TROP2-directed antibody–drug conjugate that delivers a topoisomerase I inhibitor (DXd). Binds TROP2 on tumor cells, is internalized, and releases the cytotoxic payload to induce DNA damage and cell death (with potential bystander effect).
TROP2-directed antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the DXd topoisomerase I inhibitor payload to induce DNA damage and tumor cell death, with potential bystander effect.
YES
DIRECT
TROP2-targeted ADC binds and is internalized, then releases the DXd topoisomerase I inhibitor payload inside target cells, causing DNA damage and cell death (with possible bystander effect).
TROP2-directed antibody–drug conjugate that delivers a topoisomerase I inhibitor (DXd). Binds TROP2 on tumor cells, is internalized, and releases the cytotoxic payload to induce DNA damage and cell death (with potential bystander effect).
TROP2-directed antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the DXd topoisomerase I inhibitor payload to induce DNA damage and tumor cell death, with potential bystander effect.
NO
INDIRECT
Dato-DXd targets TROP2 on the cell surface, is internalized, and releases a DXd payload that inhibits topoisomerase I to cause DNA damage and death in TROP2+ cells (with possible bystander effect). Topoisomerase I expression alone is not selectively targeted.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC), and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and opsonizes them, triggering complement-dependent cytotoxicity and Fc-mediated ADCC by NK cells/macrophages; it can also induce apoptosis of CD20+ cells.
Humanized IgG1 monoclonal antibody targeting CD20 on B cells; depletes circulating CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, reducing B-cell antigen presentation, costimulation, and proinflammatory cytokines.
Humanized IgG1 monoclonal antibody against CD20 that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, reducing B-cell antigen presentation, costimulation, and proinflammatory cytokines.
YES
DIRECT
Ocrelizumab binds CD20 on B cells and induces Fc-mediated ADCC by NK cells and other effectors, complement-dependent cytotoxicity, and apoptosis, leading to depletion of CD20+ cells.
Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
YES
DIRECT
Engineered T cells with an NKG2D-based chimeric receptor bind MICA on target cells, triggering cytolytic synapse formation and perforin/granzyme-mediated apoptosis.