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| Cas No.: | 170277-31-3 |
| pH value: | Corresponds to reference standard： PASS |
| Non-reduced CE-SDS: | 98.5% |
| SEC-HPLC: | 99.4% |
| Isoelectric Point: | Corresponds to reference standard:PASS |
| Bacterial Endotoxins Test: | ＜1 EU/ml |
| Exogenous Residual DNA: | 1 pg/mg |
| Residual protein A: | ＜1 ng/mg |
| Biological Activity: | Compared with standard, the range of biological activity is 113% |
| Osmolality: | Corresponds to reference standard: PASS |
| Peptide mapping: | Corresponds to reference standard: PASS |
| N-terminal sequence: | Corresponds to reference standard:PASS |
| 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[1][2]. |
| Target: | TNF-α |
| 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]. |
| 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]. |
| 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. [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. |