IgG1 monoclonal antibody that binds the HER2 extracellular domain IV, inhibits HER2 signaling and receptor shedding, and triggers antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 extracellular domain IV; blocks HER2 signaling and receptor shedding, suppressing downstream PI3K/AKT and MAPK pathways, and induces Fc-mediated ADCC against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 domain IV and engages Fcγ receptor–bearing immune effectors (e.g., NK cells) to trigger ADCC (and some complement activation), killing HER2+ cells; it also inhibits HER2 signaling.
An antibody–drug conjugate (IMMU-132; Trodelvy) consisting of a humanized anti–TROP-2 monoclonal antibody linked via a hydrolyzable linker to SN-38, the active metabolite of irinotecan (a topoisomerase I inhibitor). After binding TROP-2 on tumor cells, it is internalized and releases SN-38 to inhibit topoisomerase I, causing DNA damage/replication stress and apoptosis, with a bystander effect.
Humanized anti–TROP-2 monoclonal antibody linked via a hydrolyzable linker to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes Topo I–DNA complexes, causing DNA breaks, replication stress, and apoptosis; membrane-permeable SN-38 enables a bystander effect.
ADC binds TROP-2 on target cells, is internalized, and releases SN-38 (topoisomerase I inhibitor) that stabilizes Topo I–DNA complexes, causing DNA damage and apoptosis; membrane-permeable SN-38 can also produce a bystander effect.
Allogeneic gamma-delta T cells engineered to express an anti-CD19 chimeric antigen receptor, enabling MHC-independent cytotoxic depletion of CD19+ B cells to reset the B-cell compartment and reduce autoantibody-driven inflammation in SLE.
Allogeneic gamma-delta T cells engineered with an anti-CD19 chimeric antigen receptor recognize CD19 on B cells and mediate MHC-independent cytotoxic killing, depleting CD19+ B-cell subsets to reset the B-cell compartment and reduce autoantibody-driven inflammation in SLE.
Anti-CD19 CAR γδ T cells recognize CD19 on B cells and directly lyse them via MHC-independent cytotoxicity, primarily through perforin/granzyme-mediated apoptosis (and related effector pathways).
A humanized IgG1 anti-CTLA-4 monoclonal antibody checkpoint inhibitor (also known as ONC-392/BNT316); designed with pH-sensitive CTLA-4 binding to preserve peripheral CTLA-4 recycling while retaining Fc effector function to deplete intratumoral Tregs and enhance priming/expansion of tumor-reactive T cells; targets CTLA-4 and modulates the CD28–CD80/86 costimulation axis.
Humanized IgG1 anti-CTLA-4 checkpoint inhibitor with pH-sensitive binding that preserves peripheral CTLA-4 recycling while retaining Fc effector function. Blocks CTLA-4 to relieve inhibition of CD28–CD80/86 costimulation, promoting priming/expansion of tumor-reactive T cells and selectively depleting intratumoral Tregs to enhance antitumor CTL responses with reduced systemic toxicity.
IgG1 Fc effector functions recruit FcγR+ cells (NK cells/macrophages) to mediate ADCC/ADCP (± CDC), selectively depleting CTLA-4–high intratumoral Tregs; CTLA-4 blockade itself is non-cytotoxic.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
Rabbit polyclonal anti‑thymocyte IgG binds CD11a on T cells; Fc engagement activates complement and ADCC and can trigger apoptosis, directly depleting the bound cells.