HER3 (ERBB3)-targeting antibody–drug conjugate that delivers a topoisomerase I inhibitor payload; administered IV every 3 weeks; binds HER3, internalizes, and releases a DNA-damaging topo-I payload to kill HER3-expressing tumor cells; tested alone and with trastuzumab or osimertinib.
Humanized anti-HER3 IgG1 antibody-drug conjugate linked via a cleavable linker to a topoisomerase I inhibitor. After binding HER3 on tumor cells, the ADC is internalized and releases the topo I inhibitor, stabilizing the topo I–DNA complex to induce DNA breaks, block DNA replication, and trigger apoptosis in HER3-expressing tumor cells.
NO
INDIRECT
DB-1310 binds HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that stabilizes the Topo I–DNA complex, causing DNA breaks and apoptosis in HER3-expressing cells; Topo I itself is not the cell-surface target of the ADC.
Humanized anti-HER2 monoclonal antibody that blocks HER2/HER3 signaling; evaluated in combination with DB-1310.
Humanized monoclonal antibody that binds HER2 on tumor cells, blocks HER2/HER3 signaling and receptor dimerization, suppresses downstream PI3K/AKT and MAPK pathways, and mediates antibody‑dependent cellular cytotoxicity against HER2‑overexpressing cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC; it also blocks HER2 signaling, promoting growth arrest and apoptosis of HER2+ cells.
Adoptive cellular immunotherapy using autologous T lymphocytes genetically engineered to express chimeric antigen receptors that recognize tumor antigens and mediate cytotoxic activity.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that binds specific tumor-associated antigens (MHC-independent), activating the T cells to proliferate, release cytotoxic molecules and cytokines, and selectively kill antigen-expressing cancer cells.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas–FasL), inducing apoptosis of CD19+ cells.
Adoptive cellular immunotherapy using autologous T lymphocytes genetically engineered to express chimeric antigen receptors that recognize tumor antigens and mediate cytotoxic activity.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that binds specific tumor-associated antigens (MHC-independent), activating the T cells to proliferate, release cytotoxic molecules and cytokines, and selectively kill antigen-expressing cancer cells.
YES
DIRECT
BCMA-targeted CAR T cells bind BCMA on tumor cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and death-receptor signaling (e.g., Fas/FasL), with supportive cytokine-mediated apoptosis.
Polyclonal antibody that depletes T cells to reduce rejection and GVHD.
Polyclonal anti–T-cell IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent lysis and Fc-mediated ADCC/phagocytosis, producing immunosuppression to reduce rejection and GVHD.
YES
DIRECT
Anti-thymocyte globulin binds CD2 on T cells and induces complement-dependent lysis and Fc-mediated ADCC/phagocytosis, depleting the target cells.