Subcutaneous bispecific T‑cell–engaging antibody (CD3xCD20) that redirects cytotoxic T cells to CD20+ B cells, inducing immune synapse formation and perforin/granzyme-mediated apoptosis.
Bispecific CD3xCD20 antibody that binds CD3 on T cells and CD20 on B cells, redirecting cytotoxic T cells to CD20+ B cells to form an immune synapse and induce perforin/granzyme-mediated apoptosis.
NO
INDIRECT
Epcoritamab binds CD3 on T cells to recruit/activate them and simultaneously binds CD20 on B cells, forming an immune synapse. Activated T cells kill CD20+ B cells via perforin/granzyme; CD3+ T cells are not the cytotoxic target.
Intravenous anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (C1q/MAC), and apoptosis induced by CD20 crosslinking.
Autologous gene-modified T cells expressing a single CAR with two nanobody (VHH) antigen-binding domains targeting CD19 and CD22 to activate CAR signaling (CD3ζ with costimulatory domains), leading to T-cell activation, expansion, cytokine release, and cytotoxic killing of B-lineage blasts.
Autologous T cells are gene-modified to express a single tandem nanobody (VHH) CAR that binds CD19 and CD22 on malignant B cells; antigen engagement activates CD3z and costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing, with dual targeting intended to reduce antigen escape.
YES
DIRECT
CAR-T cells recognize CD19 via the tandem nanobody CAR, activate CD3z/costimulatory signaling, and kill CD19+ cells through perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Autologous gene-modified T cells expressing a single CAR with two nanobody (VHH) antigen-binding domains targeting CD19 and CD22 to activate CAR signaling (CD3ζ with costimulatory domains), leading to T-cell activation, expansion, cytokine release, and cytotoxic killing of B-lineage blasts.
Autologous T cells are gene-modified to express a single tandem nanobody (VHH) CAR that binds CD19 and CD22 on malignant B cells; antigen engagement activates CD3z and costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing, with dual targeting intended to reduce antigen escape.
YES
DIRECT
CAR-T cells bind CD22 via the tandem CAR, triggering T-cell activation and perforin/granzyme-mediated killing (with possible Fas/FasL apoptosis) of the target cell.
Bispecific T‑cell–engaging monoclonal antibody (ELREXFIO) that binds BCMA on myeloma cells and CD3 on T cells to redirect and activate cytotoxic T cells against BCMA-positive malignant plasma cells; immunotherapy with CRS/ICANS risk.
Elranatamab is a bispecific monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells, physically linking T cells to BCMA+ myeloma cells to form an immune synapse. This activates cytotoxic T cells to release perforin and granzymes and kill target cells, with associated cytokine release that can lead to CRS and ICANS.
YES
DIRECT
Elranatamab links CD3 on T cells to BCMA on target cells, forming an immune synapse and triggering T-cell degranulation (perforin/granzymes) to kill BCMA+ cells.