Laurie M. Strawn

TL;DR: 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, and intravital multifluorescence videomicroscopy of C6glioma xenografteds in the dorsal skinfold chamber model revealed thatSU6668 treatment suppressed tumor angiogenesis.

TL;DR: It is demonstrated that Flk-1 seems to be generally involved in the growth of a wide range of solid tumors, including mammary, ovarian, and lung carcinoma, as well as glioblastoma, and survival times in rats bearing intracerebral tumors were prolonged using the dominant-negative methodology.

TL;DR: Antiangiogenesis compounds that inhibit Flk-1 tyrosine kinase activity, endothelial cell mitogenesis, and blood vessel formation in the chorioallantoic membrane assay have been found.

TL;DR: The role of positive regulators in angiogenesis and tumor growth is discussed and the anti-angiogenic agents under development are described.

TL;DR: The durability of the in vitro activity of SU5416 was shown to be attributable to its long-lasting ability to specifically inhibit VEGF-dependent phosphorylation of Flk-1/KDR and subsequent downstream signaling, althoughSU5416 is not an irreversible inhibitor of FlKDR tyrosine kinase activity.