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.
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.
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.
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.
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.
Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and mediates antibody-dependent cellular cytotoxicity.
Cetuximab is an anti-EGFR IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling (e.g., RAS/RAF/MEK/ERK and PI3K/AKT), resulting in anti-proliferative effects; as an IgG1 it also mediates NK cell–driven antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to trigger ADCC (and possibly CDC), leading to lysis of EGFR-expressing cells.