Diabetes which is a state of chronic hyperglycaemia leads to increased generation of advanced glycated products (AGEs).  These AGEs are chemical moieties which can have direct effects on protein structure and function but also interact with a number of well characterised receptors including RAGE to activate a range of pathways which can induce end-organ damage.  By promoting oxidative stress and by activating intracellular signalling pathways including protein kinase C and NFkB these AGEs can promote fibrosis, inflammation and angiogenesis, cellular processes which lead to the classical hallmarks of diabetic complications.  Increasingly, dicarbonyl intermediates such as methylglyoxal which are AGE precursors are considered to also be critical in the development of diabetic complications.  A range of drugs which target the advanced glycation pathway at the level of precursors, AGE ligands or receptors have been investigated in a range of diabetic complication although currently no specific treatment has reached the stage of advanced clinical development.