Infliximab (anti-TNF-alpha)

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]

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)

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]

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)