Kimia Biosciences Limited

Benfotiamine

General Information:

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.

CAS No.

22457-89-2

Therapeutic Category:

Anti–Biotic drugs

IUPAC Name:

S-[2-{[(4-Amino-2-methylpyrimidin-5-yl)methyl] (formyl)amino}-5-(phosphonooxy)pent-2-en-3-yl] benzenecarbothioate

Molecular Formula:

C19H23N4O6PS

Molecular Weight:

C19H23N4O6PS

Molecular Structure:

Benfotiamine

Mechanism of Action

Benfotiamine exerts it beneficial effects via a number of mechanisms. In the case of diabetes, benfotiamine increases transketolase activity, an important enzyme in glucose metabolism, and as a result, blocks three of the major molecular pathways leading to hyperglycemic damage. It prevents the increase in UDP-N-acetylglucosamine (UDP-GlcNAc) and enhances hexosamine pathway activity that decreases the buildup of detrimental glucose metabolites that can lead to advanced glycation end products (AGE). Benfotiamine also normalizes protein kinase Copyright © 2006 Thorne Research, Inc. All Rights Reserved. No Reprint Without Written Permission. Alternative Medicine Review Volume, Number 3 September 2006 Monograph Benfotiamine Alternative Medicine Review u Volume 11, Number 3 u 2006 Page 239 C (PKC) activity and prevents nuclear factor-kappaB (NF-κB) activation in the retina of diabetics. In addition, benfotiamine corrects imbalances in the polyol pathway by decreasing aldose reductase activity, sorbitol concentrations, and intracellular glucose, thereby protecting endothelial cells from glucose-induced damage. Benfotiamine also corrects glucose-induced endothelial cell damage by normalizing cell replication rates and decreasing apoptosis. Animal models of diabetic limb ischemia demonstrated these mechanisms are responsible for improved post-ischemic healing. Research has also shown benfotiamine’s enhancement of transketolase activity in erythrocytes and renal glomeruli protects the kidneys from glucose-induced damage and prevents the development of diabetic nephropathy. In alcoholics and patients with chronic renal disease, benfotiamine corrects thiamine deficiency and can decrease the incidence of neuropathies.