BCMA-targeting antibody–drug conjugate (humanized anti-BCMA mAb linked to monomethyl auristatin F) that binds BCMA on malignant plasma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; Fc effector function may contribute ADCC/ADCP.
Afucosylated humanized anti-BCMA monoclonal antibody linked to the microtubule inhibitor MMAF. Binds BCMA on malignant plasma cells and is internalized; intracellular MMAF inhibits tubulin polymerization, causing G2/M arrest and apoptosis. The Fc region can also mediate ADCC/ADCP.
NO
INDIRECT
Belantamab mafodotin targets BCMA on cells; after internalization, MMAF binds beta-tubulin to inhibit microtubules, causing mitotic arrest and apoptosis (plus Fc-mediated ADCC/ADCP). Beta-tubulin expression alone does not lead to targeting or killing.
Autologous, gene-modified CD19-directed chimeric antigen receptor T-cell therapy administered intravenously; engineered patient T cells express an anti-CD19 CAR to recognize and eliminate CD19+ B cells (naive, memory, plasmablasts), inducing B-cell aplasia and reducing autoreactive B cells and pathogenic autoantibodies in SLE.
Autologous T cells are engineered ex vivo to express an anti-CD19 chimeric antigen receptor. After infusion, these CAR-T cells bind CD19 on B-lineage cells (naive, memory, plasmablasts) and kill them via T-cell activation and cytolysis, leading to B-cell aplasia and reduction of autoreactive B cells and pathogenic autoantibodies in SLE.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on B cells, become activated, and induce target-cell death via perforin/granzyme-mediated cytolysis and Fas/FasL apoptosis.
A TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to induce DNA damage and cell death (with potential bystander effect).
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to cause DNA damage and tumor cell death, with potential bystander effect.
YES
DIRECT
The ADC binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that induces DNA damage leading to apoptosis; the payload can also cause a bystander effect.
A TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to induce DNA damage and cell death (with potential bystander effect).
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to cause DNA damage and tumor cell death, with potential bystander effect.
NO
INDIRECT
The ADC binds TROP2 (not topoisomerase I); after TROP2-mediated internalization it releases a camptothecin topoisomerase I inhibitor that causes DNA damage and apoptosis, with possible bystander effect. Cells are not killed due to topoisomerase I expression itself.
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B cells and CD3 on T cells to redirect T-cell cytotoxicity against CD19-positive leukemia cells.
A BiTE antibody construct that simultaneously binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and redirect perforin/granzyme-mediated cytotoxicity against CD19-positive leukemia/lymphoma cells in an MHC-independent manner.
YES
DIRECT
Blinatumomab bridges CD3 on T cells to CD19 on target cells, activating T cells to form an immunologic synapse and kill CD19+ cells via perforin/granzyme-mediated apoptosis (MHC-independent).