$172.00 - $4,494.00

$172.00 - $4.00

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  • 100 mg - $4,494.00
  • 50 mg - $3,175.00
  • 25 mg - $2,109.00
  • 5 mg - $630.00
  • 1 mg - $172.00
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Product Description

The 177R4 monoclonal antibody reacts with mouse Fibrinogen-like protein 1 (FGL-1). FGL-1 is a member of the fibrinogen family of proteins. Under normal physiological conditions, FGL-1 is primarily secreted from hepatocytes and contributes to mitogenic and metabolic functions. FGL-1 is produced at high levels in various tumors including lung cancer and melanoma. High FGL-1 expression is associated with resistance to anti-PD-1/PD-L1 therapy and poor prognosis of cancer patients. Recently, FGL-1 has been identified as a major inhibitory ligand for LAG-3, a receptor that negatively regulates the proliferation, activation, and effector function of T cells. In murine cancer models, the 177R4 clone has been shown to block FGL-1 binding to LAG-3 resulting in boosted T cell activity and slowed tumor growth.

Specifications

Isotype Rat IgG2a, κ
Recommended Isotype Control(s) InVivoMAb rat IgG2a isotype control, anti-trinitrophenol
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Immunogen Murine FGL-1-Ig fusion protein
Reported Applications in vivo FGL-1 blockade
in vitro FGL-1 blockade
Flow cytometry
Immunohistochemistry (paraffin)
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin ≤1EU/mg (≤0.001EU/μg)
Determined by LAL gel clotting assay
Purity ≥95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Production Purified from cell culture supernatant in an animal-free facility
Purification Protein G
RRID AB_2894752
Molecular Weight 150 kDa
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

Application References

Flow Cytometry, Immunohistochemistry (paraffin), in vitro FGL-1 blockade, in vivo FGL-1 blockade
Wang, J., et al. (2019). "Fibrinogen-like Protein 1 Is a Major Immune Inhibitory Ligand of LAG-3" Cell 176(1-2): 334-347 e312.
PubMed

Lymphocyte-activation gene 3 (LAG-3) is an immune inhibitory receptor, with major histocompatibility complex class II (MHC-II) as a canonical ligand. However, it remains controversial whether MHC-II is solely responsible for the inhibitory function of LAG-3. Here, we demonstrate that fibrinogen-like protein 1 (FGL1), a liver-secreted protein, is a major LAG-3 functional ligand independent from MHC-II. FGL1 inhibits antigen-specific T cell activation, and ablation of FGL1 in mice promotes T cell immunity. Blockade of the FGL1-LAG-3 interaction by monoclonal antibodies stimulates tumor immunity and is therapeutic against established mouse tumors in a receptor-ligand inter-dependent manner. FGL1 is highly produced by human cancer cells, and elevated FGL1 in the plasma of cancer patients is associated with a poor prognosis and resistance to anti-PD-1/B7-H1 therapy. Our findings reveal an immune evasion mechanism and have implications for the design of cancer immunotherapy.

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Product Citations

  • Yap methylation-induced FGL1 expression suppresses anti-tumor immunity and promotes tumor progression in KRAS-driven lung adenocarcinoma.

    In Cancer Commun (Lond) on 1 November 2024 by Jiang, J., Ye, P., et al.

    PubMed

    Despite significant strides in lung cancer immunotherapy, the response rates for Kirsten rat sarcoma viral oncogene homolog (KRAS)-driven lung adenocarcinoma (LUAD) patients remain limited. Fibrinogen-like protein 1 (FGL1) is a newly identified immune checkpoint target, and the study of related resistance mechanisms is crucial for improving the treatment outcomes of LUAD patients. This study aimed to elucidate the potential mechanism by which FGL1 regulates the tumor microenvironment in KRAS-mutated cancer.

  • ALKBH5 enhances efficiency of anti-PD-1/PD-L1 therapy by reducing Lnc-XIST/miRNA- 124-3p mediated FGL1 expression in bladder cancer

    In Research Square on 11 October 2022 by Xia, Y., Jiang, X., et al.

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