US2002031517A1PendingUtilityA1

Methods for treating diabetes

Priority: May 6, 1998Filed: Nov 19, 2001Published: Mar 14, 2002
Est. expiryMay 6, 2018(expired)· nominal 20-yr term from priority
A61P 3/10C07K 16/30A61P 7/12A61K 2039/505C07K 16/18C07K 16/22A61K 38/18A61P 43/00A61K 38/1841C07K 2317/76A61P 5/50
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Claims

Abstract

Methods for treating diabetes by administering an inhibitor of GDF-8, or a related member of Transforming Growth Factor-beta (TGF-β) superfamily of structurally-related growth factors (e.g., GDF-11) are disclosed. Also disclosed are methods for upregulating expression of hexose transporters, such as GLUT4 and GLUT1, in a subject by administering an inhibitor of GDF-8. Also disclosed are methods for increasing glucose uptake by cells in a subject, by administering an inhibitor of GDF-8.

Claims

exact text as granted — not AI-modified
We claim:  
     
         1 . A method of increasing expression of GLUT4 in a subject comprising administering to the subject a GDF-8 inhibitor.  
     
     
         2 . A method of increasing insulin sensitivity and glucose uptake by cells in a subject comprising administering to the subject a GDF-8 inhibitor.  
     
     
         3 . A method of treating diabetes in a subject comprising administering to the subject a GDF-8 inhibitor.  
     
     
         4 . The method of any one of claims  1 - 3 , wherein the GDF-8 inhibitor is an antibody or antibody fragment.  
     
     
         5 . The method of any one of claims  1 - 3 , wherein the GDF-8 inhibitor is selected from the group consisting of a peptide fragment of GDF-8, a dominant-negative mutant of GDF-8, a GDF-8 receptor antagonist, a non-GDF-8 peptide, an antisense nucleic acid and a ribozyme.  
     
     
         6 . The method of any one of claims  1 - 3 , wherein the GDF-8 inhibitor is derived from mature GDF-8 protein.  
     
     
         7 . The method of any one of claims  1 - 3 , wherein the GDF-8 inhibitor is derived from the Pro domain of a GDF-8 protein.  
     
     
         8 . The method of  claim 2 , wherein said insulin sensitivity and glucose uptake is increased by modulating the expression of a hexose transporter selected from the group consisting of GLUT4 and GLUT1.  
     
     
         9 . The method of  claim 2 , wherein the cell is a muscle cell or a precursor thereof.  
     
     
         10 . The method of  claim 2 , wherein the cell is an adipocyte or a precursor thereof.  
     
     
         11 . The method of  claim 3 , wherein the subject is suffering from type II diabetes.

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