Benfotiamine is a derivative of vitamin B1. It was developed in Japan specifically to treat Korsakoff’s syndrome Benfotiamine reduces the extra biosynthesis and accumulation of a number of glucose metabolites, including glyceraldeyde-3-phosphate and dihydroxyacetone phosphate. Elevated levels of those glucose intermediates function as a trigger to most of the mechanisms accountable for hyperglycemia-caused cell damage. Benfotiamine increases tissue amounts of thiamine diphosphate, consequently growing transketolase activity and producing a significant decrease in glucose metabolites and precursors to AGEs. Up to now, two of the most effective AGE inhibitors in living microorganisms would be the Vitamin B1 derivative, benfotiamine and also the Vitamin B6 derivative, pyridoxamine. Additionally, benfotiamine has long been proven to lessen NF-kB activity, therefore restricting the over-production from the harmful superoxide toxin. Excess superoxide production may partly hinder a vital enzyme in glucose metabolic process, glyceraldehyde-3-phosphate dehydrogenase, directing glucose metabolites from glycolysis in to the major glucose-driven signaling paths that cause hyperglycemic damage. Theoretically, overdose with benfotiamine should cause menopausal flashes, bluish skin (because of rapid utilization of oxygen), tingling, and difficulty breathing, but used, this merely has not happened.