$235.00 - $6,391.00

$235.00 - $6.00

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  • 100 mg - $6,391.00
  • 50 mg - $4,574.00
  • 25 mg - $3,182.00
  • 5 mg - $911.00
  • 1 mg - $235.00
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Product Description

This mouse IgG2a isotype control antibody reacts with hen egg lysozyme and has low or no specific binding to any mouse sample. The D265A substitution has been shown to decrease effector functions by disrupting the Fc/Fcγ receptor interface.

Specifications

Isotype Mouse IgG2a
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Mutations D265A
Immunogen Hen egg lysozyme (HEL)
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_2927524
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

  • CREB-binding protein/P300 bromodomain inhibition reduces neutrophil accumulation and activates antitumor immunity in triple-negative breast cancer.

    In JCI Insight on 17 September 2024 by Yuan, X., Hao, X., et al.

    PubMed

    Tumor-associated neutrophils (TANs) have been shown to promote immunosuppression and tumor progression, and a high TAN frequency predicts poor prognosis in triple-negative breast cancer (TNBC). Dysregulation of CREB-binding protein (CBP)/P300 function has been observed with multiple cancer types. The bromodomain (BRD) of CBP/P300 has been shown to regulate its activity. In this study, we found that IACS-70654, a selective CBP/P300 BRD inhibitor, reduced TANs and inhibited the growth of neutrophil-enriched TNBC models. In the bone marrow, CBP/P300 BRD inhibition reduced the tumor-driven abnormal differentiation and proliferation of neutrophil progenitors. Inhibition of CBP/P300 BRD also stimulated the immune response by inducing an IFN response and MHCI expression in tumor cells and increasing tumor-infiltrated cytotoxic T cells. Moreover, IACS-70654 improved the response of a neutrophil-enriched TNBC model to docetaxel and immune checkpoint blockade. This provides a rationale for combining a CBP/P300 BRD inhibitor with standard-of-care therapies in future clinical trials for neutrophil-enriched TNBC.

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