Infliximab (Avakine) is a chimeric monoclonalIgG1antibody that specifically binds toTNF-α. Infliximab prevents the interaction ofTNF-αwith TNF-α receptor (TNFR1 and TNFR2). Infliximab has the potential for autoimmune, chronic inflammatory diseases and diabetic neuropathy research^[1][2].

TNF-α-treated adipocytes shows a significant 64% decrease in insulin-stimulated glucose uptake, whereas Infliximab (10 ng/mL) reverses TNF-α actions by significantly improving glucose incorporation in 3T3L1 adipocytes. Infliximab restores phosphorylation of substrate-2 and AKT by attenuating protein-tyrosine phosphatase 1B (PTP1B) activation. Infliximab ameliorates TNF-α-induced insulin resistance in 3T3L1 adipocytes in vitro by restoring the insulin signalling pathway via PTP1B inhibition^[1].

A single injection of Infliximab (10 μg/g in 100 μl saline/dose ip) in diabetic TNF-α^+/+) mice leads to suppression of the increased serum TNF-α and amelioration of the electrophysiological and biochemical deficits for at least 4 weeks. The increased TNF-α mRNA expression in diabetic dorsal root ganglion is also attenuated by Infliximab^[2].

Solid

170277-31-3

英夫利昔单抗

Please store the product under the recommended conditions in the Certificate of Analysis.