Benfotiamine: Benefits, Dosage, Side Effects, and How It Compares to Vitamin B1
Written by Abdul Rasheed
Abdul Rasheed is the founder and lead editor of Diabetes Knowledge Hub.
A long-time independent researcher of diabetes management and natural health strategies, he leads the site’s content direction, writing, and editorial decisions.
Medical Reviewer Wendy Castle
MPH, RD, LD, CDCES is a Registered Dietitian and Certified Diabetes Care and Education Specialist based in the United States.
She reviews Diabetes Knowledge Hub articles for medical accuracy against current ADA Standards of Care, with expertise in diabetes management, nutrition counseling, and evidence-based nutrition care.
Benfotiamine is a synthetic, fat-soluble derivative of thiamine (vitamin B1) sold in the United States as a dietary supplement. Researchers have studied it because it can raise circulating thiamine compounds and may influence pathways involved in high-glucose cellular stress.
It has not been established that benfotiamine prevents or slows diabetic neuropathy, retinopathy or kidney disease. Short-term trials have reported mixed symptom findings, while the 2026 BOND trial found no significant improvement in its primary or secondary neuropathy outcomes after 12 months (Ziegler et al., 2026). This guide separates proposed mechanisms from demonstrated clinical outcomes.
We explain what benfotiamine is, what the research says about potential benfotiamine benefits, how it compares with thiamine, the doses studied, possible side effects and interactions, and how to evaluate a benfotiamine supplement.
What Is Benfotiamine?
Benfotiamine (S-benzoylthiamine-O-monophosphate) is a synthetic, lipid-soluble derivative of thiamine, the vitamin commonly called B1. After absorption, the body converts it into thiamine and phosphorylated thiamine compounds, including thiamine diphosphate (TDP), which serves as an active coenzyme in metabolism. In the United States, benfotiamine is marketed as a dietary supplement, not an FDA-approved treatment for diabetes or its complications.
Because benfotiamine is a supplement rather than an essential nutrient with an established dietary requirement, there is no recommended dietary allowance (RDA) specifically for it. The fact that it raises thiamine biomarkers does not prove that it prevents or treats diabetic complications.
How Does It Differ From Regular Vitamin B1?
Standard thiamine is water-soluble and its intestinal absorption is influenced by dose and transporter-mediated processes. Benfotiamine is a lipid-soluble derivative of thiamine. After absorption, it is converted into thiamine and its phosphorylated forms, including thiamine diphosphate (TDP), which functions as an active coenzyme. Pharmacokinetic studies have reported higher thiamine exposure after benfotiamine than after some standard thiamine preparations, but the size of the difference depends on the formulation and study. Higher blood or tissue thiamine levels do not, by themselves, demonstrate better clinical outcomes.
Medical note: Benfotiamine is not a substitute for thiamine treatment in suspected severe thiamine deficiency or Wernicke encephalopathy. These conditions require urgent medical assessment and prompt treatment; parenteral (usually intravenous) thiamine is commonly used when clinically indicated. Do not try to manage a suspected neurological emergency with an oral supplement.
What Is Benfotiamine Good For?
Benfotiamine is a synthetic derivative of thiamine (vitamin B1) that has been studied mainly in relation to diabetic peripheral neuropathy and pathways involved in high-glucose cellular stress. Research has also examined biomarkers related to kidney disease and preliminary cognitive outcomes. However, findings in people are mixed: longer-term neuropathy trials have not demonstrated significant clinical benefit, and studies have not established that benfotiamine prevents or treats diabetic complications or Alzheimer’s disease. It should not be considered a proven therapy for any of these conditions.
Diabetic Peripheral Neuropathy
Diabetic peripheral neuropathy can cause pain, burning, numbness and tingling, usually in the feet and legs. Benfotiamine has been studied as a supplement for neuropathy, but the clinical evidence is mixed.
In the 6-week BENDIP randomized trial, 165 people with diabetic polyneuropathy were assigned to 300 mg/day, 600 mg/day or placebo. The Neuropathy Symptom Score differed significantly between groups in the per-protocol analysis (p=0.033), but the intention-to-treat result was borderline and did not meet the conventional significance threshold (p=0.055); the Total Symptom Score did not differ significantly (Stracke et al., 2008). The earlier BEDIP pilot was much smaller and lasted only three weeks; it reported improvement in a composite neuropathy score after 400 mg/day, but this is not enough to establish a treatment dose (Haupt et al., 2005).
Blood Sugar and Glucose Metabolism
Laboratory and animal studies suggest benfotiamine may increase the activity of transketolase, an enzyme in the pentose phosphate pathway. In the original experimental study, Hammes and colleagues described three major biochemical pathways involved in hyperglycaemia-related damage. The paper also discussed NF-κB activation, an inflammatory signalling response. Transketolase activation was proposed as a way to change how excess glucose-derived intermediates enter these pathways in experimental models.
The pentose phosphate pathway should not be described as a guaranteed “safe metabolic channel.” It is a normal metabolic pathway, and the proposed protective effect comes from laboratory and animal research. These mechanisms do not prove that benfotiamine blocks these pathways in people, lowers blood glucose, or prevents diabetic complications. Human clinical trials have not established those benefits.
What Longer-Term Trials Show
The long-term evidence is important when interpreting early positive findings. In the 2026 BOND study, participants with type 2 diabetes and symptomatic neuropathy received 300 mg twice daily or placebo for 12 months. Benfotiamine did not significantly improve the primary corneal nerve-fiber measure or secondary nerve-conduction, sensory or clinical outcomes; one symptom score showed only a trend. Investigators did not attribute serious adverse events to benfotiamine (Ziegler et al., 2026).
A separate 24-month trial in 67 people with type 1 diabetes found no significant between-group improvement in peripheral nerve function or inflammatory markers with 300 mg/day (Fraser et al., 2012). These results mean that benfotiamine’s role in diabetic neuropathy remains uncertain; it should not replace glucose management, foot care or evidence-based neuropathy treatment.
Diabetic Retinopathy and Nephropathy
Benfotiamine protected against experimental retinopathy in animal models, but this does not establish benefit in people. In a 12-week randomized trial in 82 people with type 2 diabetes and nephropathy, 900 mg/day did not significantly reduce urinary albumin excretion or kidney injury molecule-1 compared with placebo (Alkhalaf et al., 2010). A related 2012 analysis found no significant reductions in plasma or urinary AGEs, endothelial-dysfunction markers or inflammation markers (Alkhalaf et al., 2012).
Current human evidence therefore does not support using benfotiamine to prevent or treat diabetic kidney disease or retinopathy. People with diabetes should continue recommended kidney and eye screening and follow their clinician’s treatment plan. Our guide to diabetes complications explains why ongoing screening matters.
Alzheimer's Disease: Preliminary Evidence
A 12-month Phase IIa trial included 70 participants with amnestic mild cognitive impairment or mild Alzheimer’s dementia. Its primary cognitive outcome did not reach statistical significance (p=0.125), although some secondary measures, including clinical dementia rating, and an exploratory AGE measure favored benfotiamine. The small pilot provides a reason for further research, not evidence that benfotiamine prevents or treats Alzheimer’s disease (Gibson et al., 2020).
Evidence note: Benfotiamine remains an investigational supplement for diabetic neuropathy and other diabetes-related complications. The clinical studies discussed in this article have produced mixed results, and current evidence does not establish that it prevents or treats neuropathy, retinopathy, kidney disease or Alzheimer’s disease. It should not replace evidence-based diabetes care, prescribed medicines or routine complication screening.
How Benfotiamine Works: The Mechanism
Benfotiamine is converted into active thiamine compounds and has been studied for its effects on cellular pathways involved in glucose metabolism. Understanding these proposed mechanisms helps explain the research interest, but laboratory findings and changes in biomarkers do not necessarily translate into clinical benefits for people.
Step 1
Absorption and Bioavailability
After oral ingestion, benfotiamine’s fat-soluble structure is associated with greater circulating thiamine exposure than thiamine mononitrate in pharmacokinetic studies. The body converts benfotiamine into thiamine and phosphorylated thiamine compounds, including thiamine diphosphate (TDP), the active coenzyme form. Higher blood concentrations do not by themselves establish better clinical outcomes (Schreeb et al., 1997; Sheng et al., 2021).
Step 2
Transketolase Activation
TPP is the active form of thiamine. The enzyme transketolase needs it to work. Transketolase is part of the pentose phosphate pathway. In their original study, Hammes and colleagues described three main biochemical pathways linked to high-glucose cell damage. They also discussed NF-κB, a signal involved in inflammation. The researchers proposed that more transketolase activity could change how excess glucose products enter these pathways in experimental models.
The pentose phosphate pathway is a normal part of cell metabolism. It is not a guaranteed “safe metabolic channel.” This proposed protective effect comes from laboratory and animal research. It does not prove that benfotiamine blocks these pathways in people, lowers blood glucose, or prevents diabetic complications. Human trials have not established these benefits.
Step 3
NF-κB Inhibition
Experimental research has linked benfotiamine with transketolase activation and reduced NF-κB signalling in models of hyperglycaemia-related tissue damage. These findings help explain why the compound is being studied, but preclinical mechanisms do not establish that it prevents or treats diabetic complications in people (Hammes et al., 2003).
Benfotiamine vs Thiamine: What's the Difference?
Benfotiamine and thiamine are related but not identical — a distinction that matters clinically. The table below summarises the key differences:
Property |
Benfotiamine |
Thiamine (Vitamin B1) |
|---|---|---|
Solubility
|
Lipid-soluble thiamine derivative
|
Water-soluble vitamin
|
Absorption / metabolism
|
Converted after absorption into thiamine metabolites
|
Absorbed through thiamine transport systems
|
Relative bioavailability
|
Higher thiamine exposure in some pharmacokinetic studies; varies by metabolite
|
Reference form; different absorption kinetics
|
Cellular delivery
|
Converted to thiamine metabolites; not a direct measure of clinical benefit
|
Uses thiamine transport and phosphorylation pathways
|
Active form produced
|
Thiamine pyrophosphate (TPP)
|
Thiamine pyrophosphate (TPP)
|
Transketolase
|
May influence activity in experimental studies
|
TDP is the required cofactor
|
Use / evidence
|
Investigated for diabetic neuropathy; clinical benefit remains uncertain
|
Essential nutrient; used to prevent or treat thiamine deficiency
|
Emergency use (IV)
|
Not available
|
Yes — Wernicke's encephalopathy
|
Regulatory status (US)
|
Dietary supplement (OTC)
|
Dietary supplement / prescription IV
|
Dose context
|
No established therapeutic dose; trials have tested 300–600 mg/day
|
Adult RDA: 1.1 mg/day (women), 1.2 mg/day (men)
|
Benfotiamine is a modified thiamine derivative with different absorption and pharmacokinetic properties from standard thiamine. Some studies report higher thiamine exposure after benfotiamine, but this does not establish superior clinical outcomes or prove that it is more effective for diabetic complications. For suspected severe thiamine deficiency or a medical emergency, prompt clinician-directed thiamine treatment is essential; oral benfotiamine is not a substitute.
Benfotiamine Dosage: How Much Should You Take?
There is no official recommended daily allowance (RDA) for benfotiamine as it is classified as a dietary supplement. Dosing recommendations are drawn from clinical trials and manufacturer guidelines. The ranges below reflect what has been used in published research:
Dose |
Use Case |
Evidence Level |
Notes |
|---|---|---|---|
Benfotiamine 150 mg (capsule strength)
|
Commercial supplement strength; not an established maintenance dose
|
Not established for neuropathy
|
150 mg products are available, but no guideline supports 150 mg/day as a standard therapeutic dose
|
300 mg/day
|
Tested in BENDIP; not an established regimen
|
Mixed / limited evidence
|
BENDIP included this dose; overall symptom-score findings were borderline in the intention-to-treat analysis
|
400 mg/day
|
Small BEDIP pilot (3 weeks)
|
Preliminary
|
A small pilot reported improvement in a composite score; it is insufficient to establish a treatment dose
|
600 mg/day
|
Tested in BENDIP and BOND
|
Mixed; long-term efficacy not shown
|
BENDIP per-protocol symptom result was positive, but the 2026 BOND trial found no significant primary or secondary neuropathy benefit
|
Timing
|
Follow the product label; no proven best time
|
No established timing recommendation
|
A phase I study found food did not increase measured thiamine or TDP levels; a specific time of day or routine twice-daily schedule is not established
|
Benfotiamine Dosage for Neuropathy
For diabetic peripheral neuropathy, trials have tested 300–600 mg/day. BENDIP studied 300 mg/day and 600 mg/day for six weeks; its primary symptom-score result was statistically significant in the per-protocol analysis but borderline in the intention-to-treat analysis. The 2026 BOND trial tested 600 mg/day for 12 months and found no significant improvement in its primary or secondary neuropathy outcomes. These study doses should not be treated as a recommendation to self-start or increase benfotiamine.
There is no established dosage of benfotiamine for neuropathy. A clinician should consider a person’s health conditions, medicines and reason for use before advising any supplement.
Benfotiamine Side Effects
Available clinical studies suggest benfotiamine was generally tolerated over the periods studied, but the evidence is limited by relatively small samples and follow-up durations. Long-term safety and safety in specific populations are not fully established. Reported adverse events and the limits of available evidence are discussed below.
Reported Side Effects
Available human safety data are limited by the size and duration of the studies. In two randomized, placebo-controlled Phase I studies in healthy subjects, the incidence and severity of adverse events were similar between benfotiamine and placebo. Reported drug-related events included increased alanine aminotransferase (ALT) and urinary white blood cells (Sheng et al., 2021). In the 12-month BOND trial, adverse-event rates also showed no relevant difference between groups, although only 57 participants were randomized (Ziegler et al., 2026). These findings do not establish safety for every person, dose or duration. Discuss new symptoms and supplement use with a qualified healthcare professional.
Who Should Not Take Benfotiamine?
Benfotiamine is a dietary supplement, and people in the following groups should seek medical advice before using it:
— Individuals with a known allergy or hypersensitivity to thiamine or benfotiamine should avoid it.
— Pregnant or breastfeeding people: clinical trial data on benfotiamine use in pregnancy and lactation are lacking. Do not use doses above normal dietary requirements without advice from a qualified healthcare professional.
— People receiving 5-fluorouracil (5-FU) chemotherapy: NIH information describes concerns about changes in thiamine status during 5-FU treatment. This is not evidence that thiamine supplementation reduces the effectiveness of chemotherapy. Anyone receiving 5-FU should discuss thiamine or benfotiamine supplements with their oncology team before use.
— People with thiamine-responsive pyruvate dehydrogenase deficiency or other rare inborn errors of metabolism affecting B-vitamin handling should use supplements only under specialist supervision.
Safety note: The absence of an established tolerable upper intake level for benfotiamine does not mean unlimited doses are safe. Clinical trials have studied selected doses under supervision; do not exceed a product label or a clinician’s instructions. Keep supplements away from children.
Drug Interactions and Supplement Combinations
Clinical information about benfotiamine interactions is limited, and its interaction profile has not been fully established. The table below summarizes selected medication and supplement considerations. This is not a complete interaction check; ask a pharmacist or prescribing clinician to review your medicines and supplements before starting benfotiamine.
Agent |
Interaction Type |
Clinical Notes |
|---|---|---|
5-Fluorouracil (5-FU) / chemotherapy
|
Evidence uncertain; ask oncology team
|
A specific clinical interaction with benfotiamine is not established. People receiving chemotherapy should check with their oncology team before adding any supplement.
|
Metformin
|
No established benfotiamine interaction
|
Metformin is more clearly associated with vitamin B12 deficiency in some patients. Evidence that it routinely depletes thiamine is insufficient, and benfotiamine has not been shown to prevent metformin-related B12 deficiency.
|
Alpha-lipoic acid (ALA)
|
Often combined; added benefit unproven
|
Benfotiamine and alpha-lipoic acid are marketed together, but evidence that the combination is superior to either ingredient alone is limited. Review combined products with a clinician.
|
Vitamin B12
|
Different nutrient; assess separately
|
B12 deficiency should be assessed and treated on its own merits, especially in people taking metformin. Benfotiamine does not replace vitamin B12.
|
Vitamin B6 (pyridoxine)
|
High supplemental intake can cause neuropathy
|
Avoid excessive B6. The US adult upper limit is 100 mg/day; EFSA's adult upper limit is 12 mg/day. Check total intake across all supplements.
|
Vitamin B1 with benfotiamine / B-complex
|
No proven added benefit; check total B6
|
Combining benfotiamine with regular thiamine or a B-complex is not automatically necessary. Check all B-vitamin amounts, particularly B6, and ask a clinician or pharmacist about the combination.
|
Diabetes medicines (insulin, sulfonylureas, etc.)
|
Do not adjust medicines
|
Benfotiamine has not been shown to reliably lower blood glucose or change medication requirements. Do not change diabetes medicines based on supplement use; discuss all products with your diabetes care team
|
Dr. Berg Benfotiamine Products
Diabetes Knowledge Hub features benfotiamine products from Dr. Berg, the brand available through our affiliate partnership. The product cards below show the specific products currently offered on the Dr. Berg store: Dr. Berg Benfotiamine (300 mg, 30-day supply) and Dr. Berg Nerve Support with Benfotiamine (90 capsules). Review each product’s current Supplement Facts panel, serving size, full ingredient list, allergen information and directions before purchasing; product details and prices may change.
These are commercial product listings, not a ranking of all benfotiamine supplements and not a medical recommendation. Featuring Dr. Berg reflects product availability and our affiliate relationship; it does not mean this brand has been proven clinically superior to other brands or that either product treats or prevents diabetic neuropathy or another disease.
Affiliate disclosure: Diabetes Knowledge Hub may earn a commission if you purchase through the Dr. Berg links on this page. This does not increase your purchase price. Affiliate relationships do not determine our interpretation of the clinical research, and readers should discuss supplement use with a qualified healthcare professional.
Dr. Berg Benfotiamine
300 mg · 30-Day Supply
US$34.99
Support your daily wellness routine with Dr. Berg Benfotiamine. Each serving provides 300 mg of benfotiamine in a convenient supplement designed for everyday use.
300 mg Benfotiamine
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Affiliate link · Price may change
Dr. Berg Nerve Support
With Benfotiamine · 90 Capsules
US$34.99
Support your daily wellness routine with Dr. Berg Nerve Support. This eight-ingredient formula provides 300 mg of benfotiamine, 990 IU of vitamin D3, and 2,010 mcg of vitamin B12 per serving.
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90 Capsules
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Frequently Asked Questions
Benfotiamine is a synthetic, fat-soluble derivative of thiamine (vitamin B1). After absorption, the body converts it into thiamine and active thiamine compounds. It is sold in the United States as a dietary supplement. It has been studied for diabetic neuropathy, but clinical findings are mixed and it is not FDA-approved to treat or prevent diabetes complications.
People most often use it for nerve-health support, but evidence remains uncertain. Short trials have reported some changes in neuropathy symptom scores; the 2026 BOND trial found no significant improvement in its primary or secondary neuropathy outcomes after 12 months. Evidence for kidney, retinal or Alzheimer's benefits is insufficient. It should not replace standard diabetes care.
Benfotiamine is marketed as a supplement to increase thiamine availability and is being studied for diabetic peripheral neuropathy and glucose-related cellular stress. It is not an FDA-approved treatment for neuropathy, kidney disease, retinopathy or Alzheimer's. It is not an emergency substitute for intravenous thiamine in severe deficiency.
Benfotiamine is converted into thiamine compounds that contribute to energy metabolism. Laboratory and animal studies suggest it may influence transketolase and pathways related to advanced glycation end products. Whether these mechanisms produce meaningful benefits in people with diabetes remains uncertain; clinical trials have not consistently shown improved neuropathy outcomes.
Neither is universally better. Benfotiamine can produce higher circulating thiamine metabolites than thiamine hydrochloride in pharmacokinetic studies, but higher blood levels do not prove better clinical outcomes. Standard thiamine is an established nutrient used to prevent or treat deficiency; benfotiamine is a supplement with limited evidence for specific conditions. The appropriate choice depends on the reason for use and clinician advice.
Benfotiamine is a derivative of vitamin B1, not the same chemical form as thiamine. It is converted into thiamine and its phosphorylated metabolites after absorption. The difference is mainly its chemical structure and pharmacokinetics; it does not replace all forms of thiamine, especially injectable thiamine in emergencies.
Available trials generally report tolerability, but side-effect data are limited. Small phase I studies reported drug-related increases in ALT and urinary white blood cells; these findings require clinical interpretation. The 2026 BOND trial reported adverse events in both treatment and placebo groups, with serious events not attributed to benfotiamine by investigators. Ask a clinician if symptoms occur.
People with a known allergy or sensitivity to the product should avoid it. Safety information in pregnancy and breastfeeding is insufficient, so use only with professional guidance. People taking prescription medicines, receiving chemotherapy, or managing liver, kidney or other chronic conditions should discuss supplements with their clinician or pharmacist before starting.
There is no established recommended daily allowance or standard therapeutic dose for benfotiamine. Clinical trials have tested 300–600 mg/day for neuropathy, with mixed findings; a 12-month study using 600 mg/day did not show significant improvement in measured neuropathy outcomes. A 150 mg capsule is a commercial strength, not a proven maintenance dose. Do not self-prescribe a trial dose.
No high-quality evidence identifies a best time of day for benfotiamine or shows that taking it with dietary fat improves clinical outcomes. A phase I pharmacokinetic study found food did not increase measured thiamine or TDP levels. Follow the product label and any clinician instructions; do not split or increase doses without advice.
Benfotiamine is sold as an over-the-counter supplement in the United States through online retailers and some specialty stores. Check the current Supplement Facts panel for the amount per serving, other active ingredients, allergens, manufacturer details and quality-testing information. Product formulas and availability change, and a brand name alone does not establish clinical effectiveness.
Benfotiamine and alpha-lipoic acid are sometimes combined in supplements and studied for neuropathy support. They act through different proposed mechanisms, but evidence that the combination is more effective than either ingredient alone is limited. Review the full label and discuss the combination with a clinician, especially if you take medicines or have a chronic condition.
Medical Disclaimer: This article is for general educational and informational purposes only. It is not medical advice and does not provide a diagnosis or treatment plan. Benfotiamine is sold in the United States as a dietary supplement; it is not an FDA-approved treatment for diabetes, diabetic neuropathy, retinopathy, kidney disease or Alzheimer’s disease. Research findings remain limited and mixed, and the supplement has not been established to prevent, treat or reverse these conditions. Do not start, stop or change diabetes medicines, insulin, thiamine therapy or any prescribed treatment based on this article. Speak with a qualified healthcare professional or pharmacist before using benfotiamine, particularly if you have a medical condition, are pregnant or breastfeeding, or take prescription medicines. Suspected severe thiamine deficiency or new neurological symptoms require urgent medical assessment; oral benfotiamine must not replace emergency treatment.
References
The following peer-reviewed studies and clinical trials are cited in this guide. Links open the publication record or full text where available. Experimental and early-stage findings should not be interpreted as proof of clinical benefit in people.
- Hammes H-P, Du X, Edelstein D, et al. (2003). Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nature Medicine, 9, 294–299. doi:10.1038/nm834. Experimental research.
- Schreeb K-H, Freudenthaler S, Vormfelde S V, et al. (1997). Comparative bioavailability of two vitamin B1 preparations: benfotiamine and thiamine mononitrate. European Journal of Clinical Pharmacology, 52, 319–320.
- Haupt E, Ledermann H, Köpcke W. (2005). Benfotiamine in the treatment of diabetic polyneuropathy (BEDIP study). International Journal of Clinical Pharmacology and Therapeutics, 43, 71–77.
- Stracke H, Gaus W, Achenbach U, et al. (2008). Benfotiamine in diabetic polyneuropathy (BENDIP): a randomized, double-blind, placebo-controlled clinical study. Experimental and Clinical Endocrinology & Diabetes, 116, 600–605.
- Alkhalaf A, Klooster A, van Oeveren W, et al. (2010). A double-blind, randomized, placebo-controlled clinical trial on benfotiamine treatment in patients with diabetic nephropathy. Diabetes Care, 33, 1598–1601.
- Fraser D A, Diep L M, Hovden I A, et al. (2012). The effects of long-term oral benfotiamine supplementation on peripheral nerve function and inflammatory markers in patients with type 1 diabetes. Diabetes Care, 35, 1095–1097.
- Alkhalaf A, Kleefstra N, Groenier K H, et al. (2012). Effect of benfotiamine on advanced glycation endproducts and markers of endothelial dysfunction and inflammation in diabetic nephropathy. PLoS ONE, 7, e40427.
- Gibson G E, Luchsinger J A, Cirio R, et al. (2020). Benfotiamine and cognitive decline in Alzheimer’s disease: results of a randomized placebo-controlled Phase IIa clinical trial. Journal of Alzheimer’s Disease, 78, 989–1010.
- Sheng C C, et al. (2021). Safety, tolerability and pharmacokinetics of single and multiple ascending doses of benfotiamine in healthy subjects. Phase I randomized, placebo-controlled studies.
- Ziegler D, Sipola G, Strom A, et al. (2026). Effects of benfotiamine treatment over 12 months on morphometric, neurophysiological and clinical measures in type 2 diabetes patients with symptomatic polyneuropathy (BOND study). BMJ Open Diabetes Research & Care, 14, e005773. doi:10.1136/bmjdrc-2025-005773.
- U.S. Food and Drug Administration. Questions and Answers on Dietary Supplements. FDA information on supplement regulation and disease claims.