Antibody-drug conjugate targeting TROP2 (also known as iza-bren; izalontamab brengitecan; BMS-986507). Humanized IgG1 mAb linked via a cleavable linker to a camptothecin/topoisomerase-I inhibitor payload, leading to DNA damage and apoptosis; may have Fc-mediated effector and bystander effects.
Humanized IgG1 antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a cleavable camptothecin/topoisomerase I–inhibitor payload to induce DNA damage and apoptosis; may also elicit Fc-mediated effector functions and bystander killing.
NO
INDIRECT
BL-B01D1 is an ADC that binds a surface antigen (e.g., TROP2/EGFR/HER3), is internalized, and releases a topoisomerase I–inhibitor payload that causes DNA damage and apoptosis. DNA topoisomerase I is the intracellular enzymatic target of the payload, not the binding antigen; cells aren’t selectively killed based on topoisomerase I expression alone.
A CD3xCD20 bispecific T-cell–engager antibody that binds CD3 on T cells and CD20 on malignant B cells, activating cytotoxic T cells to kill CD20+ CLL/SLL cells via perforin/granzyme release and caspase-dependent apoptosis.
Bispecific CD3xCD20 antibody that bridges CD3 on T cells to CD20 on malignant B cells, activating cytotoxic T cells to kill CD20+ cells via perforin/granzyme release and caspase-dependent apoptosis.
YES
DIRECT
CD3xCD20 bispecific antibody crosslinks T cells to CD20+ cells, activating T-cell cytotoxicity with perforin/granzyme release and caspase-dependent apoptosis of the CD20-expressing cells.
A cellular immunotherapy in which natural killer (NK) cells are genetically engineered to express a chimeric antigen receptor (CAR) targeting CD19 on B cells; CAR engagement activates NK cytotoxic pathways (perforin/granzyme and death receptor signaling) to eliminate CD19+ B cells/plasmablasts and suppress autoantibody-driven inflammation in immune nephropathies.
Natural killer cells are genetically engineered to express a CD19-targeted chimeric antigen receptor. Upon binding CD19 on B cells, the CAR activates NK cytotoxic pathways (perforin/granzyme release and death receptor signaling), depleting CD19+ B cells/plasmablasts and reducing autoantibody-driven inflammation in immune nephropathies.
YES
DIRECT
CAR-engineered NK cells bind CD19 on target cells and trigger NK cytotoxic pathways, killing CD19+ cells via perforin/granzyme-mediated lysis and death receptor (e.g., Fas/TRAIL) signaling.
Patient-derived T cells genetically engineered ex vivo to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on myeloma cells; infused after lymphodepletion to expand and mediate antigen-specific cytotoxicity.
Autologous T cells are collected and genetically engineered ex vivo to express a chimeric antigen receptor that recognizes BCMA (TNFRSF17) on myeloma cells. Following lymphodepletion, the CAR‑T cells are infused; antigen binding activates the CAR signaling domains (CD3ζ with costimulation), driving T‑cell expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of BCMA‑expressing malignant plasma cells.
YES
DIRECT
BCMA-directed CAR-T cells bind BCMA on target cells, activate, and kill via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Subcutaneous GPRC5D×CD3 bispecific T‑cell–engaging antibody that redirects CD3+ T cells to kill GPRC5D‑positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, crosslinking T cells to GPRC5D+ tumor cells to trigger cytotoxic T-cell activation and tumor cell killing.
YES
DIRECT
Bispecific CD3×GPRC5D engagement crosslinks T cells to GPRC5D+ cells, triggering CTL-mediated killing via immunologic synapse, perforin/granzyme release and apoptosis.