Investigational bispecific monoclonal antibody that binds glypican-3 (GPC3) on tumor cells and delivers 4-1BB (CD137) costimulation to T cells to locally activate anti-tumor immunity (IV).
Bispecific antibody that binds GPC3 on tumor cells and 4-1BB (CD137) on activated T cells (and NK cells), crosslinking them to deliver local 4-1BB costimulation in the tumor microenvironment, thereby enhancing cytotoxic lymphocyte activity and lysis of GPC3-expressing tumor cells.
The bispecific crosslinks GPC3 on tumor cells with 4-1BB on T/NK cells, delivering local 4-1BB costimulation; the engaged cytotoxic lymphocytes then kill GPC3+ cells via perforin/granzyme-mediated lysis.
Autologous 'armored' chimeric antigen receptor T-cell therapy targeting glypican-3 (GPC3); genetically modified T cells with CD3ζ and co-stimulatory domains designed to enhance activation, persistence, and cytotoxicity against GPC3-positive hepatocellular carcinoma.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds glypican-3 (GPC3) on hepatocellular carcinoma cells. CAR engagement activates CD3ζ and co-stimulatory signaling, driving T-cell proliferation, cytokine release, and targeted cytotoxic killing of GPC3-positive tumor cells. The “armored” design enhances activation, persistence, and function within the immunosuppressive tumor microenvironment.
CAR engagement of GPC3 on target cells activates T-cell CD3ζ/co-stimulatory signaling, forming an immunologic synapse and inducing cytolysis via perforin/granzyme release (and death-receptor pathways), killing GPC3-positive cells.
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which a patient’s tumor-infiltrating T cells are expanded ex vivo and reinfused to recognize tumor neoantigens via TCR–MHC and mediate cytotoxic CD8+ activity against cancer cells.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens via native TCR–MHC interactions, leading to cytotoxic CD8+ T-cell–mediated killing of cancer cells and cytokine-driven antitumor activity.
Patient-derived TILs recognize the neoantigen–HLA class I complex via their native TCR and directly kill the target cell through cytotoxic CD8+ T-cell mechanisms (perforin/granzyme and Fas–FasL–mediated apoptosis).
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which a patient’s tumor-infiltrating T cells are expanded ex vivo and reinfused to recognize tumor neoantigens via TCR–MHC and mediate cytotoxic CD8+ activity against cancer cells.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused to recognize tumor neoantigens via native TCR–MHC interactions, leading to cytotoxic CD8+ T-cell–mediated killing of cancer cells and cytokine-driven antitumor activity.
Autologous TILs recognize the patient-specific neoantigen peptide–HLA class II complex via native TCRs and directly kill antigen-positive tumor cells through cytolytic granule (perforin/granzyme) release and Fas–FasL–mediated apoptosis.