US2013177533A1PendingUtilityA1

Method for treating inflammation associated with amyloid deposits and brain inflammation involving activated microglia

Assignee: UNIV RAMOTPriority: Feb 1, 2005Filed: Dec 20, 2012Published: Jul 11, 2013
Est. expiryFeb 1, 2025(expired)· nominal 20-yr term from priority
A61P 35/00A61P 25/00A61P 29/00A61P 25/28A61P 13/12A61K 35/76C12N 2795/14132C12N 2795/14171
50
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Claims

Abstract

Filamentous bacteriophage which does not display an antibody or a non-filamentous bacteriophage antigen on its surface is used to inhibit or treat brain inflammation associated with amyloid deposits and/or involving activated microglia, to inhibit the formation of amyloid deposits, and to disaggregate pre-formed amyloid deposits.

Claims

exact text as granted — not AI-modified
What is claimed is: 
     
         1 . A method of inhibiting the formation of amyloid plaques in a subject suffering from a plaque forming disease, comprising administering to the subject a pharmaceutically effective amount of a non-radioactively labeled filamentous bacteriophage that does not display an antibody and does not display a non-filamentous bacteriophage antigen on its surface. 
     
     
         2 . The method of  claim 1 , wherein the amyloid plaques are caused by aggregating protein selected from beta-amyloid, serum amyloid A, cystatin C, IgG kappa light chain, and prion protein. 
     
     
         3 . The method of  claim 2 , wherein the plaque forming disease is selected from Alzheimer's disease, SAA amyloidosis, hereditary Icelandic syndrome, senility, multiple myeloma, kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker disease, fatal familial insomnia, scrapie, bovine spongiform encephalitis, and other diseases characterized by the formation of fibrillar amyloid plaques. 
     
     
         4 . A method of disaggregating amyloid plaques in a subject suffering from a plaque forming disease, comprising administering to the subject a pharmaceutically effective amount of a non-radioactively labeled filamentous bacteriophage that does not display an antibody and does not display a non-filamentous bacteriophage antigen on its surface. 
     
     
         5 . The method of  claim 4 , wherein the amyloid plaques are caused by aggregating protein selected from beta-amyloid, serum amyloid A, cystatin C, IgG kappa light chain, and prion protein. 
     
     
         6 . The method of  claim 5 , wherein the plaque forming disease is selected from Alzheimer's disease, SAA amyloidosis, hereditary Icelandic syndrome, senility, multiple myeloma, kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker disease, fatal familial insomnia, scrapie, bovine spongiform encephalitis, and other diseases characterized by the formation of fibrillar amyloid plaques. 
     
     
         7 . A pharmaceutical composition comprising a filamentous bacteriophage and a pharmaceutically acceptable carrier or excipient, wherein substantially all of the filamentous bacteriophage is non-radioactively labeled, does not display an antibody, and does not display a non-filamentous bacteriophage antigen on its surface, and wherein the composition is formulated for administration by injection. 
     
     
         8 . A pharmaceutical composition comprising a filamentous bacteriophage and a pharmaceutically acceptable carrier or excipient, wherein substantially all of the filamentous bacteriophage is non-radioactively labeled, does not display an antibody, and does not display a non-filamentous bacteriophage antigen on its surface, and wherein the composition is formulated for intrathecal or direct intraventricular administration.

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