A humanized IgG1 bispecific T-cell–engaging monoclonal antibody (DuoBody-CD3xCD20; GEN3013) that co-binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of malignant B cells; administered subcutaneously.
Humanized IgG1 bispecific antibody (DuoBody-CD3xCD20) that co-binds CD3 on T cells and CD20 on B cells to form an immune synapse, activate T cells, and drive perforin/granzyme-mediated cytotoxic killing of CD20+ malignant B cells.
YES
DIRECT
Bispecific antibody co-binds CD20 on B cells and CD3 on T cells, forming an immune synapse that activates T cells to kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Antibody-drug conjugate targeting a tumor-associated cell-surface antigen; internalizes and releases a cytotoxic payload (e.g., topoisomerase I or microtubule-targeting warhead) to kill cancer cells.
An anti-CLDN18.2 IgG1 antibody-drug conjugate with a cleavable linker to a topoisomerase I inhibitor. After binding CLDN18.2 on tumor cells, it is internalized and the linker is cleaved to release the payload, which inhibits topoisomerase I, blocks DNA replication, and triggers cell-cycle arrest and apoptosis in CLDN18.2-expressing cancer cells.
YES
DIRECT
The ADC binds CLDN18.2 on target cells, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication, causing cell-cycle arrest and apoptosis.
A humanized IgG1 bispecific T-cell–engaging monoclonal antibody (DuoBody-CD3xCD20; GEN3013) that co-binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of malignant B cells; administered subcutaneously.
Humanized IgG1 bispecific antibody (DuoBody-CD3xCD20) that co-binds CD3 on T cells and CD20 on B cells to form an immune synapse, activate T cells, and drive perforin/granzyme-mediated cytotoxic killing of CD20+ malignant B cells.
NO
INDIRECT
Epcoritamab engages CD3 on T cells to activate them and bring them to CD20+ B cells; the T cells then kill the CD20-expressing cells via perforin/granzyme, not the CD3+ T cells.
Autologous, gene-modified T cells transduced with a lentiviral vector to express a human CD1a-specific chimeric antigen receptor (CAR) with CD3ζ signaling and costimulatory domains; upon binding CD1a on malignant T-ALL/LBL cells, the CAR T cells activate, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity in an HLA-independent manner.
Autologous T cells are lentivirally transduced to express a human CD1a-specific chimeric antigen receptor with CD3ζ signaling and costimulatory domains. Upon binding CD1a on malignant T-ALL/LBL cells, the CAR triggers HLA-independent T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells.
YES
DIRECT
CAR binding to CD1a activates the engineered T cells, which kill CD1a+ cells via perforin/granzyme-mediated cytotoxicity (HLA-independent).
Autologous patient T cells genetically engineered to express an anti-CD19 chimeric antigen receptor; targeting CD19+ B cells and plasmablasts to reduce AQP4-IgG autoantibody production in NMOSD.
Autologous T cells engineered with an anti‑CD19 chimeric antigen receptor recognize CD19 on B cells and plasmablasts, triggering T‑cell activation and cytotoxic killing (perforin/granzyme) to deplete the B‑cell lineage and reduce pathogenic AQP4‑IgG autoantibody production in NMOSD.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on B-lineage cells, form an immune synapse, and induce cytotoxicity via perforin/granzyme release (and Fas–FasL apoptosis), leading to target cell death.