Infliximab (anti-TNF-alpha)

Catalog No.A2019 Batch: A201901

Technical Data

CAS No.	170277-31-3
Formulation	PBS, pH 7.0 Contains no stabilizers or preservatives
Isotype	Chimeric IgG1
Source	Chimeric (mouse/human)
Storage (From the date of receipt)	Store the undiluted solution at 4°C in the dark to avoid freeze-thaw cycles
Purity	97.9%
Protein concentration	5.00mg/ml
Endotoxin Level	<1EU/mg

Biological Activity

Description	Infliximab (anti-TNF-alpha) is a purified, recombinant DNA-derived chimeric human-mouse IgG monoclonal antibody that consists of mouse heavy and light chain variable regions combined with human heavy and light chain constant regions. Infliximab neutralizes the biological activity of TNF-α by binding with high affinity to the soluble and transmembrane forms of TNF-α, and inhibits or prevents the effective binding of TNF-α with its receptors. MW=144.2 kDa.
In vitro	Infliximab ameliorates TNF-alpha-induced insulin resistance in 3T3L1 adipocytes in vitro by restoring the insulin signalling pathway via PTP1B inhibition.^[1] Infliximab does not exacerbate production of inflammatory cytokines, and does not affect expression of TNFR, proliferation of ARPE-19, HTLV-1 proviral load, or apoptosis of ARPE-19. Infliximab does not exacerbate HTLV-1-related inflammation in the eye and represents an acceptable treatment option under HTLV-1 infectious conditions.^[3]
In vivo	A single injection of infliximab 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 wk. Moreover, the increased TNF-α mRNA expression in diabetic DRG is also attenuated by infliximab, suggesting infliximab's effects may involve the local suppression of TNF-α. Infliximab, an agent currently in clinical use, is effective in targeting TNF-α action and expression and amelioration of diabetic neuropathy in mice.^[2] Mice given increasing doses of infliximab produces increasing levels of ADAs. Blood samples from mice given injections of human TNF and infliximab contains infliximab-TNF complexes.^[4]

Protocol (Only for Reference)

Cell Assay:	Objective: Glucose uptake assay Cells: murine 3T3L1 cell line Concentrations: 10 ng/ml Incubation Time: 2 hr Method: For glucose uptake assay, 3T3L1 mature adipocytes are in vitro cultured for 2 hr at 37°C in humidified 5% CO₂ atmosphere, using 6-well cell-culture plates at a density of 30×10⁴ cells per well. Adipocytes are stimulated twice at zero and 60 minutes with 2 μM insulin. In the infliximab-treated group, adipocytes are stimulated with 10 ng/ml infliximab at the beginning of the 2-hr in vitro assay. Reference: https://pubmed.ncbi.nlm.nih.gov/30260514 Objective: Cell Counts Cells: ARPE-19 cells, MT-2 cells, Jurkat cells Concentrations: 10 μg/ml Incubation Time: 24 h, 48 h, 72 h Method: ARPE-19 cells (2 × 10⁴) are co-cultured with three times the number of MT2 or Jurkat cells with or without Infliximab. After 0, 24, 48, or 72 h of co-culture, we remove the supernatants, trypsinized ARPE-19, and count the number of ARPE-19 cells under light microscopy. Reference: https://pubmed.ncbi.nlm.nih.gov/31620105 Infliximab can apply to humanized mice, non-humanized mice (eg: C57BL/6 mice), peripheral blood and other related assays (Only for Reference)
Animal Study:	Objective: To evaluate the effect on diabetic neuropathy Animal Models: 8-week-old C57BL/6J (WT, TNF-α+/+) and TNF-α-deficient (TNFα−/−) mice of strain B6.129S6-Tnf^tm1Gkl/J in the C57BL/6 background Formulation: Saline Dosages: 10 μg/g Administration: i.p. Reference: https://pubmed.ncbi.nlm.nih.gov/21810933 Objective: pharmacokinetic (PK) study Animal Models: 6–8 week-old female C57BL/6 mice Formulation: -- Dosages: 0.3075 μg/g, 0.384 μg/g, 0.769 μg/g, 1.538 μg/g, 6.15 μg/g, 30.75 μg/g, 246 μg/g Administration: i.p. Reference: https://pubmed.ncbi.nlm.nih.gov/31401142 Infliximab can apply to humanized mice, non-humanized mice (eg: C57BL/6 mice), peripheral blood and other related assays (Only for Reference)

Cell Assay:

Objective: Glucose uptake assay
Cells: murine 3T3L1 cell line
Concentrations: 10 ng/ml
Incubation Time: 2 hr
Method: For glucose uptake assay, 3T3L1 mature adipocytes are in vitro cultured for 2 hr at 37°C in humidified 5% CO₂ atmosphere, using 6-well cell-culture plates at a density of 30×10⁴ cells per well. Adipocytes are stimulated twice at zero and 60 minutes with 2 μM insulin. In the infliximab-treated group, adipocytes are stimulated with 10 ng/ml infliximab at the beginning of the 2-hr in vitro assay.
Reference: https://pubmed.ncbi.nlm.nih.gov/30260514

Objective: Cell Counts
Cells: ARPE-19 cells, MT-2 cells, Jurkat cells
Concentrations: 10 μg/ml
Incubation Time: 24 h, 48 h, 72 h
Method: ARPE-19 cells (2 × 10⁴) are co-cultured with three times the number of MT2 or Jurkat cells with or without Infliximab. After 0, 24, 48, or 72 h of co-culture, we remove the supernatants, trypsinized ARPE-19, and count the number of ARPE-19 cells under light microscopy.
Reference: https://pubmed.ncbi.nlm.nih.gov/31620105

Infliximab can apply to humanized mice, non-humanized mice (eg: C57BL/6 mice), peripheral blood and other related assays (Only for Reference)

Animal Study:

Objective: To evaluate the effect on diabetic neuropathy
Animal Models: 8-week-old C57BL/6J (WT, TNF-α+/+) and TNF-α-deficient (TNFα−/−) mice of strain B6.129S6-Tnf^tm1Gkl/J in the C57BL/6 background
Formulation: Saline
Dosages: 10 μg/g
Administration: i.p.
Reference: https://pubmed.ncbi.nlm.nih.gov/21810933

Objective: pharmacokinetic (PK) study
Animal Models: 6–8 week-old female C57BL/6 mice
Formulation: --
Dosages: 0.3075 μg/g, 0.384 μg/g, 0.769 μg/g, 1.538 μg/g, 6.15 μg/g, 30.75 μg/g, 246 μg/g
Administration: i.p.
Reference: https://pubmed.ncbi.nlm.nih.gov/31401142

Infliximab can apply to humanized mice, non-humanized mice (eg: C57BL/6 mice), peripheral blood and other related assays (Only for Reference)

References	[1] Lucia A Méndez-García, et al. Scand J Immunol. 2018 Nov;88(5):e12716. [2] Isamu Yamakawa, et al. Am J Physiol Endocrinol Metab. 2011 Nov;301(5):E844-52. [3] Minami Uchida, et al. Front Microbiol. 2019 Sep 18;10:2148. [4] Haggai Bar-Yoseph, et al. Gastroenterology. 2019 Nov;157(5):1338-1351.e8. + Expand

References

[4] Haggai Bar-Yoseph, et al. Gastroenterology. 2019 Nov;157(5):1338-1351.e8.

+ Expand

Selleck's Infliximab (anti-TNF-alpha) has been cited by 5 publications

Targeting autophagy overcomes cancer-intrinsic resistance to CAR-T immunotherapy in B-cell malignancies [ Cancer Commun (Lond), 2024, 44(3):408-432]	PubMed: 38407943
Modeling and therapeutic targeting of inflammation-induced hepatic insulin resistance using human iPSC-derived hepatocytes and macrophages [ Nat Commun, 2023, 14(1):3902]	PubMed: 37400454
Modeling and therapeutic targeting of inflammation-induced hepatic insulin resistance using human iPSC-derived hepatocytes and macrophages [ Nat Commun, 2023, 14(1):3902]	PubMed: 37400454
Human iPSC-Derived Proinflammatory Macrophages cause Insulin Resistance in an Isogenic White Adipose Tissue Microphysiological System [ Small, 2023, e2203725.]	PubMed: 37104853
c-Met is a novel tumor associated antigen for T-cell based immunotherapy against NK/T cell lymphoma [ Front Immunol, 2022, 13:854995]	PubMed: 35359966

FOR RESEARCH USE ONLY. NOT FOR USE IN HUMANS.

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