Humanized IgG1 monoclonal antibody targeting CCR4 that mediates antibody-dependent cellular cytotoxicity (ADCC) to deplete CCR4-positive malignant T cells and regulatory/Th2 T cells in CTCL (mycosis fungoides/Sézary syndrome).
Humanized IgG1 monoclonal antibody against CCR4 (CD194) that binds CCR4 on malignant T cells and CCR4+ Tregs/Th2 cells, blocks CCR4 chemokine signaling/trafficking, and induces Fc-mediated ADCC to deplete CCR4-positive cells, thereby reducing immunosuppressive Tregs and exerting antitumor activity in CTCL.
IgG1 anti-CCR4 binds CCR4 on target cells and engages Fc-gamma receptor-bearing effector cells (e.g., NK cells) to mediate ADCC, killing CCR4+ cells; may also trigger complement-dependent cytotoxicity.
An anti-CD20 monoclonal antibody that targets B cells to induce antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ malignant and normal B lymphocytes via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC by NK/macrophages, complement activation (CDC), and CD20-mediated apoptotic signaling.
Off-the-shelf, allogeneic iPSC-derived HER2-directed CAR T-cell therapy designed to kill HER2 (ERBB2)-expressing tumor cells.
Off-the-shelf, allogeneic iPSC-derived HER2-directed CAR T cells that recognize HER2 (ERBB2) via a 1XX CAR, triggering T-cell activation and cytotoxic killing of HER2+ tumor cells. Engineered features include CXCR2 to enhance trafficking, a TGFβ signal-redirection receptor to counter immunosuppression, CD38 knockout for persistence, an IL-7/IL-7R fusion to support T-cell stemness, TCR removal to reduce GVHD risk, and a high-affinity non-cleavable CD16a to enable antibody-dependent cellular cytotoxicity when a compatible therapeutic antibody is administered.
HER2-expressing cells are recognized by the HER2-specific CAR on FT825 T cells, triggering T-cell activation and cytolytic killing (perforin/granzyme and death receptor pathways); hnCD16 can also mediate ADCC if a compatible anti-HER2 antibody is present.
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.
Polyclonal anti-thymocyte IgG binds CD28 on T cells and depletes them via complement-dependent cytotoxicity, Fc-mediated ADCC, and apoptosis.
Chimeric IgG1 monoclonal antibody against EGFR (ERBB1); blocks EGFR signaling and induces ADCC.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR (ERBB1), blocking ligand binding, receptor activation and dimerization to inhibit downstream signaling and tumor cell proliferation; its Fc region also engages immune effector cells to mediate ADCC against EGFR-expressing cells.
IgG1 Fc engages FcγR-bearing immune cells (e.g., NK cells) to mediate ADCC, with some complement-dependent cytotoxicity; EGFR blockade is antiproliferative but cytolysis occurs via ADCC/CDC against EGFR-expressing cells.