AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts.

AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts. Research Abstract Details 

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AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts. Abstract Text:

Anthony Polverino,Angela Coxon,Charlie Starnes,Zobedia Diaz,Thomas DeMelfi,Ling Wang,James Bready,Juan Estrada,Russell Cattley,Stephen Kaufman,Danlin Chen,Yongmei Gan,Gondi Kumar,James Meyer,Sesha Neervannan,Gonzalo Alva,Jane Talvenheimo,Silvia Montestruque,Andrew Tasker,Vinod Patel,Robert Radinsky,Richard Kendall,

The growth of solid tumors is dependent on the continued stimulation of endothelial cell proliferation and migration resulting in angiogenesis. The angiogenic process is controlled by a variety of factors of which the vascular endothelial growth factor (VEGF) pathway and its receptors play a pivotal role. Small-molecule inhibitors of VEGF receptors (VEGFR) have been shown to inhibit angiogenesis and tumor growth in preclinical models and in clinical trials. A novel nicotinamide, AMG 706, was identified as a potent, orally bioavailable inhibitor of the VEGFR1/Flt1, VEGFR2/kinase domain receptor/Flk-1, VEGFR3/Flt4, platelet-derived growth factor receptor, and Kit receptors in preclinical models. AMG 706 inhibited human endothelial cell proliferation induced by VEGF, but not by basic fibroblast growth factor in vitro, as well as vascular permeability induced by VEGF in mice. Oral administration of AMG 706 potently inhibited VEGF-induced angiogenesis in the rat corneal model and induced regression of established A431 xenografts. AMG 706 was well tolerated and had no significant effects on body weight or on the general health of the animals. Histologic analysis of tumor xenografts from AMG 706-treated animals revealed an increase in endothelial apoptosis and a reduction in blood vessel area that preceded an increase in tumor cell apoptosis. In summary, AMG 706 is an orally bioavailable, well-tolerated multikinase inhibitor that is presently under clinical investigation for the treatment of human malignancies.

AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts. Publishing Authors By Initials

A Polverino,A Coxon,C Starnes,Z Diaz,T DeMelfi,L Wang,J Bready,J Estrada,R Cattley,S Kaufman,D Chen,Y Gan,G Kumar,J Meyer,S Neervannan,G Alva,J Talvenheimo,S Montestruque,A Tasker,V Patel,R Radinsky,R Kendall,

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AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Cancer research

VOLUME: 66

Page Numbers: 8715-21

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ISSN: 1538-7445

DAY: 1

MONTH: Sep

YEAR: 2006

AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts. Information

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LANGUAGE: eng

NlmUniqueID: 2984705

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Grant and Affiliation Information for AMG 706, an oral, multikinase inhibitor that selectively targets vascular endothelial growth factor, platelet-derived growth factor, and kit receptors, potently inhibits angiogenesis and induces regression in tumor xenografts.

AFFILIATION: Department of Oncology Research, Amgen, Inc., Thousand Oaks, CA 91320-1799, USA. tonyp@amgen.com

Country: United States

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MEDLINETA: Cancer Res

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