CTLA-4 Antibodies & Proteins: Reagents for Co-Stimulatory Pathway Research

CTLA-4 (cytotoxic T lymphocyte-associated protein 4, CD152) was the first immune checkpoint receptor to be therapeutically targeted in cancer.

Target Biology and Clinical Relevance

Unlike PD-1, which acts primarily in peripheral tissues (including the tumor), CTLA-4 acts early in the immune response — in lymph nodes during T cell priming. CTLA-4 competes with the co-stimulatory receptor CD28 for binding to B7 ligands (CD80 and CD86) on antigen-presenting cells. By outcompeting CD28, CTLA-4 suppresses T cell activation at the priming stage.

Ipilimumab (anti-CTLA-4) was approved in 2011 for melanoma, making it the first checkpoint inhibitor to receive FDA approval. Tremelimumab was subsequently approved in combination with durvalumab for HCC and NSCLC.

In research, anti-CTLA-4 antibodies are used for: flow cytometry (surface CTLA-4 on activated T cells, intracellular CTLA-4 in Tregs), IHC on tumor tissue, and functional blocking assays (T cell activation, MLR enhancement). Research biosimilar ipilimumab is available for PK/ADA assay development and preclinical combination studies.

CTLA-4 Ig fusion proteins (analogous to abatacept/belatacept) are available as recombinant reagents for competitive binding assays and B7 ligand blocking studies.

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References

1. Pardoll DM. The blockade of immune checkpoints in cancer immunotherapy. Nat Rev Cancer. 2012;12(4):252-264. doi: 10.1038/nrc3239

2. Sharma P, Allison JP. The future of immune checkpoint therapy. Science. 2015;348(6230):56-61. doi: 10.1126/science.aaa8172

3. Wei SC, Duffy CR, Allison JP. Fundamental mechanisms of immune checkpoint blockade therapy. Cancer Discov. 2018;8(9):1069-1086. doi: 10.1158/2159-8290.CD-18-0367

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