MedChemExpress LLC (MCE)

MedChemExpress - Model Infliximab - 170277-31-3

Infliximab (Avakine) is a chimeric monoclonal IgG1 antibody that specifically binds to TNF-α. Infliximab prevents the interaction of TNF-α with TNF-α receptor (TNFR1 and TNFR2). Infliximab has the potential for autoimmune, chronic inflammatory diseases and diabetic neuropathy research[1][2].

Infliximab

MCE China：Infliximab

Brand：MedChemExpress (MCE)

Cat. No.HY-P9970

CAS：170277-31-3

Synonyms：Avakine; CT-P13

Purity：90.30%

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

Shipping：Shipping with dry ice.

Description：Infliximab (Avakine) is a chimeric monoclonal IgG1 antibody that specifically binds to TNF-α. Infliximab prevents the interaction of TNF-α with TNF-α receptor (TNFR1 and TNFR2). Infliximab has the potential for autoimmune, chronic inflammatory diseases and diabetic neuropathy research.

In Vitro：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].

In Vivo：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].

Isotype：Human IgG1 kappa

Recommend Isotype Controls：Human IgG1 kappa, Isotype Control

References：

[1]. Lucia A Méndez-García, et al. Infliximab ameliorates tumor necrosis factor-alpha-induced insulin resistance by attenuating PTP1B activation in 3T3L1 adipocytes in vitro. Scand J Immunol. 2018 Nov;88(5):e12716. [Content Brief]

[2]. Isamu Yamakawa, et al. Inactivation of TNF-α ameliorates diabetic neuropathy in mice. Am J Physiol Endocrinol Metab. 2011 Nov;301(5):E844-52. [Content Brief]

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