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)*

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. 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, currently advancing through a Phase 1/2 clinical trial, seeks to improve therapeutic outcomes for patients with HER2-expressing tumors by targeting: 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 anti-HER2 therapies, and 3) other HER2-positive tumors not eligible for approved anti-HER2 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.

PD-L1

Checkpoint Refractory Tumors

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

PRECLINICAL

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.

MYELOID MODULATING AGONIST ANTIBODY
BDC-3042
Dectin-2

Solid Tumors with High Unmet Need

PRECLINICAL

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.

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.