Genetically engineered natural killer (NK) cells expressing a chimeric antigen receptor targeting mesothelin to enable targeted cytotoxicity against mesothelin-positive ovarian epithelial carcinoma.
Genetically engineered NK cells express a mesothelin-specific chimeric antigen receptor that binds mesothelin on tumor cells and triggers NK-cell activation, leading to targeted cytotoxicity (perforin/granzyme release and cytokine secretion) and lysis of mesothelin-positive ovarian cancer cells.
CAR-engineered NK cells bind mesothelin, activate, and kill target cells via perforin/granzyme-mediated cytotoxicity (with cytokine-mediated effects).
Anti-CD79b antibody–drug conjugate delivering MMAE to disrupt microtubules and induce B-cell apoptosis.
Anti-CD79b monoclonal antibody–drug conjugate; after binding CD79b on B cells it is internalized and linker cleavage releases MMAE, a microtubule inhibitor that blocks tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
ADC binds CD79b, is internalized, and releases MMAE that inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target-expressing B cells.
Anti-CD20 monoclonal antibody mediating ADCC/CDC and direct B-cell apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct induction of apoptosis.
Rituximab binds CD20 on B cells, inducing killing via ADCC (through Fc gamma receptor–bearing effector cells), complement-mediated cytotoxicity (CDC), and direct apoptosis signaling.
Autologous T cells genetically engineered to express a HER2 (ERBB2)-specific chimeric antigen receptor; upon binding HER2 on tumor cells, they activate cytotoxic T-cell responses leading to tumor cell killing.
Autologous T cells are genetically engineered to express a HER2-specific chimeric antigen receptor. Upon binding HER2 (ERBB2) on tumor cells, the CAR transduces activation signals (CD3ζ with costimulatory domains), driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytolytic killing of HER2-expressing cancer cells.
HER2-specific CAR-T cells bind HER2 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis (and death receptor pathways).
Autologous, genetically engineered CAR T-cell therapy that dual-targets CD19 and CD22 to deplete malignant B cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CD19 and CD22 on B cells. Upon antigen engagement, the CAR T cells activate, proliferate, release cytokines, and kill malignant B cells via cytotoxic mechanisms (perforin/granzyme), leading to depletion of CD19+/CD22+ tumor cells and on-target B-cell aplasia.
CAR T cells bind CD19 on target cells and induce killing via immune synapse formation with perforin/granzyme-mediated apoptosis (and Fas/FasL pathways).