Autologous, genetically engineered anti-CD19 CAR T-cell therapy with a CD28 costimulatory domain that targets CD19+ B cells to induce cytotoxic killing.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with a CD28 costimulatory and CD3 zeta signaling domain; after infusion they recognize CD19 on B cells and induce HLA-independent T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19-positive malignant and normal B cells.
Anti-CD19 CAR T cells bind CD19 and, upon activation via CD28/CD3ζ signaling, kill CD19+ cells through T cell cytotoxic mechanisms (perforin/granzyme and Fas–FasL), with cytokine release.
Autologous, genetically engineered anti-CD19 CAR T-cell therapy (CD28 costimulation) directed against CD19+ B-cell malignancies.
Autologous T lymphocytes genetically engineered to express an anti-CD19 chimeric antigen receptor with CD28 costimulatory and CD3 zeta signaling domains; after infusion, the CAR enables HLA-independent recognition of CD19 on B-cell malignancies, triggering T-cell activation, proliferation, and cytotoxic killing of CD19+ cells, resulting in antitumor activity and on-target B-cell aplasia.
Anti-CD19 CAR T cells bind CD19 on target cells and induce T-cell cytotoxic killing via perforin/granzyme-mediated lysis and apoptosis (HLA-independent).
Autologous, genetically engineered anti-CD19 CAR T-cell therapy with a 4-1BB costimulatory domain and defined CD4/CD8 composition, targeting CD19+ B cells.
Autologous T cells are lentivirally engineered to express an anti‑CD19 CAR with a 4‑1BB costimulatory and CD3ζ signaling domain. Upon binding CD19 on B‑cell malignancies, the CAR triggers HLA‑independent T‑cell activation, proliferation, and cytotoxic killing of CD19+ cells; an EGFRt tag enables in vivo tracking and potential cetuximab-mediated ablation.
Anti-CD19 CAR T cells bind CD19 and, via CD3ζ/4-1BB signaling, are activated to kill CD19+ cells through perforin/granzyme release and death-receptor pathways (HLA-independent).
Bispecific innate cell engager antibody that binds CD30 on tumor cells and CD16A on NK cells to bridge NK cells to CD30+ targets and trigger ADCC and cytokine release.
Tetravalent bispecific antibody that binds CD30 on tumor cells and CD16A (Fc gamma RIIIa) on NK cells, crosslinking NK cells to CD30-positive targets to activate NK-mediated cytotoxicity, induce ADCC and cytokine release, and drive tumor cell lysis.
AFM13 bridges NK cells (via CD16A) to CD30+ cells, activating NK-mediated ADCC and perforin/granzyme-dependent lysis of the target cells.