An autologous, gene-modified TCR-T cell therapy composed of engineered CD8+ and CD4+ T cells that express an HLA-A*11:01–restricted TCR specific for the KRAS G12V neoantigen, co-express a wild-type CD8α/β coreceptor to strengthen TCR signaling, and include a Fas–4-1BB switch receptor to convert Fas signals into 4-1BB costimulation, enhancing resistance to apoptosis and improving activation/persistence.
Autologous gene-modified CD8+ and CD4+ T cells engineered to express an HLA-A*11:01-restricted TCR specific for the KRAS G12V neoantigen. After infusion, the cells recognize KRAS G12V peptide presented on MHC-I and mediate tumor cell killing via TCR-driven cytotoxicity and cytokine release. A co-expressed wild-type CD8alpha/beta coreceptor strengthens TCR signaling and enables CD4+ T-cell recognition, while a Fas-4-1BB switch receptor converts FasL death signals into 4-1BB costimulation, enhancing activation, resistance to apoptosis, and persistence.
Engineered TCR-T cells recognize KRAS G12V peptide presented by HLA-A*11:01 on tumor cells and directly kill them via TCR-triggered cytotoxicity (perforin/granzyme-mediated lysis and related effector mechanisms).
Chimeric monoclonal antibody against EGFR that inhibits downstream signaling (RAS/MAPK, PI3K/AKT) and mediates antibody‑dependent cellular cytotoxicity (ADCC).
Chimeric monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream RAS/MAPK and PI3K/AKT signaling and tumor cell proliferation; also mediates NK cell–dependent ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to trigger ADCC, leading to lysis of EGFR+ cells (with possible CDC/phagocytosis); EGFR signaling blockade may also promote apoptosis.
Autologous T cells genetically engineered to express chimeric antigen receptors targeting CD19, CD20, and BCMA; upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates T-cell proliferation, cytokine release, and cytotoxic killing of malignant B-lineage and plasma cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19, CD20, and BCMA; antigen binding activates CD3zeta and costimulatory signaling, inducing T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B-lineage cells and plasma cells, with multi-antigen targeting to limit antigen escape.
CAR-T cells recognize CD19 and, upon CAR signaling, induce T-cell cytotoxicity via perforin/granzyme-mediated lysis (and apoptosis) of CD19+ cells.
Autologous T cells genetically engineered to express chimeric antigen receptors targeting CD19, CD20, and BCMA; upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates T-cell proliferation, cytokine release, and cytotoxic killing of malignant B-lineage and plasma cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19, CD20, and BCMA; antigen binding activates CD3zeta and costimulatory signaling, inducing T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B-lineage cells and plasma cells, with multi-antigen targeting to limit antigen escape.
CAR-T cells bind CD20 via the CAR; CD3ζ/costimulatory signaling activates T-cell cytotoxicity, causing perforin/granzyme-mediated lysis (and Fas/FasL apoptosis) of CD20+ cells.
Autologous T cells genetically engineered to express chimeric antigen receptors targeting CD19, CD20, and BCMA; upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates T-cell proliferation, cytokine release, and cytotoxic killing of malignant B-lineage and plasma cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors recognizing CD19, CD20, and BCMA; antigen binding activates CD3zeta and costimulatory signaling, inducing T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B-lineage cells and plasma cells, with multi-antigen targeting to limit antigen escape.
CAR-T cells recognize BCMA and, upon engagement, activate and kill BCMA+ cells via perforin/granzyme release (and death-receptor pathways).