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Experimental Therapeutics |
SUGEN, Inc., San Francisco, California 94080 [A. D. L., L. K. S., C. L., R. A. B., T. A. T. F., L. M. S., L. S., C. T., R. H., F. T., N. S., K. P. H., G. M., J. M. C.]; Department of Neurosurgery, Klinikum Mannheim, University of Heidelberg, D-68167 Mannheim, Germany [P. V., A. T.]; Department of Pharmacology, New York University Medical Center, New York, New York 10016 [M. M., J. S.]; Department of Molecular Biology, Max-Planck-Institut für Biochemie, D-82152 Martinsried, Germany [A. U.]; and Skirball Institute of Biomolecular Medicine and Department of Pharmacology, New York University Medical Center, New York, New York 10016 [S. R. H.]
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 SU6668, a novel inhibitor of these receptors. Biochemical kinetic studies using isolated Flk-1, FGF receptor 1, and PDGF receptor ß kinases revealed that SU6668 has competitive inhibitory properties with respect to ATP. Cocrystallographic studies of SU6668 in the catalytic domain of FGF receptor 1 substantiated the adenine mimetic properties of its oxindole core. Molecular modeling of SU6668 in the ATP binding pockets of the Flk-1/KDR and PDGF receptor kinases provided insight to explain the relative potency and selectivity of SU6668 for these receptors. In cellular systems, SU6668 inhibited receptor tyrosine phosphorylation and mitogenesis after stimulation of cells by appropriate ligands. Oral or i.p. administration of SU6668 in athymic mice resulted in significant growth inhibition of a diverse panel of human tumor xenografts of glioma, melanoma, lung, colon, ovarian, and epidermoid origin. Furthermore, intravital multifluorescence videomicroscopy of C6 glioma xenografts in the dorsal skinfold chamber model revealed that SU6668 treatment suppressed tumor angiogenesis. Finally, SU6668 treatment induced striking regression of large established human tumor xenografts. Investigations of SU6668 activity in cancer patients are ongoing in Phase I clinical trials.
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