Also known as AMT-754, ADCE-T02 is an intravenously administered antibody-drug conjugate (ADC) targeting Tissue Factor (TF; CD142/F3) on tumor cells. After binding and internalization, it releases a cytotoxic payload to induce cancer cell death.
Monoclonal antibody targets Tissue Factor (TF/CD142) on tumor cells; after binding and internalization, the ADC releases an intracellular cytotoxic payload that kills the cancer cell.
The ADC binds Tissue Factor (CD142) on the tumor cell, is internalized, and releases an intracellular cytotoxic payload that kills the cell (e.g., via microtubule disruption or DNA damage–induced apoptosis).
CD19xCD3 bispecific T-cell engager that redirects T cells to lyse CD19+ B-ALL blasts.
Bispecific T-cell engager that binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and induce perforin/granzyme-mediated lysis of CD19-positive B-ALL blasts.
Blinatumomab bridges CD3+ T cells to CD19+ cells, activating T cells to release perforin and granzymes that lyse/apoptose CD19-expressing cells.
Autologous T cells engineered with a CD19-specific chimeric antigen receptor to target and eliminate CD19+ B cells.
Autologous T cells are genetically modified to express a chimeric antigen receptor that binds CD19 on B cells. CAR engagement delivers CD3-zeta and costimulatory signals that activate the T cells to proliferate, release cytokines, and kill CD19-positive malignant B cells, resulting in targeted depletion of pathogenic B-cell populations.
CD19-specific CAR T cells bind CD19 on target cells and, upon CAR activation, directly kill them via perforin/granzyme-mediated cytolysis and Fas–FasL apoptotic signaling.
CD19-directed chimeric antigen receptor T-cell therapy (engineered autologous T cells) administered intravenously in split doses; recognizes CD19 and, via CAR signaling, activates cytotoxicity to kill malignant B cells, resulting in B-cell depletion.
Autologous T cells genetically engineered to express a CD19-specific chimeric antigen receptor recognize CD19 on B-lineage malignant cells; CAR signaling activates T-cell cytotoxicity and cytokine release, leading to targeted lysis and depletion of CD19+ cells.
CD19 CAR T cells bind CD19 on target cells and trigger T‑cell cytotoxicity, primarily via perforin/granzyme-mediated lysis and Fas–FasL apoptosis, leading to depletion of CD19+ cells.
Autologous CD4/CD8-enriched T cells engineered with a CD19-directed chimeric antigen receptor (CAR) that recognizes CD19 and eliminates CD19+ B-lineage cells, inducing B-cell aplasia and aiming to reset humoral autoimmunity in refractory SLE.
Autologous CD4+/CD8+ T cells engineered to express a CD19-directed chimeric antigen receptor that recognizes and eliminates CD19+ B-lineage cells, inducing B-cell aplasia, reducing autoantibody production, and aiming to reset humoral autoimmunity in refractory SLE.
CAR-T cells recognizing CD19 bind CD19+ cells and kill them via T-cell cytotoxicity (perforin/granzyme release and Fas–FasL–mediated apoptosis).