InVivoSIM anti-human TNFα (Infliximab Biosimilar)

Catalog #SIM0006

$224.00 - $7,752.00

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  • 100 mg - $7,752.00
  • 50 mg - $4,356.00
  • 25 mg - $3,030.00
  • 5 mg - $868.00
  • 1 mg - $224.00
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Product Details

This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Infliximab making it ideal for research use. This Infliximab biosimilar reacts with human TNFα (tumor necrosis factor-alpha) a multifunctional proinflammatory cytokine. TNFα exists as a soluble 17 kDa monomer, which forms homotrimers in circulation or as a 26 kDa membrane-bound form. TNFα belongs to the TNF superfamily of cytokines and signals through its two receptors, TNFR1 and TNFR2 which can be activated by both the soluble trimeric and membrane-bound and forms of TNFα. TNFα is primarily produced by macrophages in response to foreign antigens such as bacteria (lipopolysaccharides), viruses, and parasites as well as mitogens and other cytokines but can also be expressed by monocytes, neutrophils, NK cells, CD4 T cells and some specialized dendritic cells. TNFα is known to play key roles in a wide spectrum of biological processes including immunoregulation, cell proliferation, differentiation, apoptosis, antitumor activity, inflammation, anorexia, cachexia, septic shock, hematopoiesis, and viral replication. TNFα dysregulation has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Infliximab blocks the interaction of TNFα with the TNFR1 (p55) and TNFR2 (p75) resulting in a down-regulation of the inflammatory response associated with autoimmune diseases.


Isotype Human IgG1
Recommended Isotype Control(s) RecombiMAb human IgG1 isotype control, anti-hen egg lysozyme
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Immunogen Human TNFα
Reported Applications TNFα neutralization
Flow Cytometry
Western Blot
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <1EU/mg (<0.001EU/μg)
Determined by LAL gel clotting assay
Aggregation <5%
Determined by SEC
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Production Purified from cell culture supernatant in an animal-free facility
Purification Protein A
RRID AB_2894727
Molecular Weight 150 kDa
Murine Pathogen Tests Ectromelia/Mousepox Virus: Negative
Hantavirus: Negative
K Virus: Negative
Lactate Dehydrogenase-Elevating Virus: Negative
Lymphocytic Choriomeningitis virus: Negative
Mouse Adenovirus: Negative
Mouse Cytomegalovirus: Negative
Mouse Hepatitis Virus: Negative
Mouse Minute Virus: Negative
Mouse Norovirus: Negative
Mouse Parvovirus: Negative
Mouse Rotavirus: Negative
Mycoplasma Pulmonis: Negative
Pneumonia Virus of Mice: Negative
Polyoma Virus: Negative
Reovirus Screen: Negative
Sendai Virus: Negative
Theiler’s Murine Encephalomyelitis: Negative
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
in vitro TNFα neutralization
Zheng N, Fang J, Xue G, Wang Z, Li X, Zhou M, Jin G, Rahman MM, McFadden G, Lu Y. (2022). "Induction of tumor cell autosis by myxoma virus-infected CAR-T and TCR-T cells to overcome primary and acquired resistance" Cancer Cell 40(9):973-985.e7. PubMed

Cytotoxicity of tumor-specific T cells requires tumor cell-to-T cell contact-dependent induction of classic tumor cell apoptosis and pyroptosis. However, this may not trigger sufficient primary responses of solid tumors to adoptive cell therapy or prevent tumor antigen escape-mediated acquired resistance. Here we test myxoma virus (MYXV)-infected tumor-specific T (TMYXV) cells expressing chimeric antigen receptor (CAR) or T cell receptor (TCR), which systemically deliver MYXV into solid tumors to overcome primary resistance. In addition to T cell-induced apoptosis and pyroptosis, tumor eradication by CAR/TCR-TMYXV cells is also attributed to tumor cell autosis induction, a special type of cell death. Mechanistically, T cell-derived interferon γ (IFNγ)-protein kinase B (AKT) signaling synergizes with MYXV-induced M-T5-SKP-1-VPS34 signaling to trigger robust tumor cell autosis. CAR/TCR-TMYXV-elicited autosis functions as a type of potent bystander killing to restrain antigen escape. We uncover an unexpected synergy between T cells and MYXV to bolster solid tumor cell autosis that reinforces tumor clearance.