Autologous CD19-directed CAR T-cell therapy (gene-modified cellular immunotherapy). Engineered T cells express a CAR with CD3ζ signaling and costimulatory domains to target CD19 on B cells, leading to T-cell activation/expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing; expected on-target B-cell aplasia.
Autologous T cells are genetically engineered to express a CD19-directed chimeric antigen receptor (with CD3zeta signaling and costimulatory domains). Upon binding CD19 on B cells, the CAR activates T-cell signaling, leading to T-cell activation and expansion, cytokine release, and perforin/granzyme-mediated killing of malignant B cells, with expected on-target B-cell aplasia.
YES
DIRECT
CD19-directed CAR T cells bind CD19+ cells, activate, and kill them via perforin/granzyme-mediated cytolysis (and related T-cell effector mechanisms).
An IV BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that redirects CD3+ T cells to kill BCMA-expressing plasma cells, aiming to deplete IgE-producing plasma cells and lower food-specific IgE.
BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, bringing them into proximity to activate cytotoxic T cells and kill BCMA‑expressing antibody‑secreting plasma cells, thereby depleting IgE‑producing plasma cells and lowering food‑specific IgE.
YES
DIRECT
The BCMA×CD3 bispecific antibody binds BCMA on target cells and CD3 on T cells, bringing them together and activating T cells to kill BCMA-expressing cells via perforin/granzyme-mediated cytotoxicity.
An IV BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that redirects CD3+ T cells to kill BCMA-expressing plasma cells, aiming to deplete IgE-producing plasma cells and lower food-specific IgE.
BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, bringing them into proximity to activate cytotoxic T cells and kill BCMA‑expressing antibody‑secreting plasma cells, thereby depleting IgE‑producing plasma cells and lowering food‑specific IgE.
NO
INDIRECT
Linvoseltamab binds CD3ε on T cells to activate and redirect them toward BCMA-expressing cells, which are then killed via T‑cell cytolysis (perforin/granzymes). CD3+ T cells themselves are not targeted for killing.
An antibody–drug conjugate targeting CD19; an anti-CD19 monoclonal antibody linked to the PBD-dimer cytotoxic payload tesirine that induces DNA interstrand crosslinks leading to apoptosis in CD19-positive B cells.
Anti-CD19 monoclonal antibody targets CD19 on B cells and is internalized; a cleavable linker releases the PBD-dimer payload (tesirine), which binds the DNA minor groove and forms interstrand crosslinks at guanine N2 positions, blocking DNA replication and triggering apoptosis in CD19-positive tumor cells.
YES
DIRECT
The anti-CD19 ADC binds CD19 on B cells, is internalized, and releases the PBD-dimer payload (tesirine) via a cleavable linker; the payload forms DNA interstrand crosslinks (minor groove, guanine N2), blocking replication and inducing apoptosis in CD19+ cells.
An antibody–drug conjugate targeting CD19; an anti-CD19 monoclonal antibody linked to the PBD-dimer cytotoxic payload tesirine that induces DNA interstrand crosslinks leading to apoptosis in CD19-positive B cells.
Anti-CD19 monoclonal antibody targets CD19 on B cells and is internalized; a cleavable linker releases the PBD-dimer payload (tesirine), which binds the DNA minor groove and forms interstrand crosslinks at guanine N2 positions, blocking DNA replication and triggering apoptosis in CD19-positive tumor cells.
NO
INDIRECT
The ADC targets CD19 on B cells, is internalized, and then releases a PBD-dimer that binds the DNA minor groove (guanine N2) to form interstrand crosslinks, blocking replication and inducing apoptosis; DNA is the payload’s intracellular target, not the antibody’s direct targeting antigen.