CAS 170277-31-3|Infliximab
Introduction：Basic information about CAS 170277-31-3|Infliximab, including its chemical name, molecular formula, synonyms, physicochemical properties, and safety information, etc.
| Common Name | Infliximab | ||
|---|---|---|---|
| CAS Number | 170277-31-3 | Molecular Weight | / |
| Density | / | Boiling Point | / |
| Molecular Formula | / | Melting Point | / |
| MSDS | / | Flash Point | / |
Names
| Name | Infliximab |
|---|
Infliximab BiologicalActivity
| 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]. |
|---|---|
| Related Catalog | Research Areas >>Inflammation/ImmunologyResearch Areas >>Metabolic DiseaseResearch Areas >>Neurological Disease |
| Target | TNF-α |
| 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]. |
| 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. |
Chemical & Physical Properties
| Storage condition | -20℃ |
|---|
