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.
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.
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.
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.
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.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor (CAR) with CD3ζ and costimulatory signaling; metabolically armed to enhance CAR-T metabolic fitness, expansion, and persistence. Given as a single infusion to target CD19+ B-ALL cells.
Autologous T cells engineered with a CD19‑directed CAR (CD3ζ signaling plus costimulatory domains) bind CD19 on malignant B cells, triggering T‑cell activation and perforin/granzyme‑mediated cytotoxicity and cytokine release to eliminate CD19+ cells. The cells are metabolically armed to enhance metabolic fitness, expansion, and persistence in vivo, improving antitumor activity.
CD19 CAR-T cells bind CD19 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis (and death-receptor pathways), eliminating CD19+ cells.
A human afucosylated IgG1 monoclonal antibody (AMG 451/KHK4083) targeting OX40 (CD134). It blocks OX40–OX40L signaling to reduce T‑cell activation, proliferation, survival, and cytokine production, and enhances ADCC-mediated depletion of OX40+ T cells; administered subcutaneously for atopic dermatitis.
Rocatinlimab is a human afucosylated IgG1 monoclonal antibody that binds OX40 (CD134), blocking OX40–OX40L costimulatory signaling to suppress T‑cell activation, proliferation, survival, and cytokine production. Its afucosylated Fc enhances ADCC, promoting depletion of OX40+ activated/memory T cells, thereby reducing inflammatory responses in atopic dermatitis.
Afucosylated IgG1 anti‑OX40 binds OX40 on activated T cells and engages FcγRIIIa on NK cells/macrophages to drive ADCC (and ADCP), depleting/killing OX40+ T cells.