A subcutaneous CD20×CD3 bispecific T‑cell–engaging antibody that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, drive T‑cell proliferation and cytotoxic degranulation, and induce targeted B‑cell killing.
Subcutaneous bispecific antibody that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, expand and activate cytotoxic T cells, and induce perforin/granzyme‑mediated killing of CD20+ malignant B cells.
NO
INDIRECT
Epcoritamab binds CD3 on T cells to activate and redirect them to kill CD20+ B cells via perforin/granzyme cytotoxicity; CD3ε-expressing T cells are not the killed population.
Anti-CD38 IgG1κ monoclonal antibody that binds CD38 on clonal plasma cells and other CD38+ cells, inducing complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity and phagocytosis, and apoptosis; also depletes CD38+ immunosuppressive cells and can inhibit CD38 ectoenzyme (NADase) activity.
YES
DIRECT
Daratumumab binds CD38 on target cells and induces complement-dependent cytotoxicity (CDC), Fc-mediated ADCC by NK cells, ADCP by macrophages, and can trigger apoptosis upon crosslinking.
Therapeutic cancer vaccine designed to elicit MUC1-specific CD4+/CD8+ T-cell and antibody responses against tumor-associated MUC1.
Synthetic MUC1-derived peptide that is taken up by antigen-presenting cells and presented on MHC I/II to elicit MUC1-specific CD8+ cytotoxic T cells, CD4+ helper T cells, and antibodies, leading to immune-mediated killing of MUC1-expressing tumor cells and reduced tumor growth.
YES
INDIRECT
The vaccine induces MUC1-specific immunity; activated CD8+ T cells recognize MUC1 peptides on MHC I and kill via perforin/granzyme, and anti-MUC1 antibodies can mediate ADCC/complement against MUC1+ cells.
Immune-stimulating antibody conjugate (ISAC) comprising a trastuzumab-biosimilar monoclonal antibody linked via a non-cleavable, cell-impermeable linker to a TLR7/8 agonist; binds HER2 on tumor cells to localize TLR7/8 activation and trigger innate and adaptive anti-tumor immunity.
Immune-stimulating antibody conjugate: a trastuzumab-biosimilar mAb targets HER2 on tumor cells to localize a linked TLR7/8 agonist to the tumor microenvironment, activating TLR7/8 on dendritic and other antigen-presenting cells. This triggers innate immune activation, pro-inflammatory cytokine production, enhanced antigen presentation, and subsequent cytotoxic T-cell and B-cell responses leading to anti-tumor activity.
YES
INDIRECT
HER2 binding localizes a TLR7/8 agonist to the tumor, activating dendritic/APCs to drive cytokines and antigen presentation, which primes cytotoxic T cells that kill HER2+ tumor cells; Fc-mediated phagocytosis/ADCC may also contribute.
Immune-stimulating antibody conjugate (ISAC) comprising a trastuzumab-biosimilar monoclonal antibody linked via a non-cleavable, cell-impermeable linker to a TLR7/8 agonist; binds HER2 on tumor cells to localize TLR7/8 activation and trigger innate and adaptive anti-tumor immunity.
Immune-stimulating antibody conjugate: a trastuzumab-biosimilar mAb targets HER2 on tumor cells to localize a linked TLR7/8 agonist to the tumor microenvironment, activating TLR7/8 on dendritic and other antigen-presenting cells. This triggers innate immune activation, pro-inflammatory cytokine production, enhanced antigen presentation, and subsequent cytotoxic T-cell and B-cell responses leading to anti-tumor activity.
NO
INDIRECT
BDC-1001’s TLR7/8 agonist activates TLR7 on antigen‑presenting cells to drive innate activation and T‑cell priming; the resulting immune response (and Fc effector functions) kills HER2+ tumor cells, not the TLR7-expressing cells.