Human epidermal growth factor receptor 2, or HER2, is a gene that encodes a protein that promotes cell growth and differentiation. HER2 protein overexpression and gene amplification have been documented across multiple cancers.  Previous targeting of HER2 has had a major impact on the subset of patients with HER2-expressing breast and gastric cancer, but there remains a huge amount of work to be done highlighted by a significant individual and global patient need. HER2-positive has been identified in a wide range of malignancies including breast, gastric, bladder, lung, esophageal, colorectal, ovarian, salivary gland, pancreatic, cervical cancers, and others.

Our lead product candidate, BDC-1001, seeks to improve therapeutic outcomes for patients with HER2-expressing tumors: 1) HER2-positive breast and gastric cancer refractory to existing anti-HER2 therapies, 2) tumors with lower expression of HER2 that are not eligible for approved therapies, and 3) other HER2-positive tumors not eligible for approved therapies. In addition, our innovative BDC-1001 approach seeks to address this critically important unmet medical need not only in patients with advanced tumors, but also in adjuvant settings.

Our carcinoembryonic antigen (CEA) program focused on the well-known tumor antigen that is overexpressed in various solid tumors with significant unmet medical need including, but not limited to, colorectal cancer, non-small cell lung cancer, pancreatic cancer, and breast cancer.  CEA allows us to target these cancers, some of which are immunologically “cold”. CEA is upregulated on the cell surface of these cancers and displays minimal receptor-mediated internalization into the cancer cell.

Our PD-L1 Boltbody ISAC focuses on another area with significant unmet medical need, the treatment of patients with tumors that are nonresponsive or become refractory to immune checkpoint blockade. This encompasses more than 15 different tumor types impacting the lives of millions of patients yearly. Our PD-L1 program is a trifunctional therapeutic with the following mechanism: 1) antibody-dependent cellular phagocytosis of the tumor, 2) myeloid activation and adaptive T cell response, and 3) PD-L1/PD-1 checkpoint inhibition.

Our Myeloid Modulator Platform reawakens myeloid cells to attack tumor cells. We identified monoclonal antibodies that are capable of binding to and agonizing a novel cell surface protein (referred to as TAM1) on tumor-supportive macrophages. The activation of these macrophages results in the production of pro-inflammatory cytokines, consistent with the characteristics of tumor-destructive macrophages. TAM1 may have the potential to reprogram tumor-supportive macrophages into tumor-destructive macrophages to elicit a productive anti-tumor immune response. Additionally, KRAS and TP53 mutations may upregulate TAM1 on tumor-associated myeloid cells and could provide an avenue to develop precision medicine with an immune modulator.