Autologous, gene-modified CAR T-cell therapy expressing two CARs targeting the EGFR 806 epitope and IL13Rα2; delivered intrathecally to induce T-cell activation, cytokine release, and cytotoxic killing of glioblastoma cells while aiming to reduce antigen escape through dual targeting.
Autologous T cells genetically engineered (lentiviral) to co-express two chimeric antigen receptors targeting the EGFR 806 epitope and IL13Ra2. Engagement of either antigen on glioblastoma cells triggers CAR signaling to activate T cells, leading to cytokine release, clonal expansion, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape; administered intrathecally for CNS tumor access.
YES
DIRECT
CAR T cells bind IL13Rα2 on target cells, activating T cells to kill via perforin/granzyme-mediated cytotoxicity.
Fc-enhanced IgG1 anti-CTLA-4 monoclonal antibody checkpoint inhibitor that augments T-cell priming and depletes intratumoral Tregs via Fc-mediated effector functions.
Fc-enhanced IgG1 monoclonal antibody that binds CTLA-4 to block inhibitory checkpoint signaling, restoring T-cell activation and priming; its engineered Fc engages FcγR-bearing effector cells to deplete intratumoral regulatory T cells, enhancing antitumor cytotoxic T-cell responses.
Fc-enhanced IgG1 anti-CTLA-4 monoclonal antibody checkpoint inhibitor that augments T-cell priming and depletes intratumoral Tregs via Fc-mediated effector functions.
Fc-enhanced IgG1 monoclonal antibody that binds CTLA-4 to block inhibitory checkpoint signaling, restoring T-cell activation and priming; its engineered Fc engages FcγR-bearing effector cells to deplete intratumoral regulatory T cells, enhancing antitumor cytotoxic T-cell responses.
NO
INDIRECT
The antibody’s Fc binds Fcγ receptors on effector cells (e.g., NK cells, macrophages) to trigger ADCC/ADCP against CTLA-4-expressing Tregs; FcγR-positive cells are effectors, not killed.
Recombinant humanized anti-mesothelin Fab fused to de-immunized Pseudomonas exotoxin A; after mesothelin binding and internalization, the toxin ADP-ribosylates EF-2 to halt protein synthesis and induce tumor cell death.
Humanized anti-mesothelin Fab fused to de-immunized Pseudomonas exotoxin A (PE24). After binding mesothelin and internalization, the toxin ADP-ribosylates and inactivates eEF2, halting protein synthesis and inducing apoptosis in mesothelin-expressing tumor cells; engineered to reduce immunogenicity.
YES
DIRECT
LMB-100 binds mesothelin on target cells, is internalized, and its PE24 toxin ADP-ribosylates eEF2, halting protein synthesis and triggering apoptosis.
Recombinant humanized anti-mesothelin Fab fused to de-immunized Pseudomonas exotoxin A; after mesothelin binding and internalization, the toxin ADP-ribosylates EF-2 to halt protein synthesis and induce tumor cell death.
Humanized anti-mesothelin Fab fused to de-immunized Pseudomonas exotoxin A (PE24). After binding mesothelin and internalization, the toxin ADP-ribosylates and inactivates eEF2, halting protein synthesis and inducing apoptosis in mesothelin-expressing tumor cells; engineered to reduce immunogenicity.
NO
DIRECT
LMB-100 binds mesothelin on tumor cells, is internalized, and its PE24 toxin ADP-ribosylates eEF2 to block protein synthesis, inducing apoptosis; eEF2-expressing cells are not selectively targeted unless they express mesothelin.