An intravenous HER2-targeted monoclonal antibody–drug conjugate (ADC) dosed 5.4 mg/kg every 3 weeks; binds HER2 (ERBB2) on tumor cells, is internalized, and releases a DNA-damaging cytotoxic payload that inhibits proliferation, leading to tumor cell death; designed for HER2-expressing and HER2-low solid tumors.
HER2-targeted monoclonal antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases a DNA-damaging cytotoxic payload, inhibiting proliferation and inducing tumor cell death in HER2-expressing and HER2-low solid tumors.
HER2-targeted ADC binds HER2 on tumor cells, is internalized, and releases a DNA-damaging cytotoxic payload that causes cell cycle arrest and apoptosis/tumor cell death.
Human anti-CD25 (IL-2 receptor alpha) monoclonal antibody immunotherapy that blocks IL-2/IL-2R signaling and can deplete CD25+ regulatory T cells via Fc-mediated effector functions (e.g., ADCC); administered intravenously as a single agent.
Human anti-CD25 (IL-2Rα) monoclonal antibody that binds CD25 on regulatory T cells, blocks IL-2/IL-2R signaling, and depletes CD25+ Tregs via Fc-mediated effector functions (e.g., ADCC), thereby reducing tumor-associated immunosuppression and enhancing effector T-cell activity.
Anti-CD25 mAb binds CD25 on target cells and recruits FcγR-bearing effector cells to mediate ADCC (and potentially ADCP/CDC), depleting CD25+ cells.
Anti-CD20 monoclonal antibody that depletes malignant and normal B cells via CDC/ADCC and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), and induction of apoptosis.
Binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP; CD20 crosslinking can also trigger direct apoptosis.
Autologous CAR T-cell therapy in which a patient’s T cells are genetically engineered to express a chimeric antigen receptor targeting GPRC5D; upon antigen engagement, CAR signaling (CD3ζ with co-stimulation) activates T cells to proliferate and kill GPRC5D-expressing myeloma cells.
Autologous T cells are engineered to express a chimeric antigen receptor targeting GPRC5D; upon antigen binding, CD3ζ and co-stimulatory signaling activate and expand the T cells, driving cytokine release and perforin/granzyme-mediated killing of GPRC5D-positive myeloma cells.
CAR T cells recognize GPRC5D on target cells, activate via CD3ζ/costimulatory signaling, and kill through perforin/granzyme-mediated cytolysis and apoptosis.
Murine IgG1 monoclonal antibody against CA125 (MUC16); forms immune complexes with tumor-associated and circulating CA125 to enhance dendritic cell antigen uptake and elicit CA125-specific T- and B-cell responses; can mediate Fc-dependent effector functions (ADCC/complement).
Murine IgG1 monoclonal antibody against CA125 (MUC16) that binds tumor-associated and circulating CA125 to form immune complexes, enhancing dendritic cell uptake and presentation to elicit CA125-specific T- and B-cell responses; can also trigger Fc-mediated effector functions (ADCC and complement).
IgG1 antibody binds CA125 (MUC16) on tumor cells and engages Fc effector functions to mediate NK-cell ADCC and complement-dependent cytotoxicity.