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[Cancer Research 60, 5117-5124, September 15, 2000]
© 2000 American Association for Cancer Research

Experimental Therapeutics

Selective Inhibition of Vascular Endothelial Growth Factor (VEGF) Receptor 2 (KDR/Flk-1) Activity by a Monoclonal Anti-VEGF Antibody Blocks Tumor Growth in Mice1

Rolf A. Brekken2, Jay P. Overholser, Victor A. Stastny, Johannes Waltenberger, John D. Minna and Philip E. Thorpe3

Cell Regulation Program [R. A. B., P. E. T.], Hamon Center for Therapeutic Oncology Research [R. A. B., J. P. O., V. A. S., J. D. M., P. E. T.], and the Department of Pharmacology [R. A. B., J. D. M., P. E. T], University of Texas Southwestern Medical Center, Dallas, Texas 75235-8593, and the Department of Internal Medicine II (Cardiology), Ulm University Medical Center, Ulm D-89081 Germany [J. W.]

Vascular endothelial growth factor (VEGF) is a multifunctional angiogenic growth factor that is a primary stimulant of the development and maintenance of a vascular network in embryogenesis and the vascularization of solid tumors. At the present time there are two well-characterized receptors for VEGF that are selectively expressed on endothelium. VEGF receptor 2 [VEGFR2 (KDR/Flk-1)] mediates endothelial cell mitogenesis and permeability increases, whereas the role of VEGF receptor 1 [VEGFR1 (Flt-1)] has not been clearly defined. In the present study, a monoclonal antibody, 2C3, is shown to block the interaction of VEGF with VEGFR2 but not with VEGFR1 through ELISA, receptor binding assays, and receptor activation assays. 2C3 blocks the VEGF-induced vascular permeability increase in guinea pig skin. 2C3 has potent antitumor activity, inhibiting the growth of newly injected and established human tumor xenografts in mice. These findings demonstrate the usefulness of 2C3 in dissecting the pathways that are activated by VEGF in cells that express both VEGFR1 and VEGFR2, as well as highlighting the dominant role of VEGFR2 in mediating VEGF-induced vascular permeability increases and tumor angiogenesis.




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