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.
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.
A bispecific T-cell–engaging monoclonal antibody that binds CD20 on B cells and CD3 on T cells to redirect and activate T cells for targeted killing of malignant B cells.
Humanized bispecific monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, crosslinking and redirecting T cells to CD20+ malignant B cells to induce T-cell activation, immune synapse formation, cytokine release, and targeted cytotoxic lysis of the tumor cells.
Mosunetuzumab bridges CD20 on B cells to CD3 on T cells, forming an immune synapse and activating T cells to kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Humanized anti-EGFR IgG1 monoclonal antibody that binds EGFR, blocks ligand-induced signaling (e.g., RAS–RAF–MEK–ERK; PI3K–AKT), reduces proliferation/survival, may mediate ADCC, and can enhance radiosensitization.
Humanized anti-EGFR IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocks ligand-induced receptor activation and downstream signaling (RAS–RAF–MEK–ERK; PI3K–AKT), reducing tumor cell proliferation and survival; may also mediate Fc-dependent ADCC and enhance radiosensitization.
EGFR binding opsonizes tumor cells, engaging Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity (ADCC); signaling blockade is mainly cytostatic, but ADCC provides direct immune-mediated killing.
An agonistic anti-CD40 monoclonal antibody immunotherapy delivered intratumorally to activate CD40 on antigen-presenting cells, enhancing dendritic cell activation, antigen presentation, and T-cell priming.
Mitazalimab is an agonistic IgG1 monoclonal antibody that binds CD40 and activates CD40 signaling on antigen-presenting cells, enhancing dendritic cell activation, antigen presentation, and T‑cell priming/expansion; it may also mediate ADCC against CD40-expressing tumor cells.
Mitazalimab binds CD40 on target cells and its IgG1 Fc engages FcγR+ effector cells (e.g., NK cells, macrophages) to mediate antibody-dependent cellular cytotoxicity (ADCC), killing CD40+ cells.
Autologous, gene-modified T cells expressing an FMC63-derived anti-CD19 scFv with CD8 hinge, TNFRSF19 transmembrane, 4-1BB costimulatory, and CD3ζ signaling domains; designed to recognize CD19 on malignant B cells and mediate T-cell activation, proliferation, and cytotoxic killing.
Autologous T cells are gene-modified to express a CD19-directed CAR (FMC63 scFv, CD8 hinge, TNFRSF19 transmembrane, 4-1BB costimulatory, CD3ζ signaling). Upon binding CD19 on malignant B cells, the CAR triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, leading to targeted elimination of CD19+ cells and potential persistence for ongoing immune surveillance.
Anti-CD19 CAR-T cells recognize CD19 and directly kill target cells via T-cell cytotoxic mechanisms, primarily perforin/granzyme-mediated apoptosis (and death-receptor pathways).