Autologous gene-modified CAR T-cell therapy engineered to express a chimeric antigen receptor targeting DLL3. CAR engagement of DLL3 on tumor cells induces T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of DLL3-positive cancer cells, independent of native TCR; developed for DLL3-expressing neuroendocrine tumors such as small cell lung cancer and large cell neuroendocrine carcinoma.
Autologous gene-modified T cells expressing a DLL3-specific chimeric antigen receptor. Binding to DLL3 on tumor cells activates the T cells, leading to expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of DLL3-positive cancer cells independent of the native TCR.
YES
DIRECT
CAR-T cells recognize DLL3 via the CAR and, upon activation, kill DLL3-positive cells through perforin/granzyme-mediated cytolysis (with cytokine release).
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC/CDC, modulating the tumor microenvironment.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via Fc-mediated ADCC, complement-dependent cytotoxicity, and antibody-dependent phagocytosis, thereby modulating the tumor microenvironment.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated effector functions—ADCC by NK cells/macrophages, complement-dependent lysis, and antibody-dependent phagocytosis—depleting CD20+ cells.
Anti-HER2 monoclonal antibody that inhibits HER2 dimerization (especially with HER3) and mediates ADCC.
Humanized anti-HER2 monoclonal antibody that binds the HER2 extracellular dimerization domain to prevent HER2 heterodimerization (especially with HER3), thereby blocking downstream PI3K/AKT/MAPK signaling, inhibiting tumor cell proliferation and promoting apoptosis; also mediates antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Pertuzumab binds the HER2 subdomain II, recruits FcγR-expressing immune effectors (e.g., NK cells) to mediate ADCC, killing HER2+ cells; it also blocks HER2 heterodimerization, suppressing survival signaling and promoting apoptosis.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks ligand binding to EGFR, suppressing downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling; can also trigger antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor activation/dimerization, inhibiting downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling; Fc-mediated ADCC may also contribute to antitumor activity.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC (and some CDC), resulting in lysis of EGFR-expressing cells; EGFR signaling blockade is mainly antiproliferative.