Allogeneic, gene-engineered universal T cells expressing chimeric natural killer (NK) receptors, administered intravenously to harness NK receptor–mediated recognition and signaling on T cells for cytotoxic and immunomodulatory activity to dampen the pathogenic immune response in steroid-refractory or -dependent acute GVHD.
Allogeneic gene‑engineered universal T cells expressing chimeric NK receptors recognize stress‑induced ligands on pathogenic immune cells via NK receptor–derived recognition domains and signal through T‑cell activation domains to exert cytotoxic and immunomodulatory effects, depleting or suppressing alloreactive cells and inflammatory pathways that drive steroid‑refractory/dependent acute GVHD.
Engineered T cells with chimeric NK receptors bind stress‑induced ligands on target cells and, through T‑cell activation domains, trigger cytolysis via perforin/granzyme and death‑receptor pathways.
Autologous, gene-modified third-generation anti-GD2 chimeric antigen receptor T-cell therapy with CD28 and 4-1BB costimulation and CD3ζ signaling, incorporating an inducible caspase-9 (iC9) safety switch; administered as a single IV dose after lymphodepletion to target GD2-expressing CNS tumors.
Autologous T cells are gene-modified to express a third-generation anti-GD2 chimeric antigen receptor with CD28 and 4-1BB costimulatory domains and CD3ζ signaling. Binding to GD2 on tumor cells triggers T-cell activation and cytotoxic killing (perforin/granzyme, cytokines). An inducible caspase-9 safety switch enables pharmacologic elimination of the CAR T cells if severe toxicity occurs. Lymphodepleting chemotherapy facilitates CAR T expansion and persistence.
GD2-targeted CAR T cells recognize GD2 on tumor cells, activate, form an immune synapse, and induce cytolysis via perforin/granzyme (with possible Fas/FasL and cytokine-mediated apoptosis).
Bispecific antibody–drug conjugate (aka iza-bren; izalontamab brengitecan; BMS-986507) targeting EGFR and HER3. After binding, it is internalized and releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage; it also blocks EGFR/HER3 signaling.
Bispecific ADC that binds EGFR and HER3 on tumor cells; after receptor-mediated internalization it releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and cell death, while concurrently inhibiting EGFR/HER3 signaling.
BL-B01D1 binds HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) that induces DNA damage leading to cell death.
Anti-CLDN18.2 monoclonal antibody that binds Claudin 18.2 on tumor cells and mediates immune cytotoxicity (ADCC/CDC).
Anti-CLDN18.2 antibody–drug conjugate that binds Claudin 18.2 on tumor cells, is internalized, and releases the MMAE payload via a cleavable linker. MMAE binds tubulin, inhibits microtubule polymerization, and induces G2/M arrest and apoptosis in CLDN18.2-expressing cells; Fc-mediated ADCC/CDC may also contribute.
The anti-CLDN18.2 ADC binds Claudin 18.2, is internalized, and releases MMAE, which inhibits tubulin to cause G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC/CDC against CLDN18.2-positive cells.
Cord blood–derived natural killer (NK) cells genetically engineered to express a CD19-directed chimeric antigen receptor for antigen-specific recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies.
Cord blood–derived NK cells are engineered to express a CD19-specific chimeric antigen receptor, enabling antigen-dependent recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies. In this construct, IL-15 supports NK activation, proliferation, and persistence, while IL-10 modulates inflammatory responses to enhance antitumor activity and potentially reduce toxicity.
CAR-engineered NK cells recognize CD19 on target cells and directly kill them via NK-cell cytotoxicity (perforin/granzyme release and death-receptor pathways), with IL-15 supporting activation and persistence.