An oral prodrug of ganciclovir that is phosphorylated by HSV-1 thymidine kinase to cytotoxic metabolites, killing hTERT-expressing tumor cells in the suicide gene strategy.
Oral prodrug of ganciclovir; once converted to ganciclovir and phosphorylated (here by HSV‑1 thymidine kinase supplied by the suicide gene), it forms ganciclovir triphosphate that is incorporated into DNA, inhibiting DNA polymerase and DNA synthesis, leading to death of HSV‑TK–expressing tumor cells with a bystander effect.
After phosphorylation by HSV‑1 thymidine kinase, ganciclovir triphosphate inhibits DNA polymerase and causes DNA chain termination, blocking DNA synthesis and killing the activated (HSV‑TK–expressing) cells, with a bystander effect on neighbors.
Antibody–drug conjugate targeting TROP2; upon internalization it releases deruxtecan, a topoisomerase I inhibitor, causing tumor DNA damage.
Humanized anti‑TROP2 monoclonal antibody linked via a cleavable linker to deruxtecan (DXd), a topoisomerase I inhibitor. After binding TROP2 on tumor cells and internalization, the linker is cleaved to release DXd, which inhibits topoisomerase I, causing DNA damage and apoptosis; the membrane‑permeable payload can also exert a bystander effect.
Anti-TROP2 ADC binds TROP2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis in target cells; the membrane-permeable payload can also cause bystander killing.
Autologous mRNA-engineered BCMA-directed CAR T-cell therapy in which patient T cells are transiently modified to express a chimeric antigen receptor targeting B-cell maturation antigen (BCMA), resulting in CAR-mediated T-cell activation and cytotoxicity against myeloma cells.
Autologous patient T cells are transiently mRNA-engineered to express a BCMA-targeted chimeric antigen receptor; CAR binding to BCMA on myeloma cells activates the T cells to release cytotoxic effectors and kill BCMA-positive plasma cells, with transient expression limiting persistence and avoiding genomic integration.
BCMA-directed CAR T cells recognize BCMA on target cells, become activated, and kill BCMA+ cells via perforin/granzyme-mediated cytolysis and death-receptor–mediated apoptosis.
An allogeneic engineered cellular immunotherapy composed of γδ T cells expressing a chimeric antigen receptor targeting B7-H3 (CD276). Administered via local (meningeal/CSF) injection at 3×10^7 cells per dose with optional repeat dosing. CAR engagement enables MHC-independent recognition of B7-H3+ tumor cells, activating T-cell signaling for cytotoxic killing (perforin/granzyme) and cytokine release; γδ T cells contribute innate-like stress-antigen recognition (e.g., via γδ TCR/NKG2D) with lower alloreactivity.
Allogeneic γδ T cells engineered with a chimeric antigen receptor targeting B7‑H3 (CD276) recognize tumor cells independently of MHC and, upon CAR engagement, activate T‑cell signaling to mediate cytotoxic killing via perforin/granzyme and cytokine release; the γδ T-cell phenotype adds innate-like stress‑antigen recognition (e.g., via γδ TCR/NKG2D) with lower alloreactivity.
B7-H3–targeted CAR-γδ T cells bind B7-H3 on target cells and, upon CAR signaling, directly kill them via T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways).
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
ATG contains antibodies that bind CD2 on T cells, leading to complement-dependent lysis and Fc-mediated ADCC; receptor cross-linking can also induce apoptosis.