Cytotoxic T-Lymphocyte Antigen-4 (CTLA-4) Inhibitor Therapeutics -Clinical Trials & Results | Agenus, AstraZeneca, ImmunOs Therapeutics AG

Cytotoxic T-lymphocyte antigen-4 (CTLA-4) plays important role in the T-cell regulation at an early stage of naive T-cell activation, primarily in the lymph nodes. CTLA-4 has emerged as an attractive cancer immunotherapy as a part of “immune checkpoint blockade”.

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CTLA-4 pathway inhibitors enhance T-cell activation and amplify T-cell proliferation. Successful results of immune checkpoint inhibitors in cancer immunotherapy has led to the development of many new agents and strategies, including combination for the treatment of various cancers.

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Despite of many advancements in the development of anti-cancer therapies, cancer is still one of the major causes of deaths, globally. Combination therapies are proving to be more efficient than monotherapy for the treatment of cancer.

Studies have demonstrated that concurrent PD-1 and CTLA-4 blockade have shown positive results in patients with advanced melanoma. This provides huge opportunities for development of better combinatorial immunotherapeutic therapies for checkpoint blockade with molecular targeted therapies, angiogenesis inhibition and novel vaccines.

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Agenus Inc. is in the process of developing AGEN1884 as a monoclonal antibody which acts as a CTLA-4 inhibitor for the treatment of non-small cell lung cancer. It is also being studied in combination with pembrolizumab, for the treatment of cancer. Some of the other companies having pipeline of CTLA-4 inhibitor include AstraZeneca PLC, ImmunOs Therapeutics AG, Tikcro Technologies Ltd.

The report provides a comprehensive understanding of the pipeline activities covering all drug candidates under various stages of development, with detailed analysis of pipeline and clinical trials. Pipeline analysis of drugs by phases includes product description and development activities including information about clinical results, designations, collaborations, licencing, grants, technology and others.

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This release was published on openPR.