to inhibit AGE formation in the laboratory include Vitamin C, Agmatine, benfotiamine, pyridoxamine, alpha-lipoic acid, taurine, pimagedine, aspirin, carnosine, metformin, pioglitazone, and pentoxifylline. Activation of the TRPA-1 receptor by lipoic acid or podocarpic acid has been shown to reduce the levels of AGES by enhancing the detoxification of methylglyoxal, a major precursor of several AGEs. Studies in rats and mice have found that natural phenols such as resveratrol and curcumin can prevent the negative effects of the AGEs. Compounds that are thought to break some existing AGE crosslinks include Alagebrium (and related ALT-462, ALT-486, and ALT-946) and N-phenacyl thiazolium bromide. One in vitro study shows that rosmarinic acid out performs the AGE breaking potential of ALT-711. There is, however, no agent known that can break down the most common AGE, glucosepane, which appears 10 to 1,000 times more common in human tissue than any other cross-linking AGE. Some chemicals, on the other hand, like aminoguanidine, might limit the formation of AGEs by reacting with 3-deoxyglucosone. See also Glycosylation Glyoxalase system Methylglyoxal Raw foodism N(6)-Carboxymethyllysine Lipofuscin References Biomolecules Post-translational modification Senescence