Chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Chimeric anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP), and can directly induce apoptosis.
YES
DIRECT
Anti-CD20 mAb binds CD20 on B cells, triggering complement-mediated lysis (CDC), Fc-dependent ADCC/ADCP by effector cells, and can also induce apoptosis upon crosslinking.
Allogeneic engineered T cells transduced ex vivo with a lentiviral vector to express an Epstein–Barr virus–specific T-cell receptor (HLA-A*02:01/11:01/24:02–restricted). Administered at 1×10^6–1×10^8 cells/kg for adoptive cellular immunotherapy to recognize EBV-derived peptides on MHC I and eliminate EBV-infected cells in EBV-associated HLH or persistent EBV infection.
Allogeneic T cells are engineered ex vivo with a lentiviral vector to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor. Upon recognition of EBV-derived peptides presented on MHC class I of infected host cells, the introduced TCR triggers T-cell activation and cytotoxic effector functions (perforin/granzyme, Fas–FasL) and cytokine release, leading to targeted elimination of EBV-infected cells and reduction of EBV-driven inflammation (e.g., in EBV-HLH or persistent EBV infection).
YES
DIRECT
EBV-specific TCR-T cells recognize EBV-derived peptide presented on HLA-A*02:01 on target cells and directly induce apoptosis via perforin/granzyme release and Fas–FasL signaling.
Allogeneic engineered T cells transduced ex vivo with a lentiviral vector to express an Epstein–Barr virus–specific T-cell receptor (HLA-A*02:01/11:01/24:02–restricted). Administered at 1×10^6–1×10^8 cells/kg for adoptive cellular immunotherapy to recognize EBV-derived peptides on MHC I and eliminate EBV-infected cells in EBV-associated HLH or persistent EBV infection.
Allogeneic T cells are engineered ex vivo with a lentiviral vector to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor. Upon recognition of EBV-derived peptides presented on MHC class I of infected host cells, the introduced TCR triggers T-cell activation and cytotoxic effector functions (perforin/granzyme, Fas–FasL) and cytokine release, leading to targeted elimination of EBV-infected cells and reduction of EBV-driven inflammation (e.g., in EBV-HLH or persistent EBV infection).
YES
DIRECT
EBV-specific TCR on the engineered T cells recognizes EBV peptide–HLA-A*11:01 on target cells and triggers CTL killing via perforin/granzyme release and Fas–FasL-mediated apoptosis.
Allogeneic engineered T cells transduced ex vivo with a lentiviral vector to express an Epstein–Barr virus–specific T-cell receptor (HLA-A*02:01/11:01/24:02–restricted). Administered at 1×10^6–1×10^8 cells/kg for adoptive cellular immunotherapy to recognize EBV-derived peptides on MHC I and eliminate EBV-infected cells in EBV-associated HLH or persistent EBV infection.
Allogeneic T cells are engineered ex vivo with a lentiviral vector to express an EBV-specific, HLA-A*02:01/11:01/24:02–restricted T-cell receptor. Upon recognition of EBV-derived peptides presented on MHC class I of infected host cells, the introduced TCR triggers T-cell activation and cytotoxic effector functions (perforin/granzyme, Fas–FasL) and cytokine release, leading to targeted elimination of EBV-infected cells and reduction of EBV-driven inflammation (e.g., in EBV-HLH or persistent EBV infection).
YES
DIRECT
TCR-engineered T cells recognize EBV-derived peptide presented by HLA-A*24:02 on target cells and induce cytotoxicity via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous anti-BCMA chimeric antigen receptor (CAR) T-cell therapy: patient T lymphocytes are genetically engineered to express a CAR targeting BCMA and infused intravenously (3+3 dose escalation, up to 6×10^6 CAR-T cells/kg). CAR engagement activates T-cell cytotoxicity (degranulation, cytokine release, proliferation) to eliminate BCMA-positive myeloma cells. The construct includes EGFR expression as a built-in safety/control feature.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor targeting BCMA. Upon binding BCMA on malignant plasma cells, CAR signaling (CD3 zeta with costimulatory domains) activates T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate BCMA-positive cells. The construct co-expresses EGFR as a safety/control feature.
YES
DIRECT
Anti-BCMA CAR-T cells bind BCMA on target cells, triggering CAR signaling and T-cell degranulation to kill BCMA+ cells via perforin/granzyme-mediated cytotoxicity.