Allogeneic cord blood–derived natural killer cell therapy engineered to express an anti-TROP2 chimeric antigen receptor and IL-15; CAR engagement of TROP2 triggers NK cytotoxicity while IL-15 signaling sustains survival, proliferation, and in vivo persistence.
Allogeneic cord blood–derived NK cells engineered to express an anti-TROP2 chimeric antigen receptor and IL-15. CAR recognition of TROP2 on tumor cells triggers NK activation and cytotoxicity (perforin/granzyme-mediated lysis and cytokine release), while IL-15 autocrine signaling sustains NK survival, proliferation, and in vivo persistence; an inducible caspase-9 safety switch allows drug-mediated ablation if needed.
NO
INDIRECT
IL-15Rα is not the CAR target. Killing occurs only when the CAR-NK recognizes TROP2 on tumor cells, triggering perforin/granzyme-mediated lysis; IL-15 signaling merely supports NK survival/proliferation.
Allogeneic cord blood–derived natural killer cell therapy engineered to express an anti-TROP2 chimeric antigen receptor and IL-15; CAR engagement of TROP2 triggers NK cytotoxicity while IL-15 signaling sustains survival, proliferation, and in vivo persistence.
Allogeneic cord blood–derived NK cells engineered to express an anti-TROP2 chimeric antigen receptor and IL-15. CAR recognition of TROP2 on tumor cells triggers NK activation and cytotoxicity (perforin/granzyme-mediated lysis and cytokine release), while IL-15 autocrine signaling sustains NK survival, proliferation, and in vivo persistence; an inducible caspase-9 safety switch allows drug-mediated ablation if needed.
NO
INDIRECT
IL‑2/IL‑15Rβ is not targeted; IL‑15 from the engineered NK cells signals through this receptor on the NK cells to support survival. Cytotoxicity is directed at TROP2+ tumor cells via CAR-triggered NK perforin/granzyme killing.
Allogeneic cord blood–derived natural killer cell therapy engineered to express an anti-TROP2 chimeric antigen receptor and IL-15; CAR engagement of TROP2 triggers NK cytotoxicity while IL-15 signaling sustains survival, proliferation, and in vivo persistence.
Allogeneic cord blood–derived NK cells engineered to express an anti-TROP2 chimeric antigen receptor and IL-15. CAR recognition of TROP2 on tumor cells triggers NK activation and cytotoxicity (perforin/granzyme-mediated lysis and cytokine release), while IL-15 autocrine signaling sustains NK survival, proliferation, and in vivo persistence; an inducible caspase-9 safety switch allows drug-mediated ablation if needed.
NO
INDIRECT
IL-2RG (common gamma chain) is not the CAR target; it functions in IL-15 signaling on the engineered NK cells. Killing is directed to TROP2+ cells via CAR-triggered NK perforin/granzyme cytotoxicity.
Small-molecule dimerizer that activates an inducible caspase-9 safety switch to ablate the engineered cells if required.
Rimiducid (AP1903) is a synthetic dimerizer that binds FKBP12-F36V domains on the inducible caspase-9 (iCasp9) safety switch in engineered cells, inducing caspase-9 dimerization and activation, triggering the apoptotic cascade and rapid ablation of the modified cells.
YES
DIRECT
Rimiducid binds FKBP12-F36V on the iCasp9 safety switch in engineered cells, induces caspase-9 dimerization/activation, and triggers the apoptotic cascade, killing the engineered cells.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
YES
DIRECT
Autologous TILs recognize neoantigen peptides presented on tumor MHC via native TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with IFN-γ/TNF-α enhancing killing.