Autologous, gene-modified T cells engineered to express chimeric antigen receptors that target CD20 and CD30, enabling antigen-dependent T-cell activation and cytotoxic killing of malignant cells; administered intravenously after lymphodepletion for relapsed/refractory CD20/CD30-positive lymphomas.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD20 and CD30 on malignant lymphocytes, triggering antigen-dependent T-cell activation independent of the native TCR and inducing cytotoxic killing via perforin/granzyme release and cytokine secretion, leading to elimination of CD20+/CD30+ tumor cells.
CD20 recognition by the CAR triggers T‑cell activation and direct killing of CD20+ cells via perforin/granzyme-mediated cytolysis (with apoptosis signaling).
Autologous, gene-modified T cells engineered to express chimeric antigen receptors that target CD20 and CD30, enabling antigen-dependent T-cell activation and cytotoxic killing of malignant cells; administered intravenously after lymphodepletion for relapsed/refractory CD20/CD30-positive lymphomas.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD20 and CD30 on malignant lymphocytes, triggering antigen-dependent T-cell activation independent of the native TCR and inducing cytotoxic killing via perforin/granzyme release and cytokine secretion, leading to elimination of CD20+/CD30+ tumor cells.
CAR-T cells bind CD30 on target cells, triggering T-cell activation and contact-dependent killing via perforin/granzyme-mediated apoptosis (with supportive cytokine-mediated cytotoxicity).
A bispecific T-cell engager (BiTE) antibody construct given by continuous IV infusion that binds CD19 on B-lineage leukemia cells and CD3 on T cells to redirect cytotoxic T cells to kill CD19+ blasts, used as maintenance post–allo-HSCT.
A BiTE antibody construct that binds CD19 on B-lineage cells and CD3 on T cells, bringing them into proximity to activate and redirect T-cell cytotoxicity, leading to perforin/granzyme-mediated killing of CD19+ blasts.
Blinatumomab bridges CD3 on T cells and CD19 on target cells, activating T cells to form an immunologic synapse and release perforin/granzymes that kill CD19+ cells.
A bispecific tetravalent monoclonal antibody immune cell engager that binds CD123 on AML cells and CD16A on innate immune cells (primarily NK cells) to trigger ADCC and kill CD123+ leukemic cells; administered weekly IV.
A tetravalent bispecific IgG1–scFv that simultaneously binds CD123 on leukemic cells and CD16A (FcγRIIIa) on innate immune cells—primarily NK cells—cross-linking them to activate NK cell–mediated ADCC and lyse CD123+ tumor cells.
AFM28 cross-links CD123 on target cells with CD16A on NK cells (and macrophages), activating ADCC and causing lysis of CD123+ cells.
Autologous TCR-T cell therapy engineered to express a high-affinity T-cell receptor recognizing an AFP-derived peptide presented by HLA-A*02:03 on tumor cells, inducing MHC-restricted T-cell activation and cytotoxic killing; administered after lymphodepleting chemotherapy to enhance engraftment, expansion, and persistence.
Autologous T cells are genetically engineered to express a high-affinity T-cell receptor that recognizes an AFP-derived peptide presented by HLA-A*02:03 on tumor cells. Engagement of the AFP/HLA complex triggers MHC-restricted T-cell activation and cytotoxic killing via perforin/granzyme release and cytokine secretion. Lymphodepleting chemotherapy is given pre-infusion to enhance engraftment, expansion, and persistence of the infused TCR-T cells.
Engineered TCR-T cells recognize the AFP peptide presented by HLA-A*02:03 and directly induce MHC-restricted killing of target cells via perforin/granzyme-mediated apoptosis (with contributions from Fas–FasL and cytokines).