Our Pipeline
HER2
HER2+ Colorectal, Endometrial, Gastroesophageal Cancer
HER2+ Metastatic Breast Cancer*
Phase 2
Phase 2
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 significant amount of work to be done highlighted by a significant individual and global patient need.
Our lead product candidate, BDC-1001, currently advancing into a Phase 2 clinical trial, seeks to improve therapeutic outcomes for patients with HER2-positive colorectal, endometrial, gastroesophageal and metastatic breast cancer.
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 Dectin-2) 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. Dectin-2 may have the potential to reprogram tumor-supportive macrophages into tumor-destructive macrophages to elicit a productive anti-tumor immune response.
Bispecific Boltbody ISACs
Undisclosed
Discovery
† Collaboration using Bristol-Myers Squibb’s PD-1 inhibitor nivolumab
§ Collaboration using Roche’s HER2 antagonist pertuzumab
BDC-1001
BDC-1001 is a Boltbody™ ISAC that is currently in clinical development for the treatment of patients with HER2-positive colorectal, endometrial, gastroesophageal and metastatic breast cancer. We have designed BDC-1001 as an ISAC comprised of a HER2-targeting biosimilar trastuzumab conjugated to one of our proprietary TLR7/8 agonists to maximize the potential anti-tumor response.
BDC-1001 stimulates anti-tumor activity with a three-pronged approach: direct tumor cell killing by trastuzumab-mediated mechanisms, localized phagocytosis, and elimination of HER2-expressing tumor cells by activated myeloid APCs, and durable immunity manifested by T cells reactive to tumor-associated antigens or neoantigens. These mechanisms are supported by our in vivo data demonstrating tumor elimination and immunological memory when treated with our BDC-1001 surrogates.
BDC-3042
BDC-3042 is a myeloid modulating agonist antibody that 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 Dectin-2) 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. Dectin-2 may have the potential to reprogram tumor-supportive macrophages into tumor-destructive macrophages to elicit a productive anti-tumor immune response.