Benfotiamine

Catalog No.S4798 Synonyms: S-Benzoylthiamine O-monophosphate, Benzoylthiamine monophosphate

For research use only.

Benfotiamine (S-Benzoylthiamine O-monophosphate) is a synthetic S-acyl derivative of thiamine (vitamin B1) and has been investigated for the treatment and prevention of Diabetic Nephropathy and Diabetes Mellitus, Type 2. Benfotiamine suppresses oxidative stress-induced NF-κB activation and prevents the bacterial endotoxin-induced inflammation.

Benfotiamine Chemical Structure

CAS No. 22457-89-2

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Biological Activity

Description Benfotiamine (S-Benzoylthiamine O-monophosphate) is a synthetic S-acyl derivative of thiamine (vitamin B1) and has been investigated for the treatment and prevention of Diabetic Nephropathy and Diabetes Mellitus, Type 2. Benfotiamine suppresses oxidative stress-induced NF-κB activation and prevents the bacterial endotoxin-induced inflammation.
Targets
NF-κB [4]
()
In vitro

Benfotiamine improves the expression of endothelial cell markers in EPCs, restores eNOS levels, and recovers the ability of EPCs to participate in angiogenic processes. It is able to dampen glucose toxicity effects on endothelial progenitors[1]. Benfotiamine possesses antitumor activity against leukemia cells. In a panel of nine myeloid leukemia cell lines benfotiamine impairs the viability of HL-60, NB4, K562 and KG1 cells and also inhibits the growing of primary leukemic blasts. The antitumor activity of benfotiamine is not mediated by apoptosis, necrosis or autophagy, but rather occurs though paraptosis cell death induction. Benfotiamine inhibits the activity of constitutively active ERK1/2 and concomitantly increases the phosphorylation of JNK1/2 kinase in leukemic cells. In addition, benfotiamine induces the down regulation of the cell cycle regulator CDK3 which results in G1 cell cycle arrest in the sensitive leukemic cells[2].

In vivo

Benfotiamine might exert vascular and renal benefits by modulating mechanisms independent or downstream of ROS formation. Benfotiamine aids the post-ischaemic healing of diabetic animals via PKB/Akt-mediated potentiation of angiogenesis and inhibition of apoptosis[3].

Protocol (from reference)

Cell Research:

[2]

  • Cell lines: leukemia cells (HL60, AML 1, NB4 cells)
  • Concentrations: 50 μM
  • Incubation Time: 24, 48, 72, 96 h
  • Method:

    Cell viability is assessed using a colorimetric MTT metabolic activity assay.

  • (Only for Reference)
Animal Research:

[3]

  • Animal Models: diabetic animal model induced by STZ (male CD1 mice)
  • Dosages: 80 mg/kg
  • Administration: oral administration
  • (Only for Reference)

Solubility (25°C)

In vitro

DMSO 0.01 mg/mL
(0.02 mM)
Water Insoluble
Ethanol Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 466.45
Formula

C19H23N4O6PS

CAS No. 22457-89-2
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CC1=NC=C(C(=N1)N)CN(C=O)C(=C(CCOP(=O)(O)O)SC(=O)C2=CC=CC=C2)C

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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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