Biopharma company Ocean Biomedical, Inc. (NASDAQ: OCEA) on Tuesday said that new findings, co-authored by the company’s scientific co-founder Jack A. Elias in the peer-reviewed journal Immunity, have revealed the mechanisms behind the role of chitinase 3-like-1 (CHI3L1) in the growth of triple-negative breast cancer. Ocean Biomedical develops novel therapies in the areas of oncology, fibrosis, and infectious diseases, in partnership with universities, medical centers, and researchers.
Dr. Chirinjeev Kathuria, Ocean’s executive chairman and founder, commented, “We are excited to see the potential for Ocean’s cancer immunotherapy candidate demonstrated by a range of studies in some of the most aggressive cancers.”
The groundbreaking discoveries by a team led by Dr. William Muller at McGill University and in collaboration with Dr. Elias demonstrate that CHI3L1 stimulates neutrophil elaboration of NETs which block T-cells from contacting and killing the breast cancer tumor. The study also provides further evidence of the potential impact of the company’s anti-Chi3L1 antibody in reversing this process and suppressing breast cancer tumor growth.
The paper deepens the understanding of how CHI3L1 inhibits the body’s natural ability to fight breast cancer tumors. It reveals for the first time another complex pathway by which CHI3L1 inhibits the immune response to cancer, this time by inducing neutrophil recruitment and NETosis, which blocks T-cell infiltration. The paper also provides yet another preclinical demonstration of the effectiveness of Ocean’s Anti-CHI3L1 antibody in reducing tumor growth by targeting CHI3L1 and reversing the T-cell blockade. It says that the tumor control pathway is likely at work in a range of cancers beyond breast cancer, and “targeting CHI3L1 may promote anti-tumor immunity in various tumor types.”
(Source: Ocean Biomedical, Inc.)
“This complex work by our colleagues at McGill has provided one of the most exciting discoveries of my lifetime and adds another layer of understanding about the ways in which CHI3L1 functions as a ‘master regulator’ that is not only at work in many cancers, but working in multiple pathways within individual cancers,” said Dr. Jack Elias.
In April this year, an independent study published in Cancer Research demonstrated the role of CHI3L1 in modulating Glioma stem cells and the effectiveness of Ocean’s candidate in suppressing severe glioblastoma tumor growth. In October, results published in bioRxiv by Elias and colleagues at Yale revealed the role of CHI3L1 in the growth of EGFR-mutant non-small cell lung cancer and the importance of CHI3L1 in the pathogenesis of therapeutic resistance in non-small cell lung cancer.
“We are pleased to see additional research about the potential impact of cancer candidate as we continue to move towards filing an IND,” commented Elizabeth Ng, CEO of Ocean Biomedical.
The studies also demonstrated that the anti-CHI3L1 antibody effectively restored therapeutic responsiveness to tyrosine kinase inhibitors in drug-resistant non-small cell lung cancer with the combination of Ocean’s antibody and a tyrosine kinase inhibitor, stopping human tumor progression by stimulating tumor suppressor genes and inducing tumor cell death. Although these findings were defined in non-small cell lung cancer, they have potential effectiveness in other EGFR-mutation-driven cancers including Glioblastoma and Colon cancer.
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