US2003040463A1PendingUtilityA1

TIE-2 ligands, methods of making and uses thereof

48
Priority: Apr 5, 1996Filed: Jul 1, 2002Published: Feb 27, 2003
Est. expiryApr 5, 2016(expired)· nominal 20-yr term from priority
Inventors:Stanley WiegandPeter A. CampochiaroGeorge D. Yancopoulos
A01K 67/0275A61K 38/00A01K 2217/05C07K 14/515A01K 2267/0306A01K 2227/105
48
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Claims

Abstract

The present invention provides for an isolated nucleic acid molecule encoding a human TIE-2 ligand. In addition, the invention provides for a receptorbody which specifically binds a human TIE-2 ligand. The invention also provides an antibody which specifically binds a human TIE-2 ligand. The invention further provides for an antagonist of human TIE-2. The invention also provides for therapeutic compositions as well as a method of blocking blood vessel growth, a method of promoting neovascularization, a method of promoting the growth or differentiation of a cell expressing the TIE-2 receptor, a method of blocking the growth or differentiation of a cell expressing the TIE-2 receptor and a method of attenuating or preventing tumor growth in a human.

Claims

exact text as granted — not AI-modified
We claim:  
     
         1 . A method of reducing pathological neovascularization in a human comprising administering to the human an agent capable of interfering with Ang2-mediated biological effects such that pathological neovascularization is reduced.  
     
     
         2 . The method of  claim 1  wherein the pathological neovascularization is ocular neovascularization.  
     
     
         3 . The method of  claim 2 , wherein the ocular neovascularization is proliferative retinopathy.  
     
     
         4 . The method of  claim 3 , wherein the proliferative retinopathy is diabetic retinopathy, ischemic retinopathy, retinopathy of prematurity, venous obstructive disease, hemoglobinopathies, radiation retinopathy, ocular inflammation or infection, ocular neoplasias, ocular trauma, or idiopathic proliferative neovascularization.  
     
     
         5 . The method of  claim 3 , wherein the ocular neovasculariztion is choroidal neovascularization.  
     
     
         6 . The method of  claim 5 , wherein the choroidal neovascularization is lens neovascularization, corneal neovascularization, iridial neovascularization, conjunctival neovascularization, age related macular degeneration, angiod streaks, radiation retinopathy, ocular inflammation or infection, ocular neoplasias, ocular trauma, or idiopathic choroidal neovascularization.  
     
     
         7 . A method of reducing the risk of retinal detachment associated with pathological ocular neovascularization in a human comprising administering to the human an agent capable of interfering with Ang2 mediated biological effects such that retinal detachment associated with pathological ocular neovascularization is reduced.  
     
     
         8 . The method of  claim 1  or  7  wherein the administration is retrobulbar, subconjunctival, intraocular, topical, oral, subcutaneous, intramuscular, intranasal, intrathecal, intraarterial, intravenous, transvaginal, transdermal, or transanal administration.  
     
     
         9 . The method of  claim 1  wherein the pathological neovascularization is tumor neovascularization.  
     
     
         10 . The method of  claim 9 , wherein the tumor is a solid tumor.  
     
     
         11 . The method of  claim 1  wherein the pathological neovascularization is endometriosis, polycystic ovary syndrome, uterine fibroids, psoriasis, rheumatoid arthritis, or hemangioma.  
     
     
         12 . The method of claims  9  or  10  wherein the administration is topical, oral, subcutaneous, intramuscular, intranasal, intrathecal, intraarterial, intravenous, transvaginal, transdermal, or transanal administration.  
     
     
         13 . The method of  claim 1  or  7  wherein the biological effects are Ang2-mediated cell signaling, Ang2 binding to Tie1, Ang2 binding to Tie2, or Ang2 antagonism of Ang1.  
     
     
         14 . The method of  claim 1  or  7  wherein the agent is capable of interfering with Ang2 binding to Tie1 or Tie2.  
     
     
         15 . The method of  claim 1  or  7  wherein the agent is capable of interfering with Ang2-mediated cell signaling.  
     
     
         16 . The method of  claim 1  or  7  wherein the agent is capable of antagonizing Ang1 binding to Tie1 or Tie2.  
     
     
         17 . The method of  claim 14  wherein the agent is an anti-Ang2 antibody.  
     
     
         18 . The method of  claim 15  wherein the agent is an anti-Ang2 antibody.  
     
     
         19 . The method of  claim 16  wherein the agent is an anti-Tie1 or anti-Tie2 antibody.  
     
     
         20 . The method of  claim 17  wherein the antibody is a monoclonal antibody.  
     
     
         21 . The method of  claim 18  wherein the antibody is a monoclonal antibody.  
     
     
         22 . The method of  claim 19  wherein the antibody is a monoclonal antibody.  
     
     
         23 . The method of  claim 1  or  7  wherein the agent comprises a fragment of an antibody.  
     
     
         24 . The method of  claim 23  wherein the fragment is a scFv.  
     
     
         25 . The method of  claim 1  or  7  wherein the agent is a Tie1 or Tie2 receptorbody.  
     
     
         26 . The method of  claim 1  or  7  wherein the agent is an antisense molecule.  
     
     
         27 . The method of  claim 26  wherein antisense molecule is a DNA molecule.  
     
     
         28 . The method of  claim 26  wherein antisense molecule is a RNA molecule.  
     
     
         29 . The method of  claim 1  or  7  wherein the agent is a small molecule, lipid, protein, carbohydrate, nucleic acid, or aptamer capable of interfering with Ang2-mediated biological activity.

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