Date: 2015-02-01
Type of information: Presentation of results at a congress
phase: preclinical
Announcement: presentation of results at the Keystone Symposia on Tumor Immunology in Banff, Canada
Company: Compugen (Israel)
Product: CGEN-15049
Action
mechanism: CGEN-15049 is one of eleven novel B7/CD28-like immune checkpoints predicted in silico by Compugen. It was previously disclosed that this target candidate has an effect on a variety of immune cells, supporting its role as a modulator of the immune system. More specifically, CGEN-15049 has been shown to affect immune cells such as Natural Killer (NK) cells, which are important for innate anti-tumor immune responses, and various T cell types that constitute a crucial component of the adaptive immune response. The adaptive immune response includes inhibition of cytotoxic T lymphocytes, which are responsible for killing tumor cells, and promotion of inducible regulatory T cells, which play a critical role in the immunosuppressive tumor microenvironment. These data support the ability of CGEN-15049 to affect key components of the immune system involved in tumor progression and tumor elimination, thus potentially obstructing the ability of the immune system to fight the tumor. In addition, CGEN-15049 was shown to be expressed on a wide variety of cancers with high clinical unmet need, such as lung, ovarian, breast, colorectal, gastric, prostate and liver cancers.
Disease:
Therapeutic area: Cancer - Oncology
Country:
Trial details:
Latest
news: * On February 9, 2015, Speaking at the Keystone Symposia on Tumor Immunology in Banff, Canada, Arthur Machlenkin, PhD, Head of Immunology Group at Compugen Ltd, presented new experimental results for CGEN-15049, a novel immune checkpoint protein discovered by the Company as a target for cancer immunotherapy. The new data presented for CGEN-15049 demonstrate expression of this protein on tumors isolated from ovarian cancer patients, both on the cancer cells and on immune cells within the tumor. Additional new data also demonstrate expression of CGEN-15049 on a similar population of tumor infiltrating immune cells in tumor-bearing mice. The collective data generated to date by Compugen support the ability of CGEN-15049 to affect key components of the immune system known to be involved in anti-tumor immune responses, supporting its potential as a promising target for immuno-oncology antibody therapy. The CGEN-15049 studies presented at the conference examined expression of this protein on cells isolated from primary tumors of ovarian cancer patients. Expression of CGEN-15049 was observed both on cancer cells and on tumor infiltrating myeloid cells, which have been associated with immune suppression. Additional data demonstrate consistent expression of CGEN-15049 on myeloid immune cells within the tumor microenvironment in mouse cancer models. * On October 1, 2014, Compugen disclosed results from recent studies further confirming CGEN-15049 as a promising target candidate for cancer immunotherapy. These recent studies evaluated the function of this Compugen-discovered immune checkpoint candidate on immune cells derived from the tumor environment of melanoma patients. Based on these and earlier experimental results, CGEN-15049, which is expressed on various cancers including lung, ovarian, breast, colorectal, gastric, prostate and liver, is further advancing in the Company’s Pipeline Program, with ongoing therapeutic antibody development activities against this novel target. In the recent experimental studies now being disclosed, CGEN-15049 continued to demonstrate the potential to inhibit the immune system’s ability to attack cancer cells. More specifically, these studies have shown that overexpression of CGEN-15049 in human melanoma cells inhibits the activity of tumor antigen-specific cytotoxic T cells (CTLs) derived from melanoma patients’ tumors. These effector immune cells, also referred to as tumor infiltrating lymphocytes (TILs), infiltrate tumors and are known to play a major role in anti-tumor immune responses. The results suggest that CGEN-15049 can inhibit the activity of the immune system in the tumor microenvironment through its impact on TILs, which would otherwise fight the tumor. In addition, new initial experimental data from a mouse tumor model further support expression of CGEN-15049 on suppressive immune cells within the tumor microenvironment. Together with the previously reported expression on a wide variety of cancers, and combined with the immunomodulatory activity of CGEN-15049 on immune cells involved in tumor progression, these data support a potential role for this drug target in suppressing anti-tumor immune responses. Therefore, blockade of CGEN-15049 activity by monoclonal antibody therapy is anticipated to result in the stimulation of an anti-tumor immune response, leading to tumor elimination.
