Afucosylated humanized IgG1 monoclonal antibody targeting the IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, inducing antibody-dependent cell-mediated cytotoxicity (ADCC) and resulting in near-complete eosinophil depletion.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha on eosinophils and basophils; enhanced FcγRIIIa engagement drives potent ADCC, leading to near-complete depletion of eosinophils (and basophils) and functional blockade of IL-5 signaling, thereby reducing eosinophilic inflammation.
NO
INDIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils; its afucosylated Fc engages FcγRIIIa (CD16a) on NK cells to trigger ADCC against IL-5Rα+ targets. CD16a-expressing cells act as effectors and are not killed.
Genetically engineered T cells expressing a chimeric antigen receptor targeting malignant B cells; infused 2–10×10^6/kg within 7 days post-ASCT.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that recognizes B‑cell tumor antigens (e.g., CD19) independently of HLA, providing CD3ζ plus co‑stimulatory signaling (e.g., CD28 or 4‑1BB) to activate and expand the cells, leading to cytokine release and perforin/granzyme‑mediated cytotoxic killing of malignant B cells.
YES
DIRECT
CD19-directed CAR-T cells bind CD19 on target cells and kill them via perforin/granzyme-mediated cytotoxicity.
Antibody–drug conjugate (ADC) also known as izalontamab brengitecan (iza-bren; BMS-986507); administered intravenously. The monoclonal antibody binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Bispecific anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death.
YES
DIRECT
The ADC binds EGFR on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload that induces DNA damage leading to cell death.
Type II anti‑CD20 monoclonal antibody given prior to glofitamab to debulk B cells and mitigate CRS; induces direct B‑cell death and Fc‑mediated ADCC/ADCP.
Type II anti-CD20 humanized IgG1 monoclonal antibody that binds CD20 on B cells; glycoengineering increases Fc-gamma RIIIa affinity to enhance antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), and it also induces direct, caspase-independent B-cell death, depleting CD20+ B cells (used pre-glofitamab to debulk and mitigate CRS).
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages CD16a on NK cells/macrophages to trigger ADCC/ADCP that kills CD20+ B cells. CD16a-expressing cells act as effectors and are not targeted or directly killed.
Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and kills them via complement-dependent cytotoxicity (CDC), Fc-mediated effector functions (ADCC/ADCP), and induction of apoptosis.