Bispecific T-cell engager (BiTE) antibody that links CD19 on B cells to CD3 on T cells to activate cytotoxic T-cell killing of malignant B cells.
A CD19xCD3 bispecific (BiTE) antibody that binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T-cell cytotoxicity and lyse CD19-positive malignant B cells.
Blinatumomab bridges CD19 on target cells to CD3 on T cells, forming an immunological synapse and triggering T‑cell–mediated killing (perforin/granzyme and Fas–FasL apoptosis) of CD19+ cells.
Anti-CD22 antibody–drug conjugate that delivers calicheamicin intracellularly, causing DNA double-strand breaks and cytotoxicity after internalization.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; after binding CD22 on B cells and internalization, the payload is released to bind the DNA minor groove, causing double-strand breaks and apoptosis.
The anti-CD22 ADC binds CD22, is internalized, and releases calicheamicin, which binds the DNA minor groove causing double-strand breaks and apoptosis in target cells.
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.
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).
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).
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.