An allogeneic, cord blood–derived chimeric antigen receptor–engineered natural killer (CAR-NK) cell therapy targeting Claudin 18.2 for advanced gastric and pancreatic cancer; the engineered NK cells recognize CLDN18.2 on tumor cells and induce cytotoxicity via perforin/granzyme release and cytokine secretion.
Allogeneic cord blood–derived NK cells are engineered with a chimeric antigen receptor that binds Claudin 18.2 on tumor cells, activating NK cytotoxic programs to induce perforin/granzyme-mediated lysis and cytokine secretion, resulting in targeted killing of CLDN18.2-positive gastric and pancreatic cancer cells.
YES
DIRECT
CAR-NK cells recognize CLDN18.2 via the CAR and kill target cells by degranulation with perforin and granzymes, causing cytolysis/apoptosis.
An autologous, gene-modified T-cell therapy engineered to express chimeric antigen receptors against CD19 and BCMA, designed to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibodies in refractory generalized myasthenia gravis.
Autologous T cells engineered with chimeric antigen receptors targeting CD19 and BCMA bind these antigens on B cells and plasmablasts/plasma cells, triggering T-cell activation and cytotoxic killing (perforin/granzyme). This depletes autoantibody-producing compartments and reduces pathogenic autoantibodies in refractory generalized myasthenia gravis.
YES
DIRECT
CAR-T cells recognize CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
An autologous, gene-modified T-cell therapy engineered to express chimeric antigen receptors against CD19 and BCMA, designed to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibodies in refractory generalized myasthenia gravis.
Autologous T cells engineered with chimeric antigen receptors targeting CD19 and BCMA bind these antigens on B cells and plasmablasts/plasma cells, triggering T-cell activation and cytotoxic killing (perforin/granzyme). This depletes autoantibody-producing compartments and reduces pathogenic autoantibodies in refractory generalized myasthenia gravis.
YES
DIRECT
BCMA-directed CAR-T cells bind BCMA on target cells and induce T-cell cytotoxicity, killing via perforin/granzyme-mediated apoptosis.
HER2-targeted antibody–drug conjugate composed of a humanized anti‑HER2 IgG1 (trastuzumab) linked via a cleavable linker to the topoisomerase I inhibitor payload deruxtecan (DXd); binds HER2, internalizes, releases DXd to inhibit topoisomerase I and induce DNA damage; also inhibits HER2 signaling and mediates ADCC.
HER2-targeted ADC: a humanized anti-HER2 IgG1 (trastuzumab) delivers a cleavable linker–attached topoisomerase I inhibitor (deruxtecan, DXd). Upon HER2 binding and internalization, lysosomal cleavage releases DXd to inhibit topoisomerase I, causing DNA damage and cell death; the membrane-permeable payload enables a bystander effect. The antibody also inhibits HER2 signaling and mediates ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan, causing DNA damage and cell death; Fc-mediated ADCC may contribute, and the membrane-permeable payload can cause bystander killing.
HER2-targeted antibody–drug conjugate composed of a humanized anti‑HER2 IgG1 (trastuzumab) linked via a cleavable linker to the topoisomerase I inhibitor payload deruxtecan (DXd); binds HER2, internalizes, releases DXd to inhibit topoisomerase I and induce DNA damage; also inhibits HER2 signaling and mediates ADCC.
HER2-targeted ADC: a humanized anti-HER2 IgG1 (trastuzumab) delivers a cleavable linker–attached topoisomerase I inhibitor (deruxtecan, DXd). Upon HER2 binding and internalization, lysosomal cleavage releases DXd to inhibit topoisomerase I, causing DNA damage and cell death; the membrane-permeable payload enables a bystander effect. The antibody also inhibits HER2 signaling and mediates ADCC.
NO
INDIRECT
T-DXd binds HER2 (not topoisomerase I), is internalized, and releases deruxtecan that inhibits topoisomerase I to cause DNA damage and cell death in HER2+ cells; topoisomerase I expression alone is not directly targeted.