Bispecific monoclonal antibody (CD20×CD3) T‑cell engager that redirects T cells to kill CD20+ B cells.
Humanized bispecific CD20xCD3 monoclonal antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate TCR/CD3 signaling and form cytolytic synapses, leading to perforin/granzyme-mediated killing of CD20+ malignant B cells.
NO
INDIRECT
Mosunetuzumab binds CD3 epsilon on T cells to activate them and crosslink to CD20+ B cells; the activated T cells kill CD20+ cells via perforin/granzyme. CD3+ T cells are not targeted for killing.
Type I anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis; given intravenously or subcutaneously.
Chimeric type I anti-CD20 monoclonal antibody that binds CD20 on B cells and induces their depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (MAC formation), and can trigger direct apoptotic signaling upon CD20 crosslinking.
Autologous TCR-engineered T cell therapy (TCR-T) in which a patient’s T cells are transduced with a high-affinity T-cell receptor recognizing KRAS G12V peptide presented by HLA-A*11:01, enabling antigen-specific cytotoxic killing of tumor cells.
Autologous T cells are genetically engineered to express a high‑affinity TCR specific for the KRAS G12V peptide presented by HLA‑A*11:01 on tumor cells; upon infusion they recognize peptide–MHC I, activate via TCR signaling, and execute antigen‑specific cytotoxic killing via perforin/granzyme pathways (with lymphodepletion and IL‑2 support to enhance expansion).
YES
DIRECT
TCR-engineered T cells recognize the KRAS G12V peptide presented by HLA-A*11:01 on tumor cells and directly kill them via cytotoxic T-cell mechanisms (perforin/granzyme-mediated apoptosis, with possible Fas–FasL signaling).
Autologous TCR-engineered T cell therapy (TCR-T) in which a patient’s T cells are transduced with a high-affinity T-cell receptor recognizing KRAS G12D peptide presented by HLA-A*11:01, enabling antigen-specific cytotoxic killing of tumor cells.
Autologous T cells are engineered to express a high-affinity TCR that recognizes the KRAS G12D neoantigen presented by HLA-A*11:01 on tumor cells; TCR engagement triggers antigen-specific activation and cytotoxic killing via perforin/granzyme release, leading to lysis of KRAS-mutant tumor cells.
YES
DIRECT
Engineered TCR T cells recognize the KRAS G12D peptide presented by HLA-A*11:01 on tumor cells, triggering T-cell activation and perforin/granzyme-mediated killing of the target cells.
Autologous TCR-engineered T cell therapy (TCR-T) in which a patient’s T cells are transduced with a high-affinity T-cell receptor recognizing KRAS G12D peptide presented by HLA-A*11:01, enabling antigen-specific cytotoxic killing of tumor cells.
Autologous T cells are engineered to express a high-affinity TCR that recognizes the KRAS G12D neoantigen presented by HLA-A*11:01 on tumor cells; TCR engagement triggers antigen-specific activation and cytotoxic killing via perforin/granzyme release, leading to lysis of KRAS-mutant tumor cells.
NO
INDIRECT
Killing requires recognition of the KRAS G12D peptide presented by HLA-A*11:01; upon peptide–MHC recognition, engineered T cells kill via perforin/granzyme (and Fas–FasL) mediated apoptosis.