Our Pipeline

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

HER2-expressing Solid Tumors

PHASE 1

Phase 1/2 Monotherapy TrialPh 1/2 mono

PHASE 1

Phase 1/2 Combination Trial with nivolumab*Ph 1/2 combo (nivolumab)*
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 with High Unmet Need

PRECLINICAL

BOLTBODY™ ISAC COLLABORATIONS

Genmab

Bispecific Boltbody ISACs
Undisclosed

DISCOVERY

Innovent

Boltbody ISACs
Undisclosed

DISCOVERY

Toray

Boltbody ISAC
Undisclosed

DISCOVERY

*clinical collaboration using Bristol-Myers Squibb's PD-1 inhibitor nivolumab

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-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.