• Data generated from the Company’s bispecific platform demonstrate a robust, multi-pronged mechanism of action that encompasses (i) direct coupling of myeloid and cancer cells, (ii) stimulation of myeloid cells to release key cytokines that are known to reprogram TAMs and reset the immunosuppressive TME, (iii) phagocytosis and killing of tumor cells, and (iv) presentation of tumor neoantigens that activates effector and memory T cell responses that are necessary to achieve anti-tumor immunity.


• The unique biology of the phagocytic receptor enables controlled myeloid cell activation only in the presence of the target antigen. This permits localized cytokine release and increased therapeutic index and safety profile. In agreement, data from exploratory non-human primate studies with target bispecifics indicated robust pharmacodynamic activity and excellent tolerability with no adverse clinical signs, suggesting a broad therapeutic index than typically seen with other immune cell engagers.

Direct coupling of myeloid and cancer cells

• DR-02 bispecific antibodies bind with one arm to a conserved, activatory phagocytic receptor on myeloid cells, and with the second arm to a target antigen that is highly expressed on cancer cells


• DR-02 induces rapid and robust coupling of myeloid and cancer cells


• Opportunity to engage tumor-associated macrophages and cancer cells which are both abundant in the tumor microenvironment in solid tumors

Targeted immune stimulation and cytokine release

• The DR-02 target phagocytic receptor contains an ITAM motif that is activated upon bispecific antibody-induced receptor clustering


• Receptor clustering triggers the expression and release of primary (myeloid-derived) and secondary (T or NK-derived) cytokines, including IL-12, IL-23, IFNγ, TNFα, and IL-6


• Robust cytokine production via activation of phagocytic receptor on TAMs in patient tumor biopsies


• Based on observed cytokine profile, DR-02 bispecific antibodies have the potential to reprogram TAMs and reset the immunosuppressive tumor microenvironment


• Controlled stimulation of myeloid cells to release cytokines is dependent on the presence of target cell
• No systemic cytokine storms observed

Targeted Phagocytosis and killing of cancer cells

• DR-02 bispecific antibodies activate a conserved phagocytic pathway that is involved in microbial clearance


• Phagocytosis via the DR-02 target receptor is not inhibited by the SIRPα-CD47 pathway


• DR-02 bispecific antibodies demonstrated robust phagocytosis and depletion of cancer cells by tumor-associated macrophages in patient tumor biopsies

Antigen presentation

• DR-02 bispecific antibodies induce robust phagocytosis, degradation, and ultimately presentation of target cell-derived antigens by myeloid cells


• Activation of antigen-specific CD8+ T cells indicates the ability of DR-02 BsAb and target receptor pathway to induce cross-presentation


• Data suggest that DR-02 bispecific antibodies have the potential to activate memory T cell responses, and thus elicit prolonged anti-tumor immunity

Safety profile

• The unique biology of the DR-02 phagocytic receptor enables controlled myeloid cell activation only in the presence of the target antigen, thereby permitting localized cytokine release and potentially increased therapeutic index and safety profile


• No adverse events observed at 5mg/kg dose in NHP in vivo study
• Normal level of cytokines at 6h post dosing


• DR-02 provides differentiated MOA and safety profile in contrast to T or NK cell engaging therapies that are limited by narrow therapeutic windows