| Bioactivity | 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]. |
| Invitro | 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]. |
| Name | Infliximab |
| CAS | 170277-31-3 |
| Appearance | Solid |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Reference | [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. [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. |