Our Pipeline

Header divider

Proprietary Development Programs
IndicationDiscoveryPreclinicalPhase 1Phase 2

HER2+ Colorectal, Endometrial, Gastroesophageal Cancer

Phase 2

Monotherapy & nivolumab combination studyMono and nivolumab combination

HER2+ Metastatic Breast Cancer*

Phase 2

Monotherapy & pertuzumab§ combination studyMono and pertuzumab combination§
  • Triple-Negative Breast Cancer
  • Clear Cell Renal Cell Carcinoma
  • Head & Neck Cancer
  • Ovarian Cancer
  • Colorectal Cancer
  • Non-Small Cell Lung Cancer

Phase 1

Dose-escalation studyDose-escalation study
Next-Gen ISAC

Range of Solid Tumors


Next-generation Boltbody™ ISAC Collaborations


Funds 3 bispecific Boltbody ISACs through early clinical development


Funds 3 Boltbody ISACs through early clinical development


Funds 1 Boltbody ISAC through early clinical development

* Previously treated with Enhertu
Collaboration using Bristol-Myers Squibb’s PD-1 inhibitor nivolumab
§ Collaboration using Roche’s HER2 antagonist pertuzumab


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.

Learn More About BDC-1001


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.

Learn More About BDC-3042

View Publications