A monoclonal antibody Fab fragment that specifically binds and inhibits carbonic anhydrase XII (CA XII) on glioblastoma cells; used as the targeting moiety for radioimmunotherapy when labeled with lutetium-177.
A monoclonal antibody Fab fragment that binds carbonic anhydrase XII (CA XII) on glioblastoma cells and, when labeled with lutetium-177, delivers targeted beta radiation to induce localized DNA damage and tumor cell death; CA XII binding may also inhibit its enzymatic activity and disrupt tumor pH regulation.
Lutetium-177–labeled 6A10 Fab binds CA XII on tumor cells and delivers beta radiation to the bound cells, causing localized DNA damage (double‑strand breaks) and cell death; some crossfire to nearby cells may occur.
Autologous tumor-infiltrating lymphocyte (TIL) cellular therapy manufactured from a patient’s tumor, expanded ex vivo, and reinfused to mediate antitumor activity through native TCR recognition, cytotoxic mechanisms, and cytokine secretion.
Autologous TILs expanded ex vivo and reinfused; they recognize patient-specific tumor antigens via native TCR–MHC interactions and mediate antitumor effects through cytotoxic killing (perforin/granzymes) and cytokine secretion within the tumor microenvironment.
LN-145 TILs recognize the neoantigen peptide–HLA class II complex via their native TCRs and directly lyse target cells through perforin/granzyme release and, in some cases, Fas–FasL–mediated apoptosis.
A beta-emitting therapeutic radionuclide used to deliver localized radiation; in this trial it is conjugated to the 6A10 Fab to form a radiolabeled antibody (Lu-177–6A10 Fab) for intracavitary radioimmunotherapy.
Lu-177–6A10 Fab binds carbonic anhydrase XII on glioblastoma cells and delivers localized beta radiation from lutetium-177, producing DNA damage and tumor cell kill near the resection cavity; the antibody fragment targets the isotope to CA XII–expressing tumor tissue, with gamma emissions enabling imaging/dosimetry.
Lu-177–6A10 Fab binds CA XII on tumor cells and delivers beta radiation, causing DNA double-strand breaks and cell death (with some cross-fire to nearby cells).
Patient-derived T cells genetically engineered ex vivo to express a chimeric antigen receptor recognizing TM4SF1 on tumor cells, leading to T-cell activation, cytokine release, and cytotoxic killing of TM4SF1-expressing cancer cells. The CAR construct includes an EGFR-based safety switch. Administered via IV or local infusion with dose escalation (0.5–10×10^6 cells/kg).
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds TM4SF1 on tumor cells. Antigen engagement triggers CAR signaling, leading to T‑cell activation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of TM4SF1‑expressing cancer cells. An EGFR-based safety switch enables targeted elimination of the CAR T cells if required.
TM4SF1-targeted CAR T cells bind TM4SF1 on target cells and kill them via T-cell cytotoxicity, primarily perforin/granzyme-mediated apoptosis (with possible Fas–FasL signaling).
A humanized IgG monoclonal antibody given IV every 2 weeks that binds tumor-expressed CD24 to block the CD24–Siglec‑10 innate immune checkpoint, enhancing macrophage-mediated phagocytosis and potentially engaging Fc-dependent effector functions (ADCC/ADCP) in adults with advanced solid tumors.
Humanized IgG monoclonal antibody that binds CD24 on tumor cells to block the CD24–Siglec‑10 innate immune checkpoint, enhancing macrophage-mediated phagocytosis and potentially engaging Fc-dependent effector functions (ADCC/ADCP).
Anti-CD24 IgG binds CD24 on tumor cells, blocks the CD24–Siglec-10 checkpoint and engages Fcγ receptors on effector cells, triggering macrophage phagocytosis (ADCP) and NK cell ADCC of CD24+ cells; complement lysis may also contribute.