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.
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.
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.
LMB-100 binds mesothelin on target cells, is internalized, and its PE24 toxin ADP-ribosylates eEF2, halting protein synthesis and triggering apoptosis.
An antibody-drug conjugate (Trodelvy) composed of a humanized anti–TROP-2 monoclonal antibody linked to SN-38, the active metabolite of irinotecan. It binds TROP-2 on tumor cells, is internalized, and releases SN-38 to inhibit topoisomerase I, causing DNA damage and tumor cell death.
Humanized anti–TROP-2 monoclonal antibody linked to SN-38. After binding TROP-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I, stabilizes Topo I–DNA complexes, induces DNA breaks, and triggers tumor cell death; the membrane-permeable payload can produce a bystander effect.
The ADC binds TROP-2 on tumor cells, is internalized, and releases SN-38; SN-38 inhibits topoisomerase I, causing DNA damage and apoptosis. The membrane-permeable payload can also create a bystander effect.
HER2-targeted antibody-drug conjugate delivering a topoisomerase I inhibitor payload to HER2-expressing tumor cells.
HER2-targeted monoclonal antibody (trastuzumab) linked to a topoisomerase I inhibitor payload (deruxtecan, DXd). After binding HER2 and internalization, DXd is released to inhibit Top1-DNA complexes, leading to DNA replication arrest and apoptosis; the antibody also mediates ADCC and the membrane-permeable payload enables bystander killing.
The ADC binds HER2 on target cells, is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd), causing Top1-mediated DNA damage/replication arrest and apoptosis; the antibody Fc can also trigger ADCC, with some bystander killing.