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R&D Pipeline
R&D OverviewA.G.E. Crosslink BreakersALT-2074Scientific Publications
R&D Overview

Kidney

A major complication of diabetes is alteration of the nephrons of the kidney leading to depressed renal function, presence of protein in the urine, and metabolic imbalance. Alagebrium has been shown to prevent the changes in collagen deposition in the kidney in animal models of diabetic nephropathy. An A.G.E. inhibitor has been shown to ameliorate proteinuria in patients with type 1 diabetes mellitus associated) nephropathy. Treatment with compounds that inhibit formation of or break established A.G.E. crosslinks mitigates the protein loss and other hallmarks of the syndrome.


Prevention and Reversal of Diabetic Nephropathy in db/db Mice Treated with Alagebrium (ALT-711)
Author: Peppa, et al.
Source: Am J Nephrol 2006;26:430–436

Heart Failure and Nephropathy: Catastrophic and Interrelated Complications of Diabetes
Author: Gilbert, et al
Source: Clin J Am Soc Nephrol 1: 2006.

Advanced Glycation End Products and Diabetic Nephropathy
Author: Thomas, et al
Source: American Journal of Therapeutics 12, 562–572 (2005)

Interactions between Renin Angiotensin System and Advanced Glycation in the Kidney
Author: Thomas, et al
Source: J Am Soc Nephrol 16: 2976–2984, 2005

Low–Molecular Weight Advanced Glycation End Products: Markers of Tissue AGE Accumulation and More?
Author: Thomas, et al
Source: Ann. N.Y. Acad. Sci. 1043: 644–654, 2005

Superior Renoprotective Effects of Combination Therapy With ACE and AGE Inhibition in the Diabetic Spontaneously Hypertensive Rat
Author: Davis BJ, et al
Source: Diabetologia, January 2004

Accelerated Nephropathy in Diabetic Apolipoprotein E-Knockout Mouse: Role of Advanced Glycation End Products
Author: Lassila, et al.
Source: Journal of the American Society of Nephrology, 2004 15: 2125–2138

Mediators of Diabetic Renal Disease: The Case for TGF-b as the Major Mediator
Author: Ziyadeh
Source: Journal of the American Society of Nephrology, 2004, 15: S55–S57

Randomized Trial of an Inhibitor of Formation of Advanced Glycation End Products in Diabetic Nephropathy
Author: Bolton, et al.
Source: American Journal of Nephrology, 2004, 24:32–40

The Breakdown of Pre-Existing Advanced Glycation End Products is Associated With Reduced Renal Fibrosis in Experimental Diabetes
Author: Forbes, et al.
Source: Federation of American Societies in Experimental Biology (FASEB) Journal, published online, July 2003

ALT-946 and Aminoguanidine, Inhibitors of Advanced Glycation, Improve Severe Nephropathy in the Diabetic Transgenic (mREN-2)27 Rat
Author: Wilkinson-Berka, et al.
Source: Diabetes, Vol. 51, November 2002

Reduction of the Accumulation of Advanced Glycation End Products by ACE Inhibition in Experimental Diabetic Nephropathy
Author: Forbes, et al.
Source: Diabetes, Vol. 51, November 2002

Advanced Glycation End Products Cause Epithelialmyofibroblast Transdifferentiation Via the Receptor for Advanced Glycation End Products (RAGE)
Author: Oldfield, et al.
Source: The Journal of Clinical Investigation, 2001, 108:1853–1863