Bispecific T-cell engager (CD3xCD19) immunotherapy that redirects patient T cells to kill CD19-positive leukemic B cells; used here for MRD-positive B-ALL.
Blinatumomab is a CD3×CD19 bispecific T‑cell engager that links patient T cells (via CD3) to CD19‑positive B cells, inducing MHC‑independent T‑cell activation and immune synapse formation, resulting in perforin/granzyme‑mediated cytotoxicity and serial killing of CD19+ leukemic cells.
Blinatumomab bridges CD3 on T cells to CD19 on target cells, forming an immune synapse that activates T cells to release perforin and granzymes, causing cytolytic apoptosis of CD19+ cells.
Gene-modified T lymphocytes engineered ex vivo to express a chimeric antigen receptor targeting CD19 with CD3ζ and costimulatory domains; administered as a single IV infusion after lymphodepleting chemotherapy to treat relapsed/refractory CD19+ B-cell malignancies.
Ex vivo–engineered T lymphocytes expressing a CD19‑specific chimeric antigen receptor with CD3ζ and costimulatory domains recognize CD19 on B‑cell malignancies and, upon CAR engagement, trigger TCR‑independent activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxicity to eliminate CD19+ tumor cells; prior lymphodepletion supports in vivo expansion and persistence.
CD19 CAR-T cells bind CD19 on target cells, activate, and kill via T-cell effector functions—primarily perforin/granzyme-mediated cytolysis (and Fas/FasL), inducing apoptosis.
Gene-modified natural killer cells engineered ex vivo to express a chimeric antigen receptor targeting CD19; given as a single IV infusion to induce NK-mediated cytotoxicity against CD19+ B-cell malignancies.
Ex vivo gene-modified natural killer cells engineered to express a CD19-specific chimeric antigen receptor; CAR engagement of CD19 activates NK signaling (CD3zeta/costimulatory domains) to drive targeted lysis of CD19+ B cells via perforin/granzyme release and cytokine secretion.
CAR-NK cells bind CD19 via the CAR, triggering NK activation and degranulation to kill CD19+ cells through perforin/granzyme-mediated cytolysis (and death receptor pathways).
Bispecific T‑cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B-lymphoblasts to induce cytotoxic killing.
Bispecific CD19xCD3 antibody (BiTE) that binds CD19 on B-lymphoblasts and CD3 on T cells, bringing them together to form an immunologic synapse, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of CD19-positive cells (MHC-independent).
Blinatumomab bridges CD3 on T cells to CD19 on target cells, activating T cells to deliver perforin/granzyme-mediated killing of CD19+ cells (MHC-independent).
Engineered CAR T cells (lentiviral) targeting cytomegalovirus glycoprotein B (gB); dose-escalated IV infusion; designed for MHC-independent cytotoxicity against gB-expressing CMV-associated tumor cells.
Lentiviral-engineered T cells expressing a chimeric antigen receptor targeting cytomegalovirus glycoprotein B (gB); upon gB binding, the CAR drives MHC-independent T-cell activation and cytotoxicity (perforin/granzyme release and cytokine-mediated killing) against gB-expressing CMV-associated tumor cells.
CAR T cells bind CMV gB on target cells and, via MHC‑independent CAR signaling, release perforin/granzymes (and cytotoxic cytokines) to induce lysis/apoptosis of gB-expressing cells.