Bispecific IgG1-like anti-HER2 monoclonal antibody targeting ECD2 and ECD4; induces HER2 clustering/internalization, blocks signaling, and activates ADCC/ADCP/CDC.
Zanidatamab is a bispecific IgG1 monoclonal antibody that binds two non-overlapping HER2 extracellular domains (ECD2 and ECD4), promoting HER2 clustering and internalization/downregulation, blocking HER2 signaling and dimerization, and leveraging Fc-mediated effector functions (ADCC, ADCP, CDC) to kill HER2-overexpressing tumor cells.
YES
DIRECT
Zanidatamab binds HER2 (ECD2/ECD4) on target cells and engages immune effectors via its Fc to induce ADCC and ADCP, and can activate complement (CDC), leading to lysis and phagocytosis of HER2+ cells; signaling blockade/internalization contribute but cytotoxicity is via Fc-mediated effector functions.
Autologous, genetically engineered T-cell therapy expressing a single CAR with tandem scFv domains targeting CD19 or CD22 and a 4-1BB co-stimulatory domain; infused IV at 1–2×10^6 CAR-T/kg to induce T-cell cytotoxicity against malignant B cells and enhance activation, proliferation, and persistence.
Autologous T cells are genetically engineered to express a single tandem scFv CAR that recognizes CD19 or CD22 and signals via CD3zeta with a 4-1BB co-stimulatory domain. Engagement of CD19 or CD22 on malignant B cells triggers T-cell cytotoxicity and cytokine release and enhances T-cell activation, proliferation, and persistence; dual targeting helps prevent antigen-loss escape.
YES
DIRECT
CAR T cells bind CD19 via the tandem scFv, become activated through CD3ζ/4-1BB signaling, and kill target cells via perforin/granzyme-mediated lysis and death-receptor pathways.
Autologous, genetically engineered T-cell therapy expressing a single CAR with tandem scFv domains targeting CD19 or CD22 and a 4-1BB co-stimulatory domain; infused IV at 1–2×10^6 CAR-T/kg to induce T-cell cytotoxicity against malignant B cells and enhance activation, proliferation, and persistence.
Autologous T cells are genetically engineered to express a single tandem scFv CAR that recognizes CD19 or CD22 and signals via CD3zeta with a 4-1BB co-stimulatory domain. Engagement of CD19 or CD22 on malignant B cells triggers T-cell cytotoxicity and cytokine release and enhances T-cell activation, proliferation, and persistence; dual targeting helps prevent antigen-loss escape.
YES
DIRECT
CAR T cells bind CD22 via the tandem scFv, activating CD3ζ/4-1BB signaling and killing CD22+ cells via perforin/granzyme–mediated apoptosis (and Fas–FasL), with cytokine release.
Autologous double-negative (CD4−/CD8−) T cells transduced via lentiviral vector to express an anti-CD19 chimeric antigen receptor; depletes CD19+ B-lineage cells and plasmablasts to reduce autoantibody production and B cell–mediated inflammation.
Autologous double-negative (CD4-/CD8-) T cells are lentivirally engineered to express an anti-CD19 chimeric antigen receptor; CAR engagement of CD19 triggers targeted cytotoxicity against CD19+ B-lineage cells and plasmablasts, reducing autoantibody production and B cell–mediated inflammation.
YES
DIRECT
Anti-CD19 CAR-engineered double-negative T cells bind CD19 on target cells and induce cytotoxicity via immune synapse formation with perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
First-in-human antibody-drug conjugate targeting folate receptor alpha (FRα); binds FRα, is internalized, and releases a cytotoxic payload to kill FRα-expressing tumor cells.
Humanized IgG1 ADC targeting folate receptor alpha (FRα). After FRα binding and internalization, a cleavable linker releases the topoisomerase I inhibitor exatecan, causing DNA damage (single- and double-strand breaks), cell cycle arrest, and apoptosis, with potential bystander killing of neighboring tumor cells.
YES
DIRECT
ADC binds FRα on tumor cells, is internalized, cleavable linker releases exatecan (topoisomerase I inhibitor) causing DNA strand breaks, cell-cycle arrest, and apoptosis; with potential bystander killing.