A subcutaneous, full-length bispecific T‑cell–engaging monoclonal antibody (CD3×CD20) that binds CD20 on malignant B cells and CD3 on T cells to form an immune synapse, activate T cells, and induce targeted cytotoxic killing of CD20+ follicular lymphoma cells.
A subcutaneous full-length bispecific anti-CD3×CD20 monoclonal antibody that simultaneously binds CD20 on malignant B cells and CD3 on T cells, forming an immune synapse to activate and redirect T-cell cytotoxicity for targeted killing of CD20-positive follicular lymphoma cells.
YES
DIRECT
The CD3×CD20 bispecific antibody bridges CD20+ cells to T cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme–mediated lysis) to kill CD20-expressing cells.
A subcutaneous, full-length bispecific T‑cell–engaging monoclonal antibody (CD3×CD20) that binds CD20 on malignant B cells and CD3 on T cells to form an immune synapse, activate T cells, and induce targeted cytotoxic killing of CD20+ follicular lymphoma cells.
A subcutaneous full-length bispecific anti-CD3×CD20 monoclonal antibody that simultaneously binds CD20 on malignant B cells and CD3 on T cells, forming an immune synapse to activate and redirect T-cell cytotoxicity for targeted killing of CD20-positive follicular lymphoma cells.
NO
INDIRECT
Epcoritamab binds CD3ε on T cells to activate and redirect them to kill CD20-positive B cells; CD3ε-expressing T cells are not the targets of cytotoxicity.
Autologous, lentiviral-transduced dual STAR-T cell therapy targeting BCMA and LILRB4; synthetic antigen receptors engage BCMA and LILRB4 to signal via native TCR/CD3, activating T-cell cytotoxicity. Dose: 1E6–1E7 cells/kg IV; repeat dosing allowed.
Autologous T cells are lentivirally engineered to express dual synthetic antigen receptors that bind BCMA and LILRB4 and signal through the native TCR/CD3 complex. Target engagement activates T-cell cytotoxicity and cytokine release against BCMA+ myeloma cells and LILRB4+ cells in the tumor milieu, aiming to enhance efficacy and reduce antigen escape/immunosuppression.
YES
DIRECT
Engineered STAR-T cells bind BCMA and signal via TCR/CD3 to form an immunologic synapse, releasing perforin/granzymes (and Fas/FasL, cytokines) to kill BCMA+ cells.
Autologous, lentiviral-transduced dual STAR-T cell therapy targeting BCMA and LILRB4; synthetic antigen receptors engage BCMA and LILRB4 to signal via native TCR/CD3, activating T-cell cytotoxicity. Dose: 1E6–1E7 cells/kg IV; repeat dosing allowed.
Autologous T cells are lentivirally engineered to express dual synthetic antigen receptors that bind BCMA and LILRB4 and signal through the native TCR/CD3 complex. Target engagement activates T-cell cytotoxicity and cytokine release against BCMA+ myeloma cells and LILRB4+ cells in the tumor milieu, aiming to enhance efficacy and reduce antigen escape/immunosuppression.
YES
DIRECT
Engineered STAR-T cells bind LILRB4 via synthetic receptors and signal through native TCR/CD3 to trigger T-cell cytotoxicity (perforin/granzyme and death-receptor pathways) killing LILRB4+ cells.
Allogeneic, gene-edited CD19-directed CAR T-cell therapy that retains endogenous TCR and knocks out SPPL3 (Power3) to reduce alloreactivity and improve persistence; mediates CD19-specific cytotoxicity against malignant B cells.
Allogeneic, gene-edited CD19-directed CAR T cells that recognize CD19 on malignant B cells to induce T-cell activation and cytotoxic killing. The product retains the endogenous TCR to support signaling and persistence, while SPPL3 (Power3) knockout reduces alloreactivity and host-mediated rejection, enhancing expansion and durability of the donor CAR T cells.
YES
DIRECT
CAR T cells bind CD19 on target B cells, become activated, and kill via perforin/granzyme release and death receptor pathways (e.g., Fas-FasL).