Catalog #CP160

RecombiMAb mouse IgG2a isotype control, unknown specificity

Clone MOPC-21-CP160
Product Citations 1
Isotype Mouse IgG2a, κ

$235.00 - $6,391.00

$235.00 - $6.00

Choose an Option...
  • 100 mg - $6,391.00
  • 50 mg - $4,574.00
  • 25 mg - $3,182.00
  • 5 mg - $911.00
  • 1 mg - $235.00
  • Custom Amount (Quotes Only)
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Product Description

The MOPC-21-CP160 monoclonal antibody is a recombinant version of the original MOPC-21 antibody. The variable domain sequences are identical to the original MOPC-21 antibody but the constant region sequences have been switched from mouse IgG1 to mouse IgG2a. MOPC-21-CP160 contains no Fc mutations. The MOPC-21-CP160 monoclonal antibody is ideal for use as a non-reactive isotype-matched control for mouse IgG2a antibodies in in vivo and in vitro applications.

Specifications

Isotype Mouse IgG2a, κ
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin ≤0.5EU/mg (≤0.0005EU/μg)
Determined by LAL gel clotting assay
Purity ≥95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Production Purified from CHO cell supernatant in an animal free facility
Purification Protein A
RRID AB_2927528
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

Product Citations

  • The Combination of Anti-CD47 Antibody with CTLA4 Blockade Enhances Anti-Tumor Immunity in Non-Small Cell Lung Cancer via Normalization of Tumor Vasculature and Reprogramming of the Immune Microenvironment.

    In Cancers (Basel) on 19 February 2024 by Zhuang, Z., Zhou, J., et al.

    PubMed

    In solid tumors, the formidable anti-tumor impact resulting from blocking the "don't eat me" signal, arising from CD47-SIRPα interaction, is constrained, especially compared to its efficacy in hematopoietic malignancies. Activating macrophage anti-tumor activity not only necessitates the inhibition of the "don't eat me" signal, but also the activation of the "eat me" (pre-phagocyte) signal. Intriguingly, the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) antibody (Ab) has been identified to stimulate Fc receptor-mediated active phagocytes in the tumor microenvironment, thereby generating "eat me" signals. This study postulates that concurrently targeting CD47 and CTLA4 could intensify the anti-tumor effects by simultaneously blocking the "don't eat me" signal while triggering the "eat me" signal. The experimental data from this investigation confirm that the combined targeting of CD47 and CTLA4 enhances immunity against solid tumors in LLC cell-transplanted tumor-bearing mice. This effect is achieved by reducing myeloid-derived suppressor cell infiltration while increasing the presence of effector memory CD8+ T cells, NK1.1+ CD8+ T cells, and activated natural killer T cells. Meanwhile, combination therapy also alleviated anemia. Mechanistically, the anti-CD47 Ab is shown to upregulate CTLA4 levels in NSCLC cells by regulating Foxp1. Furthermore, targeting CD47 is demonstrated to promote tumor vascular normalization through the heightened infiltration of CD4+ T cells. These findings suggest that the dual targeting of CD47 and CTLA4 exerts anti-tumor effects by orchestrating the "eat me" and "don't eat me" signals, reshaping the immune microenvironment, and fostering tumor vascular normalization. This combined therapeutic approach emerges as a potent strategy for effectively treating solid tumors.

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