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Leveraging the 3D antigen design approach, we generated a new lead antibody that exclusively blocks the epitope binding surface of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4 also known as CD152), preventing its ligands CD80 and CD86 from binding to it. We focus on antibody drug-candidates that exclusively block this binding surface domain and do not block adjacent domains.
In 2011 a CTLA-4 antibody was first approved in the U.S. for clinical treatment of late stage melanoma. Revenues from this product exceeded $1.0 billion in 2016. Clinical results of a combination treatment with a PD1 antibody showed a strong synergy in the treatment of late stage melanoma, both as a first line therapy and as a second line of treatment. The U.S. FDA approved the combination treatment of both antibodies for late stage melanoma. With this synergetic clinical effect of the combination treatment, additional clinical indication in oncology for CTLA-4 antibody have shown promising results and are pending regulatory approval.
T cells or T lymphocytes are a type of lymphocyte (a type of white blood cell) that play a central role in cell-mediated immunity. T lymphocytes recognize and destroy non-self cells, including cancer cells. A natural inhibitory mechanism of binding CTLA-4, a receptor that resides on the cytotoxic T lymphocytes (CTLs) in the lymph node, by its ligands CD80 and CD86, interrupts this destruction. A CTLA-4 antibody which binds to the surface domain of CTLA-4 receptor and its ligands, CD80 and CD86, reverses this inhibitory effect on the immune system. By blocking this interaction, the “turning-off” of the cytotoxic reaction is reversed, and allows the inhibitory signal transmitted through other pathways to cause the CTLs to destroy the cancer cells.
We plan to initially focus our pre-clinical trials on models that address melanoma, alone and in combination with PD1 antibody.