Bispecific T‑cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B-lymphoblasts to induce cytotoxic killing.
Bispecific CD19xCD3 antibody (BiTE) that binds CD19 on B-lymphoblasts and CD3 on T cells, bringing them together to form an immunologic synapse, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of CD19-positive cells (MHC-independent).
YES
DIRECT
Blinatumomab bridges CD3 on T cells to CD19 on target cells, activating T cells to deliver perforin/granzyme-mediated killing of CD19+ cells (MHC-independent).
Engineered CAR T cells (lentiviral) targeting cytomegalovirus glycoprotein B (gB); dose-escalated IV infusion; designed for MHC-independent cytotoxicity against gB-expressing CMV-associated tumor cells.
Lentiviral-engineered T cells expressing a chimeric antigen receptor targeting cytomegalovirus glycoprotein B (gB); upon gB binding, the CAR drives MHC-independent T-cell activation and cytotoxicity (perforin/granzyme release and cytokine-mediated killing) against gB-expressing CMV-associated tumor cells.
YES
DIRECT
CAR T cells bind CMV gB on target cells and, via MHC‑independent CAR signaling, release perforin/granzymes (and cytotoxic cytokines) to induce lysis/apoptosis of gB-expressing cells.
Bispecific T‑cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B-lymphoblasts to induce cytotoxic killing.
Bispecific CD19xCD3 antibody (BiTE) that binds CD19 on B-lymphoblasts and CD3 on T cells, bringing them together to form an immunologic synapse, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of CD19-positive cells (MHC-independent).
NO
INDIRECT
Blinatumomab binds CD3 on T cells to activate and redirect them to kill CD19-positive cells via perforin/granzyme; CD3+ cells are effectors, not killed by the drug.
Antibody-drug conjugate that binds a tumor cell-surface target and delivers a cytotoxic payload.
Antibody-drug conjugate targeting nectin-4 on tumor cells; after binding and internalization, a cleavable linker releases the cytotoxic payload monomethyl auristatin E (MMAE), which binds tubulin and inhibits microtubule polymerization, leading to G2/M arrest and apoptosis.
YES
DIRECT
ADC binds Nectin-4, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis of the target cell.
Antibody-drug conjugate that binds a tumor cell-surface target and delivers a cytotoxic payload.
Antibody-drug conjugate targeting nectin-4 on tumor cells; after binding and internalization, a cleavable linker releases the cytotoxic payload monomethyl auristatin E (MMAE), which binds tubulin and inhibits microtubule polymerization, leading to G2/M arrest and apoptosis.
NO
INDIRECT
Enfortumab vedotin must bind nectin-4 on the cell surface, be internalized, and then release MMAE; MMAE binds beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis. Beta-tubulin expression alone does not confer killing.