Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
AgenT-797 iNKT cells express NKG2D, which binds ULBP4 on target cells and triggers direct cytotoxic killing via perforin/granzyme release (with supportive Th1 cytokines).
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
AgenT-797 iNKT cells express NKG2D, which binds ULBP5 on target cells, activating the iNKT cells to kill via immune-synapse–mediated cytotoxicity (perforin/granzyme and death-receptor pathways).
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
ULBP6 is an NKG2D ligand. AgenT-797 iNKT cells express NKG2D; engagement with ULBP6 activates iNKT cells to directly lyse target cells via perforin/granzyme (and death receptor) pathways, with Th1 cytokines supporting cytotoxicity.
Fc-engineered IgG1 anti-CTLA-4 monoclonal antibody that blocks CTLA-4 to enhance T-cell priming and depletes intratumoral Tregs via Fc effector function.
Fc-engineered IgG1 anti-CTLA-4 monoclonal antibody that blocks CTLA-4 inhibitory signaling to enhance T-cell priming and activation; its optimized Fc domain mediates depletion of intratumoral regulatory T cells via effector functions (e.g., ADCC/ADCP) and extends half-life, promoting antitumor immunity.
Anti-CTLA-4 IgG1 binds CTLA-4 on T cells (notably Tregs) and its Fc engages FcγR-expressing effectors to mediate ADCC/ADCP, depleting CTLA-4+ cells.
Autologous, genetically modified CAR T-cell therapy made from PD-1–positive T cells transduced via lentivirus to express a TROP2-directed CAR plus an additional enhanced receptor; administered as a one-time IV infusion for TROP2-expressing advanced solid tumors.
Autologous PD-1-positive T cells are transduced with a lentiviral vector to express a TROP2-directed chimeric antigen receptor plus an enhancement receptor. After infusion, the CAR recognizes TROP2 on tumor cells and triggers CD3zeta/costimulatory signaling, leading to T-cell activation, cytokine release, and cytotoxic killing of TROP2-expressing cancer cells; the enhancement receptor is intended to improve function within the tumor microenvironment.
CAR T cells bind TROP2 via the engineered CAR, triggering CD3ζ/costimulatory signaling and T‑cell effector functions that lyse TROP2+ cells (perforin/granzyme and death-receptor pathways, with cytokine release).