Our Pipeline

Program
(Target)
IndicationPRECLINICALPHASE 1PHASE 2
BOLTBODY™ ISACs
BDC-1001
HER2

HER2-expressing Solid Tumors

  • HER2+ Breast Cancer
  • HER2+ Gastric Cancer
  • HER2-low Breast Cancer

PHASE 1

Multi-arm Phase 1/2 Trial
BDC-2034
CEA
  • Non-Small Cell Lung Cancer
  • Colorectal Cancer
  • Pancreatic Cancer
  • Breast Cancer

PRECLINICAL

PD-L1

Checkpoint refractory Tumors

  • Non-Small Cell Lung Cancer
  • Head and Neck Cancer
  • Breast Cancer

PRECLINICAL

MYELOID MODULATING AGONIST ANTIBODY
BDC-3042
Dectin-2

Solid Tumors

  • KRAS mutated tumors
  • TP53 mutated tumors

PRECLINICAL

BDC-1001

BDC-1001 is a Boltbody™ ISAC that is currently in clinical development for the treatment of patients with HER2-expressing solid tumors, including subsets with HER2-low tumors. 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-2034

BDC-2034 is a Boltbody™ ISAC in development for the treatment of various solid tumors. In designing BDC-2034, we selected a monoclonal antibody with selective binding to CEACAM5, also known as carcinoembryonic antigen (CEA), that displays high levels of antibody-dependent cellular phagocytosis of CEA-expressing cancer cells. We then created an ISAC by conjugating one of our proprietary TLR7/8 agonists to this mAb. In our preclinical studies, we have observed robust myeloid cell activation in vitro and promising anti-tumor activity in vivo.

CEA is a well-known tumor antigen that is overexpressed in various solid tumors where there is significant unmet medical need including, colorectal cancer, non-small cell lung cancer, pancreatic cancer, and breast cancer. CEA is upregulated on the cell surface of these cancers and displays minimal receptor-mediated internalization into the cancer cell. Therefore, CEA allows us to target these cancers, some of which are immunologically “cold,” with an ISAC and offers the potential to turn these “cold” tumors into “hot” tumors with a robust immunological response.

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. Additionally, KRAS and TP53 mutations may upregulate Dectin-2 on tumor-associated myeloid cells and could provide an avenue to develop precision medicine with an immune modulator.