Investigational antibody-drug conjugate (humanized IgG1) targeting B7-H4 on tumor cells; after binding and internalization, a protease-cleavable linker releases a topoisomerase I inhibitor payload (DAR ~6) that causes DNA damage/replication stress and apoptosis.
Humanized IgG1 ADC that binds B7-H4 on tumor cells and is internalized; a protease-cleavable linker releases a topoisomerase I inhibitor payload that stabilizes TOP1–DNA cleavable complexes, preventing DNA re-ligation, inducing DNA damage/replication stress, cell-cycle arrest, and apoptosis in B7-H4–expressing cancer cells.
NO
INDIRECT
HS-20089 binds B7-H4 on tumor cells, is internalized, and releases a TOP1 inhibitor that traps TOP1–DNA complexes, causing DNA damage and apoptosis in B7-H4–expressing cells; DNA topoisomerase I is not the antigen targeted for cell selection.
Anti-GD2 IgG1 monoclonal antibody (ch14.18/CHO) that binds GD2 on neuroblastoma cells to mediate NK cell/macrophage Fc-dependent ADCC and complement-dependent cytotoxicity.
Chimeric IgG1 anti-GD2 monoclonal antibody that binds GD2 on tumor cells and induces immune-mediated killing via Fc receptor-mediated antibody-dependent cellular cytotoxicity (by NK cells and macrophages) and complement-dependent cytotoxicity.
YES
DIRECT
The antibody binds GD2 on target cells and engages effector functions via its Fc: NK cell/macrophage FcγR-mediated ADCC and complement-dependent cytotoxicity (C1q→MAC), leading to lysis of GD2+ cells.
Afucosylated human IgG1 monoclonal antibody targeting the IL-5 receptor alpha on eosinophils and basophils; blocks IL-5 signaling and induces NK cell-mediated ADCC to deplete eosinophils; administered subcutaneously for severe eosinophilic asthma.
Afucosylated human IgG1 monoclonal antibody that binds IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, blocking IL-5 signaling and engaging FcγRIIIa on NK cells to induce ADCC-mediated depletion of eosinophils, thereby reducing type 2/eosinophilic inflammation in severe asthma.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and, via its afucosylated Fc, engages FcγRIIIa on NK cells to induce strong ADCC, depleting IL-5Rα-expressing cells.
Afucosylated human IgG1 monoclonal antibody targeting the IL-5 receptor alpha on eosinophils and basophils; blocks IL-5 signaling and induces NK cell-mediated ADCC to deplete eosinophils; administered subcutaneously for severe eosinophilic asthma.
Afucosylated human IgG1 monoclonal antibody that binds IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, blocking IL-5 signaling and engaging FcγRIIIa on NK cells to induce ADCC-mediated depletion of eosinophils, thereby reducing type 2/eosinophilic inflammation in severe asthma.
NO
INDIRECT
Benralizumab binds IL-5Rα on eosinophils and uses its Fc to engage CD16a on NK cells, triggering ADCC that kills IL-5Rα+ eosinophils. CD16a-expressing cells (NK cells) are engaged as effectors, not killed.
An anti-HER2 antibody–drug conjugate (RC48-ADC) that delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells and can mediate ADCC/bystander killing.
Anti-HER2 IgG1 antibody–drug conjugate that delivers monomethyl auristatin E (MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the Fc can mediate ADCC, and the membrane-permeable payload enables bystander killing.
YES
DIRECT
The ADC binds HER2 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; Fc-mediated ADCC and some bystander killing can also occur.