Anti-CD20 chimeric IgG1 monoclonal antibody that mediates ADCC/ADCP, complement-dependent cytotoxicity, and direct apoptosis, leading to B-cell depletion.
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via Fc-mediated ADCC/ADCP, complement-dependent cytotoxicity, and direct induction of apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces killing via FcγR-mediated ADCC/ADCP, complement-dependent cytotoxicity (CDC), and can directly trigger apoptosis upon CD20 cross-linking.
Anti-CD19 humanized, Fc-engineered IgG1 monoclonal antibody that enhances ADCC/ADCP and induces apoptosis, depleting malignant and normal B cells.
Fc‑engineered, humanized anti‑CD19 IgG1 monoclonal antibody that binds CD19 on B cells and engages Fcγ receptors on NK cells and macrophages to enhance ADCC and ADCP, while also inducing apoptosis, leading to depletion of malignant and normal CD19+ B cells.
YES
DIRECT
Binds CD19 on B cells and engages Fc gamma receptor–bearing effector cells (NK cells, macrophages) to trigger ADCC and ADCP, and can also induce apoptosis, leading to killing of CD19+ cells.
Anti-CD19 humanized, Fc-engineered IgG1 monoclonal antibody that enhances ADCC/ADCP and induces apoptosis, depleting malignant and normal B cells.
Fc‑engineered, humanized anti‑CD19 IgG1 monoclonal antibody that binds CD19 on B cells and engages Fcγ receptors on NK cells and macrophages to enhance ADCC and ADCP, while also inducing apoptosis, leading to depletion of malignant and normal CD19+ B cells.
NO
INDIRECT
Tafasitamab binds CD19 on B cells; its Fc engages CD16A on NK cells/macrophages to trigger ADCC/ADCP that kills CD19+ cells. CD16A-expressing cells act as effectors and are not killed by the drug.
Gene-modified autologous macrophages expressing an anti-HER2 chimeric antigen receptor (CAR). Derived from patient PBMCs, differentiated to macrophages, transduced ex vivo via an adenoviral vector, and administered intraperitoneally to induce HER2-dependent tumor cell phagocytosis and cytotoxicity and remodel the tumor microenvironment.
Autologous macrophages engineered to express an anti-HER2 chimeric antigen receptor bind HER2 on tumor cells, activating macrophage phagocytosis and cytotoxicity and remodeling the tumor microenvironment to enhance anti-tumor immunity.
YES
DIRECT
HER2-directed CAR macrophages bind HER2 on tumor cells and directly kill them via CAR-triggered phagocytosis and macrophage cytotoxic effector functions (phagolysosomal killing, ROS/cytotoxic mediators).
Anti-CD19 humanized, Fc-engineered IgG1 monoclonal antibody that enhances ADCC/ADCP and induces apoptosis, depleting malignant and normal B cells.
Fc‑engineered, humanized anti‑CD19 IgG1 monoclonal antibody that binds CD19 on B cells and engages Fcγ receptors on NK cells and macrophages to enhance ADCC and ADCP, while also inducing apoptosis, leading to depletion of malignant and normal CD19+ B cells.
NO
INDIRECT
Tafasitamab binds CD19 on B cells; its Fc engages CD32A (Fc gamma receptor IIA) on effector cells to trigger ADCC/ADCP that kills CD19+ cells. CD32A+ cells serve as effectors and are not targeted or killed by the drug.