Our Pipeline

PlatformTargetIndicationDISCOVERYPRE-CLINICALPHASE I/II
Boltbody ISAC HER2
  • HER2+ Breast Cancer
  • HER2 Low Breast Cancer
  • HER2+ Gastric Cancer
  • Other HER2+ Cancers

PHASE I/II

BDC-1001
Boltbody ISAC CEA
  • Non-Small Cell Lung Cancer
  • Colorectal Cancer
  • Pancreatic Cancer
  • Breast Cancer

PRE-CLINICAL

BDC-2034
Boltbody ISAC PD-L1
  • Checkpoint Inhibitor Refractory Tumors

PRE-CLINICAL

Myeloid ModulatorDectin-2*
  • KRAS mutated cancer
  • TP53 mutated cancer

PRE-CLINICAL

BDC-1001

BDC-1001 is 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 that is 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 with significant unmet medical need including, but not limited to, 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.


*Dectin-2, also known as TAM1