Autologous T-cell receptor–engineered T-cell therapy in which patient T cells are lentivirally transduced ex vivo to express an HLA-A*02:01–restricted TCR that recognizes mutant NPM1 (dNPM1) peptides; the cells are expanded and reinfused to mediate antigen-specific cytotoxicity against NPM1-mutant AML.
Autologous T cells are lentivirally transduced ex vivo to express an HLA-A*02:01–restricted T-cell receptor specific for mutant NPM1 (dNPM1) peptides; after expansion and reinfusion, these engineered T cells recognize the HLA-A*02:01/dNPM1 peptide complex on NPM1-mutant AML cells and mediate antigen-specific cytotoxic killing.
YES
DIRECT
Engineered TCR T cells recognize the HLA-A*02:01–presented mutant NPM1 peptide on AML cells and kill them via cytotoxic T-lymphocyte mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Autologous, gene-engineered T cells expressing a dual chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells to activate T-cell cytotoxicity and eliminate malignant plasma cells.
Autologous T cells are gene-engineered to express dual chimeric antigen receptors recognizing BCMA (TNFRSF17) and GPRC5D on myeloma cells. Binding triggers CAR signaling (CD3z with costimulatory domains), activating T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate malignant plasma cells while reducing antigen escape.
YES
DIRECT
CAR-T cells bind GPRC5D on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (and death-receptor pathways), directly killing GPRC5D+ cells.
Chimeric anti-CD20 monoclonal antibody that depletes CD20-positive B cells from pre-B to mature stages, lowering precursors of ANCA-producing cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B to mature B lymphocytes and depletes them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (and apoptosis), reducing precursors of ANCA-producing cells.
YES
DIRECT
Anti-CD20 antibody binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and apoptosis), leading to depletion of CD20+ cells.
An intravenously administered antibody–drug conjugate (ADC) targeting folate receptor alpha (FRα). A monoclonal antibody binds FRα on tumor cells, undergoes FRα-mediated endocytosis, and releases an intracellular cytotoxic payload to induce tumor cell death. Intended for FRα-positive advanced solid tumors (e.g., ovarian, endometrial, lung adenocarcinoma, triple-negative breast cancer, PDAC, mesothelioma).
Monoclonal antibody binds folate receptor alpha (FRα) on tumor cells, undergoes receptor-mediated endocytosis, and releases an intracellular cytotoxic payload (mechanism unspecified) to kill the cancer cell.
YES
DIRECT
The ADC binds FRα on tumor cells, is internalized via receptor-mediated endocytosis, and releases an intracellular cytotoxic payload that kills the FRα-expressing cell.
A subcutaneous bispecific T‑cell–engaging monoclonal antibody (CD20×CD3) that binds CD20 on malignant B cells and CD3 on T cells to form an immune synapse, activating T cells to kill CD20+ B-ALL blasts via cytotoxicity and cytokine release.
CD20×CD3 bispecific antibody that simultaneously binds CD20 on malignant B cells and CD3 on T cells, forming an immune synapse that activates T cells via CD3/TCR signaling to lyse CD20+ B cells through cytotoxicity and cytokine release.
YES
DIRECT
The CD20×CD3 bispecific antibody redirects and activates T cells to CD20+ cells, forming an immune synapse and inducing T‑cell–mediated killing via perforin/granzyme release and apoptotic signaling with cytokine support.