TROP2-targeting antibody–drug conjugate (izalontamab brengitecan; also referred to as BMS-986507) that delivers a DNA topoisomerase I inhibitor payload to tumor cells, causing DNA damage and cell death with potential bystander effect.
TROP2-targeting antibody–drug conjugate (izalontamab brengitecan; BMS-986507) that binds TROP2 on tumor cells, is internalized, and releases a DNA topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death with a potential bystander effect.
YES
DIRECT
BL-B01D1 is a bispecific ADC that binds HER3 (and EGFR) on tumor cells, is internalized, and releases a cytotoxic payload inside the cell, leading to death of HER3-expressing cells.
Anti–IL-5Rα monoclonal antibody that induces antibody-dependent cell-mediated cytotoxicity to deplete eosinophils and basophils.
Afucosylated humanized anti–IL-5Rα monoclonal antibody that binds the IL-5 receptor alpha on eosinophils and basophils and, through enhanced FcγRIIIa engagement, induces antibody‑dependent cell‑mediated cytotoxicity and apoptosis, depleting these cells and suppressing IL‑5 signaling to reduce eosinophilic inflammation.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and, via enhanced FcγRIIIa engagement, triggers NK cell–mediated ADCC leading to apoptosis and depletion of target-expressing cells.
Anti–IL-5Rα monoclonal antibody that induces antibody-dependent cell-mediated cytotoxicity to deplete eosinophils and basophils.
Afucosylated humanized anti–IL-5Rα monoclonal antibody that binds the IL-5 receptor alpha on eosinophils and basophils and, through enhanced FcγRIIIa engagement, induces antibody‑dependent cell‑mediated cytotoxicity and apoptosis, depleting these cells and suppressing IL‑5 signaling to reduce eosinophilic inflammation.
NO
INDIRECT
Benralizumab binds IL-5Ralpha on eosinophils/basophils; its afucosylated Fc engages CD16a on NK cells to trigger ADCC that kills IL-5Ralpha+ cells. CD16a+ cells act as effectors, not targets.
Fully human, Fc-enhanced anti-CTLA-4 monoclonal antibody that blocks CTLA-4 to enhance T-cell priming/activation and can deplete intratumoral regulatory T cells via Fc receptor engagement.
Fc-engineered human IgG1 anti-CTLA-4 monoclonal antibody that blocks CTLA-4 checkpoint signaling to enhance T-cell priming/activation; Fc receptor engagement can deplete intratumoral regulatory T cells, promoting cytotoxic T-cell-mediated antitumor responses.
YES
DIRECT
Fc-engineered IgG1 engages FcγR-bearing effector cells (e.g., NK cells/macrophages) to mediate ADCC/ADCP and deplete CTLA-4–expressing intratumoral regulatory T cells.
Gene-modified autologous T cells engineered with a chimeric antigen receptor targeting BCMA and FcRL5 to mediate targeted cytotoxicity against multiple myeloma cells; dual targeting aims to reduce antigen escape.
Autologous T cells are gene-modified to express a chimeric antigen receptor that recognizes BCMA and FcRL5 on multiple myeloma cells. CAR engagement triggers TCR signaling (CD3ζ with costimulatory domains), leading to targeted T-cell activation, proliferation, and cytotoxic killing of BCMA+/FcRL5+ tumor cells. Dual targeting is intended to reduce antigen escape and enhance tumor clearance.
YES
DIRECT
Anti-BCMA CAR T cells bind BCMA on target cells, activating TCR/CD3ζ signaling and directly killing BCMA+ cells via perforin/granzyme-mediated cytolysis and apoptosis (and Fas/FasL).