Dren develops therapeutic antibodies to execute robust depletion of disease-causing cells and agents. We selectively engage an effector cell for the targeted depletion in correlation with the pathogenesis and status of immune cells in the disease. Our pipeline is currently comprised of two distinct drug discovery programs.
  • DR-01: Utilizes enhanced antibody-dependent cellular cytotoxicity (“ADCC”)

  • DR-02: Targeted Myeloid Engager and Phagocytosis Platform derived bispecific antibodies


DR-01 is a nonfucosylated antibody that binds to a cell surface receptor selectively expressed on cytotoxic cells and that are aberrantly proliferated in various leukemias and lymphomas. In addition to the opportunity in liquid cancers, DR-01 will be evaluated in auto-immune indications driven by the cytotoxic immune cells.
  • Lead candidate DR-01 is a high affinity, fully human, ligand non-competing and NHP cross-reactive antibody

  • The antibody is engineered to induce enhanced antibody-dependent cellular cytotoxicity (“ADCC”)

  • Initially targeting leukemic and lymphoma cells with NK or CD8 T cell type

  • DR-01 engages the cytotoxic malignant cells to execute fratricide

  • POC demonstrated in vitro, ex vivo and in vivo including multiple NHP and disease model studies

  • IND-enabling toxicology study

  • Accelerated approval opportunity in orphan hem-onc indications

  • Expansion into well defined subsets of autoimmune disease


DR-0201: Targeted Myeloid Engager and Phagocytosis Platform for the treatment of B cell malignancies (click on platform link to learn more)
  • B cell lymphomas are characterized by high levels of CD163+ M2-like macrophages and myeloid-derived suppressor cells (MDSCs) in patients with late-stage disease
    • Elevated levels of these immuno-suppressive myeloid cells are associated with disease severity and poor prognosis

  • DR-0201 bispecific antibody binds on one arm to a phagocytic receptor on myeloid cells, and on the second arm to a surface receptor that is highly expressed on B cells in various B cell malignancies, including DLBCL, MCL, FL, and CLL

  • DR-0201 demonstrated superior B cell depletion and cytokine release compared to benchmark therapies like Rituximab, Obinutuzumab, and T cell engagers

  • DR-0201 induced target antigen cross-presentation suggesting the potential to activate effector and memory T cells, and therefore promote lasting anti-tumor immunity

  • In exploratory non-human primate studies, DR-0201 demonstrated robust pharmacodynamic activity and excellent tolerability with no adverse clinical signs, suggesting a broad therapeutic index than typically seen with other immune cell engagers

  • Fundamentally differentiated MOA of DR-0201 may warrant benefit for patients with B cell malignancies

DR-02 Solid Cancer

Targeted Myeloid Engager and Phagocytosis Platform for the treatment of solid tumors (click on platform link to learn more)
  • Bispecific Abs for clinically-validated; cell surface receptor that is highly expressed in multiple solid tumors, including breast, urothelial, glioblastoma, and endometrial cancers
    • Approved therapies in some of the cancers have low response rates and result in adverse reactions, such as neutropenia, diarrhea, and vomiting

  • Bispecific candidates demonstrated robust cytokine release and cancer cell depletion in multiple tumor biopsies

  • Bispecific candidates cross-presentation and activation of cytotoxic CD8+ T cells in ex vivo assays, highlighting the potential to achieve lasting anti-tumor immunity

  • Notably, DR-0202 has the potential to restrict anti-tumor activity to the tumor microenvironment where target cancer cells and myeloid cells are abundant
    • DR-02 bispecifc Abs activity is tightly regulated by the presence of cancer cells; after cancer cells are eliminated, the antibody activity is attenuated

DR-02 Non-Oncology

Targeted Myeloid Engager and Phagocytosis Platform for the treatment of Light Chain Amyloidosis (click on platform link to learn more)
  • Light chain (AL) amyloidosis is the most common form of systemic amyloidosis affecting the heart, kidney, nervous system, liver, and gastrointestinal tract

  • In AL amyloidosis, abnormal plasma cells make excessive amounts of light chain proteins
    • Free light chains become misfolded and deposit as amyloids in various organs
    • AL amyloid deposits are toxic and drives morbidity and mortality

  • Current therapies have low response rates and do not address unmet need adequately
    • There are no approved drugs that directly target amyloid deposits

  • In co-cultures of myeloid cells and AL amyloid fibrils, DR-02 bispecific Abs demonstrated robust immune stimulation and targeted phagocytosis