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Infliximab

  Cat. No.:  A012   Featured
Chemical Structure
170277-31-3
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More than 5000 active chemicals with high quality for research!
Field of application
Infliximab is a tumor necrosis factor TNF-α blocker and a chimeric monoclonal IgG1 antibody and it is used to treat rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and severe or disabling plaque psoriasis.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
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.
MSDS
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MSDS_20535_A012_170277-31-3
COA
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