Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
NKG2D-CAR NK cells bind ULBP5 on target cells, triggering NK activation and degranulation (perforin/granzyme) and death receptor pathways, leading to apoptosis of the target cells.
Chimeric monoclonal antibody against EGFR that blocks ligand binding and receptor signaling.
Chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocks ligand binding and receptor dimerization/activation, suppressing downstream RAS–MAPK and PI3K–AKT signaling to inhibit tumor cell proliferation and survival; may also induce receptor internalization and ADCC.
Cetuximab binds EGFR on tumor cells and its IgG1 Fc engages FcγR-bearing effector cells to trigger ADCC (and sometimes complement-mediated cytotoxicity), causing target-cell lysis; it also blocks EGFR signaling (primarily cytostatic).
An antibody–drug conjugate targeting HER2 that delivers a topoisomerase I inhibitor (DXd). After HER2 binding and internalization, DXd is released to induce DNA damage and apoptosis; it also has a bystander effect and can inhibit HER2 signaling/mediate ADCC.
HER2-targeted antibody–drug conjugate: trastuzumab binds HER2 and is internalized; a cleavable linker releases the DXd topoisomerase I inhibitor to induce DNA damage and apoptosis. The membrane-permeable payload produces a bystander effect, and the antibody component can inhibit HER2 signaling and mediate ADCC.
Trastuzumab deruxtecan binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; the membrane-permeable payload enables a bystander effect, and the Fc can mediate ADCC.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement activation, ADCC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells, inducing B‑cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and direct apoptosis.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP by immune effector cells; CD20 crosslinking can also induce apoptosis.
Autologous CD19-directed CAR T-cell therapy using a CD19 scFv with CD28/CD3ζ signaling domains, engineered to constitutively secrete interleukin-18 (IL-18) to enhance Th1/IFN-γ responses, cytotoxicity, proliferation, and persistence against CD19+ B-ALL.
Autologous T cells engineered to express a CD19-specific CAR with CD28/CD3ζ signaling (19-28z) that triggers T-cell activation and cytotoxic killing of CD19+ B-ALL cells upon antigen engagement. The cells are further engineered to constitutively secrete IL-18, which enhances Th1/IFN-γ signaling, boosts T and NK cell activation, cytotoxicity, proliferation, and persistence, and modulates the tumor microenvironment to improve anti-leukemic activity.
CD19-directed CAR T cells bind CD19 on target cells and, upon CD28/CD3zeta signaling, directly kill them via perforin/granzyme-mediated cytolysis and Fas-FasL apoptosis; IL-18 secretion enhances T/NK activation and persistence.