Abstract: Aminobenzoic acid derivatives represented by Formula (1) as follows: (wherein, R1 represents a hydrogen atom, a C1-6alkyl group, or the like; R2 represents a hydrogen atom, a C1-6alkyl group, or the like; R3 represents a C8-25alkyl group, or the like; R4 represents a hydrogen atom or a group represented by OR9 or CO2R10 (wherein R9 and R10 represent a hydrogen atom or a C1-6 alkyl group); A represents a group represented by S(O)qR15 (wherein q is 0, 1, or 2, R15 represents a C1-6alkyl group, a phenyl C1-3alkyl group, or a group represented by (CH2)mOR16 (wherein m is 2 or 3, and R16 represents a hydrogen atom or a methoxymethyl group), or the like; X represents O, a single bond, CH═CH, or a group represented by NR27 (wherein R27 represents a hydrogen atom or a t-butoxycarbonyl group); Y represents O, CONH, NHCO, or a group represented by NR28 (wherein R28 represents a hydrogen atom or a t-butoxycarbonyl group); and n is an integer of 0 to 15) or pharmaceutically acceptable salts of the

Abstract: An object of the present invention is to provide a chimera VEGF-E having a reduced antigenicity while maintaining the activity of VEGF-E. The present invention provides a chimera protein having an activity of growing vascular endothelial cells, which is obtained by substituting a part of the sequence of a VEGF analogous protein having an activity of vascularization that binds to KDR (VEGF receptor-2) but does not bind to Flt-1 (VEGF receptor-1) with a corresponding sequence of a human-derived VEGF analogous protein.

Abstract: The present invention provides an antibody or peptide which immunologically reacts with human VEGF receptor Flt-1 and cells in which human VEGF receptor Flt-1 is expressed on the cell surface and an antibody or peptide which inhibits binding of human VEGF to human VEGF receptor Flt-1. It also provides a means for the diagnosis or treatment of diseases in which their morbid states progress by abnormal angiogenesis, such as proliferation or metastasis of solid tumors, arthritis in rheumatoid arthritis, diabetic retinopathy, retinopathy of prematurity, psoriasis, and the like.

Abstract: The present invention provides a substance which inhibits binding of a signal transduction molecule to 1175-tyrosine phosphorylated KDR/Flk-1 and inhibits cell growth by VEGF. Also, the present invention provides a method for inhibiting KDR/Flk-1 signal transduction, a method for inhibiting cell growth, a method for inhibiting angiogenesis, a method for screening a cell growth inhibitor, a method for screening an angiogenesis inhibitor, a method for screening a substance which inhibits KDR/Flk-1 signal transduction, a method for determining whether or not a tested substance can inhibit KDR/Flk-1 signal transduction, a method for detecting angiogenesis in tissue and a method for screening a substance which inhibits 1175-tyrosine phosphorylated KDR/Flk-1, in which each method comprises using the substance.

Abstract: An object of the present invention is to provide a low molecular weight VEGF inhibitor that can be utilized to treat diseases accompanying neovascularization, such as solid tumors. It was found that a polypeptide containing immunoglobulin-like domain 1 and immunoglobulin-like domain 2 but neither immunoglobulin-like main 6 nor immunoglobulin-like domain 7 of the extracellular domain of the VEGF receptor FLT possess VEGF inhibitory activity.