Autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy that recognizes and kills malignant B cells.
Autologous T cells genetically engineered (gammaretroviral vector) to express an anti‑CD19 CAR with CD28 costimulation and CD3ζ signaling. After infusion, CAR T cells recognize CD19 on B‑cell malignancies independent of MHC, leading to T‑cell activation, proliferation, cytokine release, and cytotoxic killing of CD19‑positive cells (resulting in depletion of malignant and normal B cells).
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on B cells, become activated, and kill target cells via T-cell cytotoxic pathways (perforin/granzyme release and death receptor–mediated apoptosis).
Autologous CD19-directed CAR T-cell therapy composed of defined CD4+ and CD8+ T-cell subsets to target malignant B cells.
Autologous CD4+ and CD8+ T cells are engineered with a lentiviral vector to express a CD19-specific chimeric antigen receptor containing an anti-CD19 scFv, 4-1BB costimulatory domain, and CD3-zeta signaling domain. Upon binding CD19 on B-cell malignancies, the CAR activates T-cell cytotoxicity and proliferation to kill target cells. A truncated EGFR tag enables in vivo tracking and potential cetuximab-mediated elimination of the infused cells.
YES
DIRECT
CD19-specific CAR T cells bind CD19 on target cells, triggering T-cell effector functions that kill via perforin/granzyme-mediated lysis and Fas–FasL-induced apoptosis.
Investigational intravenous bispecific T‑cell–redirecting antibody that binds BCMA on malignant plasma cells and CD3 on T cells to activate T‑cell–mediated cytotoxicity in multiple myeloma.
ABBV-383 (etentamig) is an IgG4 bispecific T-cell–redirecting antibody that binds BCMA on malignant plasma cells and CD3 on T cells, forming an immune synapse that activates cytotoxic T cells to kill BCMA-expressing myeloma cells, with a low-activating CD3 design to limit excess cytokine release.
YES
DIRECT
Bispecific T-cell engager binds BCMA on tumor cells and CD3 on T cells, forming an immune synapse that activates cytotoxic T cells to kill BCMA+ cells via perforin/granzyme-mediated apoptosis.
Investigational intravenous bispecific T‑cell–redirecting antibody that binds BCMA on malignant plasma cells and CD3 on T cells to activate T‑cell–mediated cytotoxicity in multiple myeloma.
ABBV-383 (etentamig) is an IgG4 bispecific T-cell–redirecting antibody that binds BCMA on malignant plasma cells and CD3 on T cells, forming an immune synapse that activates cytotoxic T cells to kill BCMA-expressing myeloma cells, with a low-activating CD3 design to limit excess cytokine release.
NO
INDIRECT
ABBV-383 binds CD3ε on T cells and BCMA on myeloma cells to form an immune synapse; activated T cells kill BCMA+ tumor cells (perforin/granzyme), while CD3+ T cells are engaged, not targeted for killing.
Autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy given as a single IV infusion to deplete CD19+ B-lineage cells in SLE.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with a 4-1BB costimulatory domain; after infusion, they recognize CD19 on B-lineage cells and induce cytotoxic killing, depleting B cells and plasmablasts to reduce autoantibody production and reset immune tolerance in SLE.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on B-lineage cells and induce T-cell cytotoxicity (perforin/granzyme-mediated apoptosis and/or Fas–FasL), depleting CD19+ cells.