For the same reason that repair is better than good maintenance, AGE-breakers should be better than AGE inhibitors when it comes to reducing the contribution of AGE buildup to aging. Few groups are effectively working on either, however, so I am always pleased to see more published research on the topic: "The reno- and cardiovascular-protective effects of angiotensin II receptor blockers (ARBs), have been ascribed, at least in part, to their ability to inhibit the formation of advanced glycation end products (AGEs), independently of their effect on blood pressure. They act through decreased oxidative stress, unlike previously reported AGE inhibitors which entrap reactive carbonyl (RCOs) precursors of AGEs. The hypotensive effects of ARBs', however, may limit their use. In the present study, we report the synthesis of a new AGE inhibitor, TM2002, and its effects in vitro and in vivo. ... In vivo, TM2002, given acutely or for 8 weeks, has no adverse effects. In four different rat models of renal injury [and cardiovascular injury] TM2002 improves renal and cardiovascular lesions without modification of blood pressure." Inhibitors may be useful for the class of AGEs that are in fact broken down in the body, just more slowly than they accumulate. Unfortunately, animal studies have proven to be misleading for AGE-breakers in the past; the types of AGEs important in other mammals turn out to be much less important in humans.

Link: http://www.ncbi.nlm.nih.gov/pubmed/17928329