CONQR SIGNED

Project "CONQR" data sheet

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 Project objective

The high number of cancer cases worldwide points to the large global demand for therapeutics for adenocarcinomas (the majority of lung, breast, and pancreatic cancers). Cancer metastases cause more than 90% of cancer patient deaths. There is thus great need to develop more targeted cancer therapies, as well as therapies that enhance the delivery and penetration of chemotherapies to reduce side effects and increase efficacy. A specific societal need is improved therapies for triple-negative breast cancer (TNBC), to which the targeted therapies developed for other breast cancers are not applicable. TNBC treatment, particularly for women with BRCA1 gene mutations, typically involves aggressive chemotherapy, mastectomy, and radiation treatment, with preventive oophorectomy also recommended. The physical and psychological impact of this regimen on young mothers and their families is unquantifiable, and the risk of relapse imposes continuing psychological stress.

We have made a revolutionizing discovery that significantly controlled cancer cell adhesion, cell migration, primary tumor growth, and metastasis. We found that inhibition of the secreted enzyme QSOX1 by a monoclonal antibody inhibitor counteracts extracellular matrix ECM matrix stiffening and prevents tumor cell adhesion and migration. The QSOX1 inhibitor showed an added benefit in controlling primary tumor growth and metastasis when provided together with standard chemotherapy in a TNBC model in mice. The antibody drug we are developing based on these exciting discoveries has great promise for commercialization as a new therapeutic agent for TNBC and for other oncology indications.

The goal of the CONQR project is to perform key preclinical experiments and explore market entering opportunities for commercialization of a novel QSOX1-inhibitory reagent against ECM remodeling in cancer. The intended outcome will be a development and commercialization plan to best position the product for out-licensing.