Autologous T cells engineered ex vivo via non-viral transposon electroporation to express a PSMA-targeting chimeric antigen receptor with co-expressed factors intended to augment innate and adaptive immune activation; administered to target PSMA-positive prostate cancer.
Autologous T cells engineered ex vivo via non-viral transposon electroporation to express a PSMA-targeted chimeric antigen receptor. CAR engagement of PSMA activates T-cell signaling, proliferation, and cytotoxic killing of PSMA-positive tumor cells through perforin/granzyme release and cytokine secretion; co-expressed enhancement factors are intended to boost innate and adaptive immune activation and T-cell persistence.
YES
DIRECT
PSMA-targeted CAR T cells bind PSMA and directly kill target cells via T-cell cytotoxicity, primarily perforin/granzyme-mediated lysis (and death-receptor signaling).
Fourth-generation dual-target autologous chimeric antigen receptor T cells engineered to recognize CD19 on B cells and BCMA (TNFRSF17) on plasmablasts/plasma cells, inducing cytolytic depletion of autoreactive B-lineage cells to reduce autoantibody production.
Autologous fourth-generation CAR T cells engineered to recognize CD19 and BCMA activate upon antigen binding and mediate cytolytic killing of B cells, plasmablasts, and plasma cells, thereby depleting autoreactive B-lineage populations and reducing autoantibody production.
YES
DIRECT
CD19-directed CAR-T cells bind CD19 on B-lineage cells, activate, and kill targets via immunologic synapse formation with perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
Autologous cell-based immunotherapy consisting of a patient’s fresh peripheral blood mononuclear cells (primarily T cells) armed ex vivo with an anti-CD3 x anti-EGFR bispecific antibody; upon reinfusion, redirects and activates T-cell cytotoxicity against EGFR-expressing tumor cells.
Autologous PBMCs (primarily T cells) are armed ex vivo with an anti-CD3×anti-EGFR bispecific antibody. After reinfusion, the bispecific antibody bridges CD3 on T cells to EGFR on tumor cells, activating and redirecting cytotoxic T-cell activity to lyse EGFR-expressing cancer cells without genetic modification.
NO
INDIRECT
The bispecific antibody binds CD3ε on T cells to activate and redirect them to EGFR-expressing tumor cells; T cells (CD3ε+) are not killed. Cytotoxicity is T-cell mediated (perforin/granzyme) against EGFR-positive targets.
A bispecific antibody that binds CD3 on T cells and EGFR on tumor cells, bridging and activating T cells to kill EGFR-positive cancer cells; used ex vivo to arm autologous PBMCs prior to infusion.
A bispecific antibody that binds CD3 on T cells and EGFR on tumor cells, bridging them to activate and redirect T-cell cytotoxicity against EGFR-positive cancer cells. In this trial, autologous PBMCs are armed ex vivo with the bispecific before infusion to provide immediate T-cell engagement without genetic modification.
NO
INDIRECT
Binding CD3 activates and redirects T cells; the engaged T cells kill EGFR-positive tumor cells via perforin/granzyme cytotoxicity, not the CD3+ T cells themselves.
A bispecific antibody that binds CD3 on T cells and EGFR on tumor cells, bridging and activating T cells to kill EGFR-positive cancer cells; used ex vivo to arm autologous PBMCs prior to infusion.
A bispecific antibody that binds CD3 on T cells and EGFR on tumor cells, bridging them to activate and redirect T-cell cytotoxicity against EGFR-positive cancer cells. In this trial, autologous PBMCs are armed ex vivo with the bispecific before infusion to provide immediate T-cell engagement without genetic modification.
YES
DIRECT
The bispecific links CD3 on T cells to EGFR on target cells, activating T cells to kill EGFR+ cells via immune-synapse–mediated perforin/granzyme cytotoxicity (and Fas/FasL).