Last Updated: November 17, 2022

Benfotiamine is a relative of the vitamin Thiamine (B1) that appears to have a therapeutic role in pain reduction and diabetic complications (neuropathies and nephropathies); confers bioavailable Vitamin B1 after oral ingestion.

Benfotiamine is most often used for.

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Sources and Structure



Benfotiamine is a molecule with the proper name of S-benzoylthiamine O-monophosphate and is a derivative of Vitamin B1, Thiamine.[1][2] After oral ingestion, it can be converted to Thiamin and is thus considered a prodrug for Thiamin.

Benfotiamine is hydrophobic (fat soluble)[3][4] and is structurally stable unless dephosphorylated, in which case it may degrade into Thiamin.[5]






The absorption rates (bioavailability) of Benfotiamine are approximately 5-fold that of Thiamin and 3.7-fold higher than Thiamin Hydrochloride according to one study,[1] with another suggesting that to reach the same circulating levels of Thiamin only 40% an oral dose of Benfotiamine is needed.[6]

This enhanced bioavailability is thought to be related to the structure, where the novel open thiazole-ring enables passive membrane transport secondary to being phosphorylated (in the brush border of the intestines) to S-benzoylthiamine by ecto-alkaline phosphatase.[1][7]

Benfotiamine appears to have better absorption than other Thiamin-related structures that get metabolized into free Thiamin



Serum increases in Thiamin and phosphorylated metabolites can be detected in serum within one hour of ingesting Benfotiamine.[5]

Relatively quick serum spikes in Thiamin resulting from Benfotiamine ingestion



One hour after oral gavage of Benfotiamine, elevated tissue concentrations of Thiamine, Thiamine monophosphate, and Thiamine Diphosphate can be detected in the liver and kidneys with most relative increase between 100-300mg/kg.[5]

These metabolites can also be detected in dorsal root ganglia and the dorsal spinal cord of rats, but to a much lesser degree in neural tissue (2.3-fold increase at 300mg/kg);[5] this has been noted elsewhere.[8]

Benfotiamine can increase tissue concentrations of Thiamin and Thiamin-related compounds after oral administration to rats



Benfotiamine appears to be substrate of the enzyme Prostatic Acid phosphatase (or in the intestines, ecto-alkaline phosphatase) which dephosphorylates Benfotiamine into S-benzoylthiamine,[5] this then passively degrades into O-benzoylthiamine and is converted into active Thiamin via a thioesterase-dependent mechanism; some passive degradation may occur to Thiamin under alkaline conditions in vitro.[5] Metabolism in the liver to Thiamin by thoiesterase enzymes also yields free benzoic acid.[7]




Alzheimer's Disease

In isolated HEK293 cells, Benfotiamine at 20-40ug/mL is able to attenuate the glucose-induced increase in β-amyloid protein synthesis and theoretically aid the pathology of Alzheimer's disease.[9]

In mice (either diabetic by streptozotocin or normal mice) given Benfotiamine at 100mg/kg for 14 days was able to normalize the glutathione:glutathione disulfide (GSSG) ratio in the cerebral cortex (by decreasing GSSG to control levels), although it did not affect normal mice.[10] These benefits occurred prior to any changes in AGEs or TNF-α (and thus were independent).[10]



Studies measuring the antinociorecptive effects against heat-pain in mice note an EC50 of 69.1mg/kg following oral administration[5] and against capsaicin-induced (injections) writhing, the ED50 dose of Benfotiamine injections appears to be 529.4+/-85.2mg/kg; this was lower than resveratrol (ED50 104+/-8.2mg/kg) but the two appears to be synergistic.[11] Pain reduction has also been noted in chronic models of pain such as CFA injection (a chemical mimetic of Rheumatoid Arthritis) with near complete normalization at 300mg/kg oral ingestion.[5] Other rat studies conducted on pain note that both diabetic and non-diabetic rats experience reduction in pain at 75-300mg/kg Benfotiamine (10mg/kg not being statistically significant).[12]

One study in Diabetic Polyneuropathy has noted that while the Global rating scores slightly failed to reach statistical significance, 300-600mg of Benfotiamine daily was associated with significant reductions on the pain subset of the Diabetic Polyneuropathy rating scale in particular.[13]

Able to reduce pain perception following intravenous and oral dosing, with varying potency depending on the manner of stressor (chemical or environmental)

The enzyme Prostatic Acid phosphatase is required for pain relief from Benfotiamine, although it appears to be required for Thiamin-induced pain relief and may be indepedent of metabolism from Benfotiamine into Thiamin.[5] Metabolism of Benfotiamine to Thiamin was not actually attenuated in this study, suggesting that PAP is not mandatory for conversion yet has novel pain interactions.[5]


Cardiovascular Health


Cardiac Tissue

In periods of hyperglycemia, accumulation of Advanced Glycemic End products (AGEs) and the subsequent upregulation of their receptor (Receptor for AGE; known as RAGE) appears to contribute to cardiomyopathy from high serum glucose; this study noted the diabetes induced decrease in LVDP of the heart did not occur in mice lacking RAGE, and attenuating AGE formation with 80mg/kg Benfotiamine (confirmed to reduce AGE without influencing TGs or cholesterol) and secondary to this attenuated collagen crosslinking and Methylglycoxal formation.[14]

High dose intravenous Benfotiamine therapy (100mg/kg) for 14 days appears to benefit cardiac function in streptozotocin-induced diabetic mice independent of AGE formation.[15] Benfotiamine (70mg/kg oral ingestion for four weeks) was later shown to preserve signalling via an Akt/Pim-1 pathway (PI3K dependent) secondary to its transketolase inducing ability.[16] This pathway is protective of cardiomyocyte cells, but is hindered during periods of high blood glucose since STAT3 is downregulation (normally preserves Pim-1) and then PP2A is induced (suppresses Pim-1); Benfotiamine prevented STAT3 downregulation (without affecting PP2A) and preserved Pim-1, which then preserved the cardioprotective signalling via Akt/Pim-1.[16]

Appears to protect cardiomyocytes (cardiac muscle cells) in response to stressors, either prolonged during reducing AGE formation (which ties into diabetic cardiomyopathy) or acutely via anti-oxidative effects. Has not yet been demonstrated to benefit cardiac tissue when a stressor is not otherwise incubated, suggesting preventative but not enhancing properties



Protein phosphatase A2 (PPA2) appears to be activated during periods of hyperglycemia which contributes to glucose-induced endothelial cell death via NF-kB activation; incubation with Benfotiame can attenuate these adverse changes.[17]

A small study (n=13 Type II Diabetics) involving a high heat processed meal (to concentrate AGE content, also had a high carbohydrate content) before and after a 3 day period where they were given 1050mg Benfotiamine noted that supplementation was able to preserve flow-mediated vasodilation (which was reduced following the meal prior to Benfotiamine) and Benfotiamine abolished the reactive hyperemia without influencing blood pressure or endothelium-dependent vasorelaxation at either time point.[18] This study also noted that postprandial glucose concentrations were reduced at 2 hours (10%), 4 hours (40%), and 6 hours (22%) relative to the control meal.[18] A similar study design also noted that the postprandial reduction in adiponectin is prevented with supplementation of Benfotiamine.[19]


Blood Flow

One study using 2x50mg Benfotiamine (alongside methylcobalamin at 2x500mcg and pyridoxine at 2x50mg) noted that over 12 weeks in persons with Rheumatoid Arthritis was associated with an improvement in endothelial dependent blood flow, but not endothelial independent; suggesting an ability to increase nitric oxide bioavailability.[20]


Interactions with Glucose Metabolism



In states of hyperglycemia (acute, but clinical problems manifest during chronic exposure), the mitochondrial influx of energy is coupled with an increased production of the superoxide radical; superoxide can partially inhibit the enzyme Glyceraldehyde Phosphate Dehydrogenase (GAPDH) and divert glucose away from glycolysis towards alternate pathways.[21][22] Partial inhibition of GAPDH causes a relative accumulation of the metabolites prior to that enzyme in the glycolytic chain, which include fructose-6-phosphate (F6P) and glyceraldehyde-3-phosphate (G3P); accumulation of these contribute to increased Advanced Glycemic End product (AGE) and Diacylglycerol (DAG) production, and increased metabolic activity of the Hexosamine pathways all of which contribute to microvascular damage and complications associated with Diabetes.[21][22] Another contributing factor to complications of Microvascularity, increased Polyol synthesis, is independent of F6P and G3P and more related to the Aldose Reductase enzyme.[23]

Benfotiamine is seen as helpful in this scenario due to being a transketolase enzyme inducer at concentrations exceeding 50uM, where activity of the enzyme can increase fourfold.[22] Transketolase is a thiamine diphosphate dependent enzyme with a normally low activity in glycolysis,[24] and its activity is further reduced in diabetic patients (as measured in the erythrocytes).[25] Transketolase can reversibly interchange the two products seen as problematic in states of hyperglycemia (F6P and G3P) to D-xylulose-5-phosphate and Erythrose-4-phosphate, and secondary to that reduce the complications that occur with excess cellular accumulation of F6P and G3P.[22] This is sometimes referred to as redirecting glucose substrates towards the pentose phosphate shunt.

Benfotiamine can increase activity of a normally low-active enzyme (transketolase), and in the state of hyperglycemia reduce the buildup of two metabolites which (when in excessive concentrations) contribute to the pathology of diabetic microvasculature damage (damage to small arteries; which is tied to retinopathy, nephropathy, and neuropathy)

Additionally, Benfotiamine appears to have direct anti-oxidant properties,[26][27] which attenuates hyperglycemia induced oxidative damage to the endothelium.[28]



80mg/kg oral Benfotiamine is able to abolish the increase in acellular capillary segments in the retina of diabetic rats over 36 weeks, conferring complete protection against diabetic retinopathy according to this rat study.[22]

Redirection of G3P and F6P via the pentose phosphate shunt and activation of transketolase appears to prevent the decrease in cardiac progenitor cells and may be cardioprotective in states of diabetes.[29]

Various benefits to rats at the above doses

A small study (n=9) in Type 1 Diabetics given 300mg Benfotiamine (twice a day to total 600mg) with Alpha Lipoic Acid (600mg twice a day to total 1200mg) over 28 days was able to enhance transketolase activity (measured in monocytes) 2-3 fold and by 15 days completely normalized serum angiopoietin-2 (a biomarker of methylgloxal adducts in endothelial cells), and effectively normalized (as such that it was not statistically different than non-diabetic control) N-acetylglucosamine modified proteins (indicative of AGE status) and 6-keto-PGF.[30]

In diabetics with high-normal proteinuria (protein losses in the urine, in the range of 15–300 mg/24h urinary albumin excretion) taking 300mg thrice a day (totalling 900mg) for a period of 12 weeks failed to provide a significant reduction in serum or urinary Advanced Glycation End products (AGEs); this study also failed to find significant differences in biomarkers of endothelial stress and adhesion factors yet confirmed an increase in thiamine status and transketolase activity.[31]

A two year long trial in type I diabetics (over 15 years of diabetes, thought to have reduced nerve conductance velocity) given 300mg Benfotiamine daily failed to note changes in albumin excretion (urinary), HbA1c, nerve conductance measures, or various inflammatory measures.[32] This study has been commented upon and subsequently responded to,[33] but was mostly a defense of methodology.


Skeletal Muscle and Bone



In cultured myotubes derived from healthy participants, normal (5.5uM) and high glucose (20uM) conditions both experienced an increase in glucose oxidation at 100uM Benfotiamine (35% normal; hyperglycemic not statistically significant) and 200uM Benfotiamine (49% normal, 70% hyperglycemic) with a concomitant increase in glucose uptake (lesser at 17%); Glucose uptake but not oxidation was also affected by Thiamine (30% as much potency as Benfotiamine) while lipid metabolism and glycogen synthesis remained unaffected under all conditions.[34]

This former study noted that around 100 and 200 genes were upregulated or downregulated (respectively) after 200uM Benfotiamine, with notable downregulations being NOX4 (2.5-3.1fold), Thymidine phosphorylase (2.2-2.8fold), and MDK (3.3-fold) and notable upregulations of SERPINB7 (2.3-3.4fold increase; more efficacy in normoglycemia) and Carboxypeptidase A4 (1.57-3.16fold; also more efficacy in normoglycemia).[34] Differentiation factors MyoD and Myogenin were not significantly affected.[34]

Possible increase in glucose utilization in skeletal muscle, which may not be related to the two most common pathways (insulin receptor signalling and AMPK activation) and is potentially novel

Type 1 diabetes was associated with an increase in adipocyte content, Reactive Oxygen Species (ROS), and microangiopathy in bone marrow with reduced density and volume;[35] these effects are prevented in vitro with antioxidants such as N-AcetylCysteine, and oral administration of 70mg/kg Benfotiamine for 24 weeks lessens the degree of oxidative damage in diabetic rats as well as these adverse pathological changes, with the degrees of improvement either trending towards normalization (Bone marrow blood flow), were normalized (LSK cells and density) were were more beneficial than non-diabetic control (TK, Mitochondrial ROS, and G6PDH activity in BMMNCs,).[35]


Inflammation and Immunology



Benfotiamine appears to weakly attenuate Advanced Glycemic End product (AGE) bound to serum albumin (a complex known as AGE-alubmin) from activating macrophages and inducing oxidative stress via NADPH oxidase.[36] AGE-Albumin is known to interefere with the cholesterol efflux transporters ABCG1 and ABCA1[37][38] which appears to be mediated via oxidation.[36] Anti-oxidants in general may reduce these effects (as was established with aminoguanidine), with Benfotiamine confering weak protective effects.[36]

Benfotiamine incubation in macrophages has been noted to attenuate LPS induced mitochondrial membrane potential loss in the macrophages, which was thought to be downstream of preventing NF-kB translocation secondary to anti-oxidant effects.[39]

Appears to be an anti-oxidant in immune cells, but is fairly weak at this role

Benfotiamine has been demonstrated to inhibit arachidonic acid (AA) release form RAW264.7 cells, with 100uM Benfotiamine inhibiting approximately 90% of AA release, a similar magnitude of cPLA2 suppression (medites AA release) which was thought to be through a reduction in oxidative stress causing less activation of the pro-inflammatory signalling proteins NF-kB and Er-1;[40] similar mechanisms have been noted elsewhere.[39]



One study using Benfotiamine (50mg) alongside methylcobalamin (500mcg) and pyridoxamine (50mg) twice daily in persons with Rheumatoid Arthritis (without diabetes) for a period of 12 weeks was associated with an improvement of endothelial dependent blood flow (no effect on endothelial independent vasodilation assessed by nitroglycerin) associated with a reduction on TBARS (23%), C-Reactive Protein (36%), and serum Uric Acid (11%); no significant changes were noted in serum AGEs, blood glucose, or blood pressure.[20] Significant improvements were noted in Rheumatoid arthritis disease state as assessed by DAS28 ratings, which was correlated with improvements in inflammatory biomarkers.[20]


Interaction with Oxidation


Genomic Damage

When measuring the lymphocytes of hemodialysis patients (pilot study followed by single blind study), Benfotiamine at 600mg was able to decrease the micronucleus frequency (16+/-1.2 to 11.1+/-1.1 micronuclei per 1,000 binucleated cells; 30% reduction) in the pilot study and by 15% in the single blind study, which occurred alongside a reduction in AGEs (both intervention and placebo) and an increase in Thiamin levels in serum but did not exist alongside an increase in transketolase activity. This reduction in MNF is thought to be indicative of less oxidative damage to the genome.[41] It was thought that the observed effects were due to direct anti-oxidant properties, as antioxidants in general reduce genomic damage in lymphocytes[42] and Benfotiamine has shown direct anti-oxidant properties that protect the genome in vitro.[27] A significant correlation was noted between transketolase activity and micronucleus frequency though.[41]

Direct anti-oxidant properties that protect DNA have once been shown to be relevant after oral ingestion of Benfotiamine (600mg) by persons at higher risk of genomic damage


Interactions with Organ Systems



A study in 20 otherwise healthy smokers (18.3+/-12.1 pack years) where Benfotiamine was taken thrice a day (350mg x 3) for two days and then an acute bolus of 1050mg an hour prior to smoking, Benfotiamine was able to attenuate the 50% reduction in Flow-Mediated Vasodilation (FMD) from 50% to 25% and abolished the small increase of sVCAM seen with smoking; the changes of blood pressure and heart rate induced by smoking were unaffected.[43]



In a rat model of peritoneal dialysis in uremia (SNX), benfotiamine at 80mg/kg did not significantly reduce serum urea or creatinine but increase transketolase activity; this was associated with less advanced glycemic end products measured in the peritoneum and biomarkers of inflammation and angiogenesis.[44] An approximate halving of albuminuria was noted (in mg/24h) and showed benefit on histological analysis and fibrosis ratings, although not to a remarkable degree.[44] Usage of 70mg/kg Benfotiamine for 24 weeks has been noted to prevent a diabetes-induced increase in AGE adduct formation of renal glomeruli,[45] which is equally potent as a same dose of Thiamin.

One human trial has been conducted measuring the degree of urinary albumin excretion (UAE) and and serum levels of KIM-1 (biomarker of kidney damage) in Type II diabetic patients (10-12 disease years) who did not respond to Angiotensin Receptor Blockers (ARBs) or ACE inhibitors who were then given 900mg of Benfotiamine (3x300mg) for 12 weeks, but although there was a trend to reduce UAE rates there was no significant effect on any measured parameter including HbA1c, KIM-1, blood pressure, or cholesterol.[46]



In cultured human pericytes, high glucose conditions can induce DNA fragmentation and apoptosis (vicariously through producting extracellular matrix (ECM) proteins, not directly by glucose) which are prevented with incubation with either Thiamin (medium normally had 12nM which is similar to diabetic patients,[47] was increased to 50-100umol for the Thiamin condition) or Benfotiamine (50-100umol).[48] High glucose conditions (to mimick diabetes) did not alter cell adhesion or proliferation, and the increase in apoptosis from ECM was abolished with all tested doses.[48] This study built off previous studies in bovine pericytes where thiamin acted in a similar manner to aminoguanidine,[49][50] but was replicated in human pericytes due to species differences.[51] Preventing apoptosis of pericytes is though to be preventative in the early stages of diabetic retinopathy.[52]

7-70mg/kg Benfotiamine in diabetic rats for 24 weeks is also associated with less Advanced Glycemic End product (AGE) adduct formation in the retina, although an equal dose of Thiamin appeared to be more effective;[45] this may be related to transketolase activation.[53]

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