Infliximab
Modify Date: 2024-01-09 19:32:00
Infliximab structure
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Common Name | Infliximab | ||
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| CAS Number | 170277-31-3 | Molecular Weight | N/A | |
| Density | N/A | Boiling Point | N/A | |
| Molecular Formula | N/A | Melting Point | N/A | |
| MSDS | N/A | Flash Point | N/A | |
Use of InfliximabInfliximab (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]. |
| Name | Infliximab |
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| 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]. |
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| Related Catalog | |
| 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 |
| Storage condition | -20℃ |
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