Autologous CD19-directed CAR T-cell therapy that redirects T cells to CD19+ B cells to induce cytotoxicity.
Autologous CD19-directed chimeric antigen receptor T-cell therapy. Patient T cells are engineered to express a CAR (with 4-1BB costimulatory and CD3ζ signaling domains) that binds CD19 on B cells, triggering T-cell activation, proliferation, and cytotoxic killing of CD19+ malignant B cells.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity and complement.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and phagocytosis.
YES
DIRECT
Rituximab binds CD20 and triggers Fc-mediated immune killing: NK-cell ADCC, complement-dependent cytotoxicity (MAC formation), and macrophage phagocytosis of CD20+ cells.
Autologous T cells genetically engineered to express an anti-CD20 chimeric antigen receptor, redirecting T cells to recognize CD20 on malignant B cells and induce TCR-independent activation, cytokine release, cytotoxic killing, and in vivo expansion.
Autologous T cells are genetically engineered to express an anti-CD20 chimeric antigen receptor that recognizes CD20 on malignant B cells and triggers TCR-independent activation through CAR signaling, leading to cytokine release, proliferation, and targeted cytotoxic killing of CD20-positive cells.
YES
DIRECT
Anti-CD20 CAR engagement activates the infused T cells to kill CD20+ cells via perforin/granzyme-mediated cytolysis and apoptosis (± Fas/FasL), with associated cytokine release.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor targeting CD19-positive B-cell malignancies, mediating TCR-independent activation, cytokine release, cytotoxicity, and in vivo expansion.
Autologous T cells are genetically engineered to express an anti-CD19 chimeric antigen receptor. Upon binding CD19 on malignant B cells, the CAR provides TCR/MHC-independent activation signals that trigger T-cell activation, cytokine release, proliferation, and cytotoxic killing of CD19-positive tumor cells.
YES
DIRECT
CD19-directed CAR-T cells bind CD19 and, upon activation, kill target cells via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas/FasL).
Human IgG1 monoclonal antibody immune checkpoint inhibitor targeting PD-L1; blocks PD-L1 interaction with PD-1/B7.1 to restore cytotoxic T-cell activity and can mediate ADCC.
Human IgG1 monoclonal antibody that binds PD-L1, blocking its interaction with PD-1 and B7.1 to lift inhibitory signaling and restore cytotoxic T-cell activity; its Fc region can mediate antibody-dependent cellular cytotoxicity (ADCC) against PD-L1–expressing tumor cells.
YES
DIRECT
Avelumab binds PD-L1 on target cells and its IgG1 Fc engages Fc gamma receptors on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), directly killing PD-L1-expressing cells; it also blocks PD-L1/PD-1 to restore CTL killing (indirect).