Abstract:
The present invention describes methods for inhibition of angiogenesis in tissues using vitronectin &agr;v&bgr;3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing &agr;v&bgr;3 antagonists.
Abstract:
The present invention describes methods for inhibition angiogenesis in tissues using vitronectin αvβ3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing αvβ3 antagonists.
Abstract:
The present invention describes methods for inhibition angiogenesis in tissues using vitronectin αvβ3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing αvβ3 antagonists.
Abstract:
The present invention describes methods for inhibition angiogenesis in tissues using vitronectin αvβ3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing αvβ3 antagonists.
Abstract:
The present invention describes methods for inhibiting angiogenesis in tissues using vitronectin αvβ5 antagonists. The αvβ5-mediated angiogenesis is correlated with exposure to cytokines including vascular endothelial growth factor, transforming growth factor-α and epidermal growth factor. Inhibition of αvβ5-mediated angiogenesis is particularly preferred in vascular endothelial ocular neovascular diseases, in tumor growth and in inflammatory conditions, using therapeutic compositions containing αvβ5 antagonists.
Abstract:
The present invention describes methods for inhibition angiogenesis in tissues using vitronectin αvβ3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing αvβ3 antagonists.
Abstract:
The present invention describes methods for modulating angiogenesis in tissues using Src protein, modified Src protein, and nucleic acids encoding for such. Particularly the invention describes methods for inhibiting angiogenesis using an inactive Src protein, or nucleic acids encoding therefor, or for potentiating angiogenesis using an active Src protein, or nucleic acids encoding therefor. The invention also describes the use of gene delivery systems for providing nucleic acids encoding for the Src protein, or modified forms thereof.
Abstract:
The present invention describes methods for modulating vascular permeability (VP) in tissues using Src or modified Src protein, Yes protein or modified Yes protein, or mixtures thereof, and nucleic acids capable of expression such proteins. In particular, the invention describes methods for inhibiting VP using an inactive Src or Yes protein or a mixture thereof, or nucleic acids encoding therefor, or for potentiating VP using an active, Src or Yes protein or a mixture thereof, or nucleic acids encoding therefor. Related compositions and articles of manufacture are also disclosed.
Abstract:
The present invention describes methods for inhibition of angiogenesis in tissues using vitronectin .alpha..sub.v .beta..sub.3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing anti-.alpha..sub.v .beta..sub.3 monoclonal antibodies.
Abstract:
Angiogenesis, tumor growth, and metalloproteinase 2 (MMP2) interaction with integrin-αvβ3 are inhibited by an inhibitor compound of formula: wherein G1 and G2 are each independently —NH—C(O)—O—(CH2)v—(C6H4)—X3 ; Y1 and Y2 are each independently —OH or C1-C4 alkoxy; X1 and X2 are each independently halo or C1-C4 alkoxy; X3 is fluoro, nitro, C1-C4 alkyl, C1-C4 alkoxy, or C1-C4 perfluoroalkyl; Z is —C≡C—, —C6H4—, cis-CH═CH—, trans-CH═CH—, cis-CH2—CH═CH—CH2—, trans-CH2—CH═CH—CH2—, 1,4-naphthyl, cis-1,3-cyclohexyl, trans-1,3-cyclohexyl, cis-1,4-cyclohexyl, or trans-1,4-cyclohexyl; A is H or a covalent bond; m and n are each 1; t is an integer having a value of 0 or 1; p and r are each 2, and v is 1; with the proviso that when A is H, t is 0, and when A is a covalent bond, t is 1.