HER2-targeted antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death with potential bystander effect.
HER2-targeted ADC (trastuzumab rezetecan). The trastuzumab antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases a camptothecin-derived payload that inhibits topoisomerase I by stabilizing Topo I–DNA complexes, leading to DNA breaks, replication arrest, apoptosis, and tumor cell death, with potential bystander killing; the IgG1 backbone may also inhibit HER2 signaling and mediate ADCC.
YES
DIRECT
HER2-targeted ADC binds HER2, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that causes DNA damage, replication arrest, and apoptosis in HER2-expressing cells; IgG1 Fc may also mediate ADCC and bystander killing.
Fc-engineered anti-CTLA-4 monoclonal antibody that enhances T-cell activation and can deplete Tregs.
Fc-engineered anti-CTLA-4 IgG1 monoclonal antibody that blocks CTLA-4 to relieve inhibitory signaling and enhance T-cell priming/activation; the engineered Fc increases stability/half-life and enhances Fc-gamma receptor engagement to deplete intratumoral Tregs, promoting CTL-mediated antitumor immunity.
YES
DIRECT
Antibody binds CTLA-4 on Tregs and its engineered Fc engages FcγR-bearing effectors (NK cells/macrophages), inducing ADCC/antibody-dependent phagocytosis (and possibly CDC) to deplete CTLA-4–high intratumoral Tregs.
HER2-targeted antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death with potential bystander effect.
HER2-targeted ADC (trastuzumab rezetecan). The trastuzumab antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases a camptothecin-derived payload that inhibits topoisomerase I by stabilizing Topo I–DNA complexes, leading to DNA breaks, replication arrest, apoptosis, and tumor cell death, with potential bystander killing; the IgG1 backbone may also inhibit HER2 signaling and mediate ADCC.
NO
INDIRECT
The ADC binds HER2 (not topoisomerase I), is internalized, and releases a camptothecin payload that inhibits topoisomerase I to cause DNA damage and apoptosis. Expression of topoisomerase I alone does not direct killing; only HER2-targeted delivery (with possible bystander effect) leads to cytotoxicity.
Afucosylated humanized monoclonal antibody against IL-5Rα that depletes eosinophils via antibody-dependent cell-mediated cytotoxicity.
Afucosylated humanized anti–IL-5Rα monoclonal antibody that binds IL-5 receptor alpha on eosinophils and basophils, enhances FcγRIIIa engagement, and induces antibody-dependent cell-mediated cytotoxicity to deplete these cells, thereby suppressing IL-5 signaling and eosinophilic inflammation.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and its afucosylated Fc engages FcγRIIIa on NK cells to trigger strong ADCC, causing apoptosis/depletion of IL-5Rα+ cells.
Afucosylated humanized monoclonal antibody against IL-5Rα that depletes eosinophils via antibody-dependent cell-mediated cytotoxicity.
Afucosylated humanized anti–IL-5Rα monoclonal antibody that binds IL-5 receptor alpha on eosinophils and basophils, enhances FcγRIIIa engagement, and induces antibody-dependent cell-mediated cytotoxicity to deplete these cells, thereby suppressing IL-5 signaling and eosinophilic inflammation.
NO
INDIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils; its afucosylated Fc engages FcγRIIIa (CD16a) on NK cells to trigger ADCC that kills IL-5Rα+ cells. FcγRIIIa-expressing cells are effectors, not targets.