Allogeneic NK-92 cell therapy engineered to express a PD-L1–targeting CAR and high-affinity CD16, enabling killing of PD-L1–positive tumor/immunosuppressive cells and ADCC.
Allogeneic NK-92 cells engineered to express a PD-L1–targeting chimeric antigen receptor and high-affinity CD16 (FcγRIIIa), enabling direct killing of PD-L1–positive tumor and immunosuppressive cells and enhancing antibody-dependent cellular cytotoxicity (ADCC).
CAR-engineered NK-92 cells bind PD-L1 on target cells and directly lyse them via NK cytotoxic pathways (perforin/granzyme); high-affinity CD16 also enables ADCC when antibodies are present.
Afucosylated anti–IL-5Rα monoclonal antibody that depletes eosinophils (and basophils) via antibody-dependent cellular cytotoxicity (ADCC).
Afucosylated anti-IL-5Ralpha monoclonal antibody that binds IL-5 receptor alpha on eosinophils and basophils, triggering strong ADCC to deplete these cells and thereby suppress IL-5 signaling and type 2 inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and, via its afucosylated Fc, strongly engages FcγRIIIa on NK cells to trigger ADCC (perforin/granzyme-mediated killing), depleting IL-5Rα+ cells.
Type II glycoengineered anti-CD20 monoclonal antibody administered IV; depletes B cells via enhanced ADCC, direct cell death, and some complement activation.
Type II glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC/ADCP, direct non-apoptotic cell death, and limited complement-dependent cytotoxicity.
Anti-CD20 mAb depletes CD20+ B cells via enhanced Fc-mediated ADCC/ADCP (NK cells, macrophages), direct non-apoptotic cell death (type II), and some complement-dependent cytotoxicity.
An anti-HER2 antibody–drug conjugate (T-DXd, Enhertu) composed of trastuzumab linked via a cleavable linker to a DXd topoisomerase I inhibitor payload; binds HER2, is internalized, releases DXd to induce DNA damage and cell death with a bystander effect, and the antibody component also inhibits HER2 signaling and mediates ADCC.
Humanized anti‑HER2 mAb (trastuzumab) targets HER2 on tumor cells and is internalized; a cleavable linker releases the DXd payload (a topoisomerase I inhibitor), causing DNA damage, replication arrest, and apoptosis. The membrane‑permeable payload enables a bystander killing effect, and the antibody component also inhibits HER2 signaling and mediates ADCC.
The ADC binds HER2, is internalized, and releases a DXd topoisomerase I inhibitor that causes DNA damage and apoptosis; Fc can also trigger ADCC, with a membrane-permeable payload enabling bystander killing.
Anti-CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases an MMAE payload to disrupt microtubules causing mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
Anti-CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases an MMAE payload to disrupt microtubules, causing mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
Anti-CLDN18.2 ADC binds CLDN18.2, is internalized, and releases MMAE to disrupt microtubules causing mitotic arrest and apoptosis; Fc-mediated ADCC may also contribute.