Autologous T lymphocytes genetically modified to express dual chimeric antigen receptors targeting CD19 and CD22; antigen engagement triggers CAR signaling with costimulation, leading to T-cell expansion, cytokine release, and cytotoxic killing of malignant B cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19 and CD22 on B cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains such as CD28/4-1BB), driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with on-target B-cell aplasia and reduced antigen-loss escape.
YES
DIRECT
CAR-engineered T cells recognize CD19 on target cells, activate via CD3ζ with costimulation, and kill through perforin/granzyme-mediated cytolysis (and death receptor apoptosis).
Autologous T lymphocytes genetically modified to express dual chimeric antigen receptors targeting CD19 and CD22; antigen engagement triggers CAR signaling with costimulation, leading to T-cell expansion, cytokine release, and cytotoxic killing of malignant B cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19 and CD22 on B cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains such as CD28/4-1BB), driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with on-target B-cell aplasia and reduced antigen-loss escape.
YES
DIRECT
CAR-T cells recognize CD22 on target cells; CAR signaling (CD3ζ with costimulation) activates T cells to kill via perforin/granzyme release and death-receptor pathways, leading to lysis/apoptosis of CD22+ cells.
Autologous T lymphocytes genetically modified to express dual chimeric antigen receptors targeting CD19 and CD20; binding activates CAR signaling to mediate expansion and cytotoxic elimination of B-cell malignancies while aiming to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express dual chimeric antigen receptors recognizing CD19 and CD20 on B cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains), driving T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of malignant B cells. Dual targeting aims to reduce antigen‑loss escape; on‑target effects include B‑cell aplasia.
YES
DIRECT
CAR-T cells recognize CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous T lymphocytes genetically modified to express dual chimeric antigen receptors targeting CD19 and CD20; binding activates CAR signaling to mediate expansion and cytotoxic elimination of B-cell malignancies while aiming to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express dual chimeric antigen receptors recognizing CD19 and CD20 on B cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains), driving T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of malignant B cells. Dual targeting aims to reduce antigen‑loss escape; on‑target effects include B‑cell aplasia.
YES
DIRECT
CAR-T cells bind CD20 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (plus death-receptor pathways).
Human IgG1 monoclonal antibody (VAY736) administered subcutaneously (300 mg) that targets the BAFF receptor (BAFF-R/TNFRSF13C). It blocks BAFF/BLyS binding to BAFF-R and depletes BAFF-R–positive B cells via Fc-mediated ADCC, reducing BAFF-driven survival/maturation signals and lowering autoreactive B-cell activity and autoantibody production.
Fully human IgG1 monoclonal antibody targeting the BAFF receptor (BAFF-R/TNFRSF13C). It blocks BAFF/BLyS binding and downstream BAFF-R signaling and depletes BAFF-R–positive B cells via Fc-mediated ADCC, reducing BAFF-driven B-cell survival/maturation and autoantibody production.
YES
DIRECT
Ianalumab is an anti–BAFF-R IgG1 that opsonizes BAFF-R+ B cells and recruits FcγR-expressing effector cells to mediate ADCC (and possibly complement-mediated lysis), depleting the target cells.