MICHAEL A BROWNLEE, MD
Osteopathic Medicine in Bronx, NY

2002011, Aug 22, 2002

Sep 17, 2001

09/954514

Anthony Cerami - New York NY, US
Peter Ulrich - Old Tappan NJ, US
Michael Brownlee - New York NY, US

A61K031/155

514/634000

The present invention relates to methods for inhibiting protein aging. Accordingly, methods are disclosed for treating an animal to inhibit the formation of advanced glycosylation end products of target proteins with the animal by adminstering a pharmaceutical composition comprising an agent capable of reacting with the carbonyl moiety of the early glycosylation product, whereby the subsequent cross-linking of the early glycosylation product is inhibited. Agents of the present invention comprise aminoguanidine, its pharmaceutically acceptable salts, and mixtures thereof.

RE35465, Feb 25, 1997

May 9, 1995

8/437064

Helen Vlassara - Shelter Island NY
Michael Brownlee - New York NY
Anthony Cerami - Shelter Island NY

The Rockefeller University - New York NY

A61K 31415

514402

The present invention relates to a method and associated agents for the inhibition and treatment of protein aging in animals by stimulating the bodies of the animals to increase their recognition and affinity for advanced glycosylation end products. Specifically, the method contemplates the administration of certain agents such as advanced glycosylation endproducts, such endproducts as are bound to the carrier, monokines that stimulate phagocytic cells to increase their activity toward advanced glycosylation endproducts, and mixtures of these materials either alone, or in conjunction with other co-stimulatory agents. Numerous diagnostic and therapeutic applications are defined, and pharmaceutical compositions are also contemplated.

4900747, Feb 13, 1990

Sep 3, 1987

7/091534

Helen Vlassara - New York NY
Michael Brownlee - New York NY
Anthony Cerami - Shelter Island NY

The Rockefeller University - New York NY

A61K 31415

514402

The present invention relates to a method and associated agents for the inhibition and treatment of protein aging in animals by stimulating the bodies of the animals to increase their recognition and affinity for advanced glycosylation end products. Specifically, the method contemplates the administration of certain agents such as advanced glycosylation endproducts, such endproducts as are bound to the carrier, monokines that stimulate phagocytic cells to increase their activity toward advanced glycosylation endproducts, and mixtures of these materials either alone, or in conjunction with other co-stimulatory agents. Numerous diagnostic and therapeutic applications are defined, and pharmaceutical compositions are also contemplated.

6491909, Dec 10, 2002

Aug 1, 2000

09/630042

Michael Brownlee - New York NY
Marshall S. Horwitz - Larchmont NY
Howard J. Federoff - Rochester NY
Shimon Efrat - Bronx NY

Albert Einstein College of Medicine of Yeshiva University - Bronx NY

A61K 4800

424 9321, 424 932, 514 44, 435325, 435455, 435456

The invention provides a method and vectors to express a gene or genes, derived from a virus, which block allograft rejection. One class of genes blocks the intracellular transport and/or intracellular maturation within the cells of proteins called MHC class I products. Without limitation as to theory, it is believed that blocking the appearance of this class of proteins on the transplanted cells surface, prevents the hosts immune system from rejecting the graft. Another class of proteins acts to permit TNF -mediated cell cytolysis. In one embodiment, the invention is directed towards engrafting the cells that secrete insulin, which are called alternatively, pancreatic -cells and islet cells, and thereby provide a treatment of diabetes mellitus.

2008016, Jul 3, 2008

May 27, 2004

10/558532

Michael Brownlee - New York NY, US

A61K 48/00, A61K 38/17, A61K 39/395, A61K 31/455, A61K 31/454, A61K 31/51, A61K 31/165

514 44, 514620, 514300, 514298, 514400, 4241331, 5303871, 435 71, 514276, 514323, 514356, 514 12

The present invention provides methods of inhibiting the development or progression of atherosclerotic, microvascular, or neurologic disease due to diabetes or insulin resistance in a mammal, or conditions resulting therefrom. The methods involve specifically inhibitingpoly(ADP-ribose) polymerase (PARP) activity or accumulation in the mammal. Also provided are antibodies that specifically react with Nα-acetyl-Nδ (5-hydro-5-methyl)4-imidazolone. Additionally, the invention provides methods of monitoring the effectiveness of an anti-diabetic or anti-insulin resistance treatment or an anti-diabetic or anti-insulin resistance complication treatment in a mammal. The methods involve measuring ADP-ribosylated protein levels, or measuring methylglyoxyl AGE levels in the mammal using an antibodies that specifically react with Nα-acetyl-Nδ (5-hydro-5-methyl)4-imidazolone, or measuring GlcNAc-modified protein levels in the mammal.

2006028, Dec 14, 2006

Dec 7, 2005

11/297808

Geoffrey Gurtner - Stanford CA, US
Michael Brownlee - New York NY, US

A61K 31/5377, A61K 31/496, A61K 31/4196

514235500, 514254050, 514383000

One aspect of the present invention relates to a method of treating or preventing pathologic effects of hyperglycemia and/or increased fatty acid flux in a subject in need of such treatment or preventive therapy. This method involves administering a composition containing a therapeutically effective amount of a ROS inhibitor to a subject in need thereof.