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.
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.
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.
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.
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).
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.
Anti-FCRL5 CAR T cells bind FCRL5 on target cells, triggering TCR/CD3zeta signaling and cytolytic killing via perforin/granzyme (and Fas/FasL)–mediated apoptosis of FCRL5+ cells.
Intravenous HER2-targeted antibody-drug conjugate: a humanized anti-HER2 IgG1 linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd); binds HER2, is internalized, releases DXd to induce DNA damage, with Fc-mediated ADCC and bystander killing.
Humanized anti-HER2 IgG1 linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd). After binding HER2, the ADC is internalized and the linker is cleaved to release DXd, which induces DNA damage and cell death. The Fc domain can mediate ADCC, and the membrane-permeable payload enables bystander killing of adjacent tumor cells.
Anti-HER2 ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and cell death; Fc-mediated ADCC can contribute, with some bystander killing from membrane-permeable payload.