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Benfotiamine NF-κB inhibitor

Cat.No.S4798

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. This compound suppresses oxidative stress-induced NF-κB activation and prevents the bacterial endotoxin-induced inflammation.
Benfotiamine NF-κB inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 466.45

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Chemical Information, Storage & Stability

Molecular Weight 466.45 Formula

C19H23N4O6PS

 Storage (From the date of receipt)
CAS No. 22457-89-2 -- Storage of Stock Solutions

Synonyms S-Benzoylthiamine O-monophosphate, Benzoylthiamine monophosphate 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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In vitro
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5%TFA : 6 mg/mL

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Mechanism of Action

Targets/IC50/Ki
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]. This compound possesses antitumor activity against leukemia cells. In a panel of nine myeloid leukemia cell lines this chemical impairs the viability of HL-60, NB4, K562 and KG1 cells and also inhibits the growing of primary leukemic blasts. The antitumor activity of this compound is not mediated by apoptosis, necrosis or autophagy, but rather occurs though paraptosis cell death induction. It inhibits the activity of constitutively active ERK1/2 and concomitantly increases the phosphorylation of JNK1/2 kinase in leukemic cells. In addition, this chemical 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. This compound aids the post-ischaemic healing of diabetic animals via PKB/Akt-mediated potentiation of angiogenesis and inhibition of apoptosis[3].
References

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