1. Apoptosis
  2. TNF Receptor
  3. Infliximab

Infliximab (Synonyms: Avakine; CT-P13)

Cat. No.: HY-P9970
Handling Instructions

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.

For research use only. We do not sell to patients.

Custom Peptide Synthesis

Infliximab Chemical Structure

Infliximab Chemical Structure

CAS No. : 170277-31-3

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Estimated Time of Arrival: December 31
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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].

IC50 & Target[1]

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].

CAS No.

170277-31-3

Storage

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Keywords:

InfliximabAvakineCT-P13TNF ReceptorTumor Necrosis Factor ReceptorTNFRTNFR2TNFR1anti-TNF-αmonoclonalautoimmuneanti-inflammatoryPTP1BdiabeticneuropathyInhibitorinhibitorinhibit

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Infliximab
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