Abstract: The present invention describes methods for inhibition angiogenesis in tissues using organic peptidomimetic ?v?3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing ?v?3 antagonists. The antagonists are organic compounds having a basic group and an acidic group spaced from one another by a distance in the range of about 10 Angstroms to about 100 Angstroms, as described in detail herein.

Abstract: Myocardial infarction in a mammal is treated by administering to the mammal a therapeutically effective amount of a chemical Src family tyrosine kinase protein inhibitor and the use of such inhibitor compounds for the preparation of a medicament for treating myocardial infarction. Myocardial infarction can be prevented by administering to the mammal a prophylactic amount of the inhibitor. The inhibitor preferably is an inhibitor of Src protein selected from the group consisting of a pyrazolopyrimidine class Src family tyrosine kinase inhibitor, a macrocyclic dienone class Src family tyrosine kinase inhibitor, a pyrido[2,3-d]pyrimidine class Src family tyrosine kinase inhibitor, a 4-anilino-3-quinolinecarbonitrile class Src family tyrosine kinase inhibitor, and a mixture thereof. The Src family tyrosine kinase inhibitors can be used to prepare medicaments for the treatment of myocardial infarction. Also disclosed are articles of manufacture containing a chemical Src family tyrosine kinase inhibitor.

Abstract: Angiogenesis inhibitors and methods of use thereof are disclosed. The inhibitors are substantially pure oligopeptides consisting essentially of 7–20 amino acid residues and comprising a proline-rich sequence of five amino acid residues PPXPP, SEQ ID NO: 1, wherein X is an amino acid residue selected from the group consisting of alanine, glycine, serine, threonine, valine, leucine and methionine. In a preferred embodiment, the proline-rich polypeptide is covalently bound to a transport molecule such as a Tat-derived transport polypeptide.

Abstract: The invention teaches methods for treating tumors and tumor metastases in a mammal comprising administering, to a mammal in need of treatment, a therapeutic amount of an antagonist sufficient to inhibit angiogenesis in combination with a therapeutic amount of anti-tumor immunotherapeutic agent, such as a anti-tumor antigen antibody/cytokine fusion protein having a cytokine and a recombinant immunoglobulin polypeptide chain sufficient to elicit a cytokine-specific biological response.

Abstract: Angiogenesis, tumor growth, and metalloproteinase 2 (MMP2) interaction with integrin-?v?3 are inhibited by an inhibitor compound of formula (I): wherein G1 and G2 are each independently NH—C(O)—O—R1, —NH—C(O)—O—(CH2)v—(C6H4)—X3, —NH—C(O)—NH—(CH2)v—(C6H4)—X3, —O—C(O)—NH—(CH2)v—(C6H4)—X3, —O—C(O)—O—(CH2)v—(C6H4)—X3, or NH—C(O)—CH2—(C6H4)—X3; Y1 and Y2 are each independently OH, C1–C4 alkyl, C1–C4 hydroxyalkyl, C1–C4 alkoxy, phenyl, benzyl, or NH2; R1 is C1–C4 alkyl; X1 and X2 are each independently halo or C1–C4 alkoxy; X3 is halo, 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 independently an integer having a value of 0 or 1; t is an integer having a value of 0 or 1; and p, r, and v are each independently an integer having a value of 1 or 2; with provisos that when A

Abstract: Angiogenesis, tumor growth, and metalloproteinase 2 (MMP2) interaction with integrin-?v?3 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.

Abstract: ?v?3 Integrin receptor targeting liposomes comprise a cationic amphiphile such as a cationic lipid, a neutral lipid, and a targeting lipid. The targeting lipid includes a non-peptidic ?v?3 integrin antagonist.

Abstract: The present invention describes methods for inhibiting angiogenesis in tissues using vitronectin ?v?5 antagonists. The ?v?5-mediated angiogenesis is correlated with exposure to cytokines including vascular endothelial growth factor, transforming growth factor-? and epidermal growth factor. Inhibition of ?v?5-mediated angiogenesis is particularly preferred in vascular endothelial ocular neovascular diseases, in tumor growth and in inflammatory conditions, using therapeutic compositions containing ?v?5 antagonists.

Abstract: The present invention describes methods for inhibiting angiogenesis in tissues using vitronectin ?v?5 antagonists. The ?v?5-mediated angiogenesis is correlated with exposure to cytokines including vascular endothelial growth factor, transforming growth factor-? and epidermal growth factor. Inhibition of ?v?5-mediated angiogenesis is particularly preferred in vascular endothelial ocular neovascular diseases, in tumor growth and in inflammatory conditions, using therapeutic compositions containing ?v?5 antagonists.

Abstract: ?v?3 Integrin receptor targeting liposomes comprise a cationic amphiphile such as a cationic lipid, a neutral lipid, and a targeting lipid. The targeting lipid includes a non-peptidic ?v?3 integrin antagonist.

Abstract: The present invention describes methods for modulating angiogenesis in tissues using Raf and/or Ras protein, modified Raf or Ras protein, and nucleic acids encoding for such. Particularly the invention describes methods for inhibiting angiogenesis using an inactive Raf and/or Ras protein, or nucleic acids encoding therefor, or for potentiating angiogenesis using an active Raf and/or Ras protein, or nucleic acids encoding therefor. The invention also describes the use of gene delivery systems for providing nucleic acids encoding for the Raf or Ras protein, or modified forms thereof.

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 inhibition angiogenesis in tissues using vitronectin ?v?3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing ?v?3 antagonists.

Abstract: The present invention describes methods for inhibition angiogenesis in tissues using vitronectin ?v?3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing ?v?3 antagonists.

Abstract: The present invention describes methods for inhibition 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 &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: Myocardial infarction in a mammal is treated by administering to the mammal a therapeutically effective amount of a chemical Src family tyrosine kinase protein inhibitor and the use of such inhibitor compounds for the preparation of a medicament for treating myocardial infarction. Myocardial infarction can be prevented by administering to the mammal a prophylactic amount of the inhibitor. The inhibitor preferably is an inhibitor of Src protein selected from the group consisting of a pyrazolopyrimidine class Src family tyrosine kinase inhibitor, a macrocyclic dienone class Src family tyrosine kinase inhibitor, a pyrido[2,3-d]pyrimidine class Src family tyrosine kinase inhibitor, a 4-anilino-3-quinolinecarbonitrile class Src family tyrosine kinase inhibitor, and a mixture thereof.

Abstract: Compounds which inhibit tumor growth and angiogenesis, of general formula (II) are provided. These compounds include glycyl lysine derivatives bound to a central aromatic linking core.

Abstract: Angiogenesis inhibitors and methods of use thereof are disclosed. The inhibitors are substantially pure oligopeptides consisting essentially of 7-20 amino acid residues and comprising a proline-rich sequence of five amino acid residues PPXPP, SEQ ID NO: 1, wherein X is an amino acid residue selected from the group consisting of alanine, glycine, serine, threonine, valine, leucine and methionine. In a preferred embodiment, the proline-rich polypeptide is covalently bound to a transport molecule such as a Tat-derived transport polypeptide.

Abstract: The present invention describes methods for inhibition angiogenesis in tissues using organic peptidomimetic &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. The antagonists are organic compounds having a basic group and an acidic group spaced from one another by a distance in the range of about 10 Angstroms to about 100 Angstroms, as described in detail herein.