Infliximab Is A Chimeric Monoclonal IgG1 Antibody

Infliximab Is A Chimeric Monoclonal IgG1 Antibody

English name:Infliximab
CAS number:170277-31-3
Another name:
Avakine; Immunoglobulin G, anti-(human tumor necrosis factor) (human-mouse monoclonal ca2 heavy chain), disulfide with human-mouse monoclonal ca2 light chain, dimer; Remicade; Unii-B72hh48flu; CT-P 13; Infliximab USP/EP/BP; Research Grade Infliximab(DHB94403); TNFR1, Infliximab, anti-inflammatory, Avakine, Tumor Necrosis Factor Receptor, autoimmune, diabetic, TNFR, PTP1B, neuropathy, Inhibitor, TNFR2,monoclonal, TNF Receptor, inhibit, CT-P13
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Products Description

 

English name:Infliximab

CAS number:170277-31-3

molecular formula

Molecular weight: 0

EINECS No

Related category: mAb 12; control product; chemical reagent

The Mol file: Mol File

structural formula:

 

Nature of infliximab administration

Storage conditions: Store at-30 C

Form: solid

Color: white to off-white

 

Use and synthesis method of infliximab

 

Bioactivity

Infliximab (Avakine) is a chimeric monoclonal IgG 1 antibody that binds specifically to TNF- α. Infliximab Prevent the interaction of TNFChemicalbook- α with TNF- α receptor 1 (TNFR 1) and TNFR 2. Infliximab Can be used in the study of autoimmune, chronic inflammatory diseases and diabetic neuropathy.

 

Target spot

TNF-α

 

In vitro study

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.

 

In vivo research

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.

 

Security information

Toxic substances data: 170277-31-3 (Hazardous Substances Data)

 

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