Type II anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-mediated cytotoxicity, and direct cell death.
Glycoengineered type II anti-CD20 humanized IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced antibody-dependent cellular cytotoxicity (increased FcγRIIIa affinity), complement-dependent cytotoxicity, and direct caspase-independent apoptosis.
Binds CD20 on B cells and induces killing via Fc-enhanced ADCC (NK cells/macrophages), complement-dependent cytotoxicity, and direct caspase-independent apoptosis/type II signaling.
Autologous T cells engineered with a chimeric antigen receptor to recognize and kill malignant B cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds B-cell surface antigens (e.g., CD19) independent of HLA, activating T-cell signaling, proliferation, and cytotoxicity to eliminate malignant B cells via perforin/granzyme release and cytokine-mediated killing.
CAR-T cells bind CD19 on target cells, trigger T-cell activation and immunologic synapse formation, then kill via perforin/granzyme-mediated apoptosis (with additional Fas/FasL and cytokine-mediated cytotoxicity).
Off-the-shelf allogeneic CAR NK cell therapy targeting GPC3 for advanced hepatocellular carcinoma; armed with calibrated-release IL-15 to support NK-cell survival, proliferation, and persistence.
Off-the-shelf allogeneic NK cells engineered with a CAR targeting glypican-3 (GPC3) recognize GPC3-expressing tumor cells and trigger NK-mediated cytotoxicity (perforin/granzyme and cytokine release). The product includes calibrated-release IL-15 to enhance NK-cell survival, proliferation, and persistence in vivo.
CAR-engineered NK cells bind GPC3 on target cells and directly kill them via NK degranulation (perforin/granzyme–mediated cytotoxicity) and related apoptotic pathways; IL-15 supports NK survival/persistence.
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
rATG contains antibodies that bind CD28 on T cells and deplete them via complement-dependent lysis and Fc-mediated ADCC/phagocytosis, with additional apoptosis induction.
Autologous anti-CD19 CAR T-cell therapy; patient T cells are engineered to express a CD19-directed chimeric antigen receptor, activating T-cell cytotoxicity to eliminate CD19+ malignant and normal B cells (often causing B-cell aplasia).
Autologous T cells are engineered ex vivo to express a CD19-directed chimeric antigen receptor; upon binding CD19 on malignant and normal B cells, CAR signaling activates T-cell cytotoxicity and cytokine release, resulting in targeted lysis and depletion of CD19+ cells (often causing B-cell aplasia).
Anti-CD19 CAR T cells bind CD19 on target B cells; CAR signaling triggers a cytolytic synapse and release of perforin/granzymes (and Fas–FasL), inducing apoptosis/lysis of CD19+ cells.