Autologous gene-modified T-cell therapy engineered via Sleeping Beauty to express a ROR1-targeted CAR, membrane-bound IL-15, an EGFRt/HER1t safety switch, and intrinsic PD-1 downregulation to recognize and kill ROR1+ tumor cells with enhanced persistence and resistance to PD-1/PD-L1 suppression.
Autologous T cells engineered with a ROR1-targeted chimeric antigen receptor to recognize and kill ROR1-positive tumor cells; membrane-bound IL-15 enhances T-cell survival and expansion; intrinsic PD-1 downregulation resists PD-1/PD-L1–mediated inhibition; an EGFRt/HER1t safety switch allows conditional ablation of the cells.
NO
INDIRECT
Membrane-bound IL-15 on the CAR-T cells enhances their survival/expansion; cytotoxicity occurs when the CAR targets ROR1 on tumor cells and kills them via T cell effector mechanisms (perforin/granzyme). IL-15-expressing cells are not targeted for killing.
Autologous gene-modified T-cell therapy engineered via Sleeping Beauty to express a ROR1-targeted CAR, membrane-bound IL-15, an EGFRt/HER1t safety switch, and intrinsic PD-1 downregulation to recognize and kill ROR1+ tumor cells with enhanced persistence and resistance to PD-1/PD-L1 suppression.
Autologous T cells engineered with a ROR1-targeted chimeric antigen receptor to recognize and kill ROR1-positive tumor cells; membrane-bound IL-15 enhances T-cell survival and expansion; intrinsic PD-1 downregulation resists PD-1/PD-L1–mediated inhibition; an EGFRt/HER1t safety switch allows conditional ablation of the cells.
NO
INDIRECT
EGFRt is a safety tag on the CAR-T cells; they are not targeted by the CAR. EGFRt+ CAR-T cells can be conditionally ablated only if an anti-EGFR antibody (e.g., cetuximab) is given, triggering ADCC/complement-mediated killing.
Autologous gene-modified T-cell therapy engineered via Sleeping Beauty to express a ROR1-targeted CAR, membrane-bound IL-15, an EGFRt/HER1t safety switch, and intrinsic PD-1 downregulation to recognize and kill ROR1+ tumor cells with enhanced persistence and resistance to PD-1/PD-L1 suppression.
Autologous T cells engineered with a ROR1-targeted chimeric antigen receptor to recognize and kill ROR1-positive tumor cells; membrane-bound IL-15 enhances T-cell survival and expansion; intrinsic PD-1 downregulation resists PD-1/PD-L1–mediated inhibition; an EGFRt/HER1t safety switch allows conditional ablation of the cells.
NO
INDIRECT
PD-1 is not targeted for killing; PD-1 is downregulated on the CAR T cells to resist PD-1/PD-L1 inhibition. Cytotoxicity is directed against ROR1+ tumor cells via CAR-mediated T-cell killing, not PD-1–expressing cells.
Anti-CD38 IgG1 monoclonal antibody (Sarclisa) that induces ADCC, CDC, ADCP, direct apoptosis, and inhibits CD38 ectoenzyme activity.
Isatuximab is an IgG1 monoclonal antibody targeting CD38 on plasma cells. It mediates antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis, can trigger direct apoptosis, and inhibits CD38 ectoenzyme (NADase) activity, leading to depletion/lysis of CD38-expressing tumor cells.
YES
DIRECT
Anti-CD38 IgG1 mAb binds CD38 on target cells and induces ADCC, CDC, and ADCP, and can trigger direct apoptosis, leading to lysis of CD38-expressing cells.
Subcutaneous long-peptide therapeutic cancer vaccine targeting indoleamine 2,3-dioxygenase (IDO), designed to elicit IDO-specific CD4+ and CD8+ T cells to eliminate IDO-expressing tumor and immunosuppressive cells.
Long‑peptide therapeutic cancer vaccine targeting indoleamine 2,3-dioxygenase (IDO); induces IDO‑specific CD4+ and CD8+ T‑cell responses that recognize and eliminate IDO‑expressing tumor and immunosuppressive cells, reversing IDO‑mediated tryptophan catabolism/kynurenine immunosuppression and restoring antitumor immune activity.
YES
INDIRECT
Peptide vaccine induces IDO1-specific CD8+ (and CD4+) T cells that recognize IDO1 peptides on MHC of IDO1-expressing cells and kill them via CTL effector mechanisms (perforin/granzyme, Fas–FasL).