000-08-17)
Vascular endothelial growth factor, fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF) and their cognate receptor tyrosine kinases are strongly implicated in angiogenesis associated with solid tumors. Using rational drug design coupled with traditional screening technologies, we have discovered
R M Shaheen et al.
Cancer research, 59(21), 5412-5416 (1999-12-20)
Increased vascular endothelial growth factor (VEGF) expression is associated with colon cancer metastases. We hypothesized that inhibition of VEGF receptor activity could inhibit colon cancer liver metastases. BALB/c mice underwent splenic injection with CT-26 colon cancer cells to generate metastases.
Klaus Godl et al.
Cancer research, 65(15), 6919-6926 (2005-08-03)
Knowledge about molecular drug action is critical for the development of protein kinase inhibitors for cancer therapy. Here, we establish a chemical proteomic approach to profile the anticancer drug SU6668, which was originally designed as a selective inhibitor of receptor
L Sun et al.
Journal of medicinal chemistry, 42(25), 5120-5130 (1999-12-22)
Receptor tyrosine kinases (RTKs) have been implicated as therapeutic targets for the treatment of human diseases including cancers, inflammatory diseases, cardiovascular diseases including arterial restenosis, and fibrotic diseases of the lung, liver, and kidney. Three classes of 3-substituted indolin-2-ones containing
A Douglas Laird et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 16(7), 681-690 (2002-04-30)
SU6668 is a small molecule inhibitor of the angiogenic receptor tyrosine kinases Flk-1/KDR, PDGFRbeta, and FGFR1. In mice, SU6668 treatment resulted in regression or growth arrest of all large established human tumor xenografts examined associated with loss of tumor cellularity.
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