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Biotech / Medical : Alteon (ALT) -- Ignore unavailable to you. Want to Upgrade?

To: Bill Tomko who wrote (284)	3/14/2000 4:59:00 PM
From: tnsaf	Read Replies (1) \| Respond to of 318

AGEs results in dogs Jason ------------------------ Published online before print March 7, 2000, 10.1073/pnas.040558497; Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 6, 2809-2813, March 14, 2000 Medical Sciences An advanced glycation endproduct cross-link breaker can reverse age-related increases in myocardial stiffness Mohammad Asif, John Egan, Sara Vasan, Garikiparthy N. Jyothirmayi, Malthi R. Masurekar, Santos Lopez, Chandra Williams, Ramon L. Torres, Dilip Wagle, Peter Ulrich, Anthony Cerami, Michael Brines, and Timothy J. Regan,õ University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, NJ 07103; Alteon Inc., Ramsey, NJ 07446; and The Kenneth S. Warren Laboratories, 765 Old Saw Mill River Road, Tarrytown, NY 10591 Contributed by Anthony Cerami, December 21, 1999 Decreased elasticity of the cardiovascular system is one of the hallmarks of the normal aging process of mammals. A potential explanation for this decreased elasticity is that glucose can react nonenzymatically with long-lived proteins, such as collagen and lens crystallin, and link them together, producing advanced glycation endproducts (AGEs). Previous studies have shown that aminoguanidine, an AGE inhibitor, can prevent glucose cross-linking of proteins and the loss of elasticity associated with aging and diabetes. Recently, an AGE cross-link breaker (ALT-711) has been described, which we have evaluated in aged dogs. After 1 month of administration of ALT-711, a significant reduction (40%) in age-related left ventricular stiffness was observed [(57.1 ñ 6.8 mmHgúm2/ml pretreatment and 33.1 ñ 4.6 mmHgúm2/ml posttreatment (1 mmHg = 133 Pa)]. This decrease was accompanied by improvement in cardiac function.