Catalog #SIM0014

InVivoSIM anti-human IL-6R (Tocilizumab Biosimilar)

Clone Tocilizumab
Reactivities Human
Applications Functional assays
ELISA
Isotype Human IgG1

$243.00 - $8,425.00

$243.00 - $8.00

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  • 100 mg - $8,425.00
  • 50 mg - $4,734.00
  • 25 mg - $3,293.50
  • 5 mg - $943.00
  • 1 mg - $243.00
  • Custom Amount (Quotes Only)
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US Customers - Order within 4 hours, 47 minutes to receive by October 23.

Product Description

This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Tocilizumab making it ideal for research use. This Tocilizumab biosimilar reacts with human IL-6 receptor also known as CD126. IL-6R is an 80 kDa type I cytokine receptor and a member of the immunoglobulin superfamily. IL-6R is expressed by activated T and B lymphocytes, monocytes, hepatocytes, and plasma cells. The IL-6 receptor α chain binds IL-6 but requires association with gp130 to initiate signal transduction. Upon IL-6 binding the IL-6R complex influences antigen-specific immune responses, inflammatory responses, neuronal development, and is a major mediator of the acute phase reaction. Tocilizumab binds to both soluble and membrane bound IL-6R and blocks the binding of IL-6 to IL-6R.

Specifications

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 IL-6R
Reported Applications Functional assays
ELISA
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin ≤0.5EU/mg (≤0.0005EU/μg)
Determined by LAL 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_2894735
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.
Need a Custom Formulation? See All Antibody Customization Options

Product Citations

  • TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells.

    In Nat Commun on 7 July 2026 by Nissen, T. A. D., Baig, A., et al.

    PubMed

    Adult hippocampal neurogenesis is essential for learning, memory, and mood regulation, and its disruption is implicated in ageing, neurodegeneration, and mood disorders. However, the mechanisms linking inflammation to adult hippocampal neurogenesis impairment remain unclear. Here, we identify chronic tumour necrosis factor-alpha signalling as a key driver of neurogenic dysregulation via a previously unrecognised type I interferon autocrine/paracrine loop in human hippocampal progenitor cells. Using a female-derived human in vitro neurogenesis model, single-cell RNA sequencing, and functional T cell migration assays, we show that tumour necrosis factor-alpha induces a robust type I interferon response in hippocampal progenitor cells, promoting chemokine-mediated and CXC motif chemokine receptor 3-dependent T cell recruitment and suppressing neurogenesis. This inflammatory signalling cascade drives a fate switch in hippocampal progenitor cells from a neurogenic trajectory towards an immune-defensive phenotype, with critical implications for infectious and inflammatory disease pathogenesis. These findings uncover a key inflammatory checkpoint regulating human adult hippocampal neurogenesis and highlight potential therapeutic targets to restore neurogenesis in chronic inflammatory states.

  • TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells

    In bioRxiv on 24 June 2025 by Nissen, T. A. D., Baig, A., et al.

  • Inflammatory arthritis immune related adverse events represent a unique autoimmune disease entity primarily driven by T cells, but likely not autoantibodies

    In medRxiv on 6 June 2025 by Zhu, X., Yu, Y., et al.

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