The multifaceted therapeutic potential of benfotiamine

Long-Term Cognitive Improvement After Benfotiamine Administration in Patients with Alzheimer’s Disease

“…Here, we present the results of a clinical case study showing the potential of benfotiamine as a disease-modifying drug for AD. As a derivative of thiamine with better bioavailability, benfotiamine has been demonstrated to exert beneficial effects against abnormal glucose metabolism and its consequences via multiple mechanisms, including the elimination of oxidative stress [16,17] and the inhibition of glycogen synthase kinase-3 [18], which are both considered to be major pathogenic factors that cause neurodegeneration in AD. The better bioavailability and the pharmacological effects via multiple mechanisms against abnormal glucose metabolism and its consequences may explain why benfotiamine administration but not thiamine supplementation [24] had a long-term beneficial effect on cognitive ability in AD patients.…”

“…Benfotiamine is a synthetic thiamine derivative with better bioavailability than thiamine and has been shown to prevent abnormal glucose metabolism via multiple pathways [16,17]. Our previous study demonstrated that benfotiamine improves cognitive impairment in a mouse model of AD (amyloid precursor protein/presenilin-1 (APP/PS1) transgenic mice) [18].…”

Benfotiamine increases glucose oxidation and downregulates NADPH oxidase 4 expression in cultured human myotubes exposed to both normal and high glucose concentrations

“…GSEA analysis also suggested that fatty acids could be channeled to peroxisomes for oxidation after treatment with benfotiamine. Most previous research into the biochemical effects of benfotiamine has focused on cells, such as endothelial cells, susceptible to hyperglycemic-associated damage (Balakumar et al 2010). The clinical implications of the results from the present study are that oral benfotiamine has marked metabolic effects on cells i.e., skeletal muscle, other than those typically associated with diabetic microvascular complications.…”

“…These effects are believed to occur secondary to a buildup of glucose and glycolytic intermediates in the cytosol during bouts of hyperglycemia when intracellular glucose concentrations are abnormally increased (Brownlee 2001). Benfotiamine, a synthetic thiamine monophosphate analogue with improved intestinal absorption as compared with thiamine, prevents the adverse cellular changes associated with hyperglycemia and can prevent the development of diabetic retinopathy in mice (Balakumar et al 2010;Hammes et al 2003). These effects are believed to be mediated by increasing the activity of thiamine-dependent and rate-limiting enzyme of the pentose phosphate pathway (PPP), transketolase (TK), which shifts excess glycolytic metabolites away from central biochemical pathways of hyperglycemic damage (Hammes et al 2003).…”

Benfothiamine Administration in Patients with Dilated Cardiomyopathy and Advanced Heart Failure with Chronic Diuretic Treatment

“…Benfothiamine has an open thiazole ring, which closes once benfothiamine is absorbed passively through intestinal mucosa, generating active thiamine. Benfothiamine is available in a proportion of at least 25%, for 8 days in tissues, much longer than water soluble thiamine [8,9]. It is very efficient in the treatment of macrovascular and microvascular endothelial dysfunction and oxidative stress, in patients with diabetes mellitus and secondary complications [10,11,12].…”