CAR T cells generated via lentiviral transduction to recognize CD133; IV dose-escalated infusion; targets CD133+ myeloid progenitors/blasts using CAR-mediated T-cell activation and cytotoxicity.
Autologous/allogeneic T cells are lentivirally engineered to express a chimeric antigen receptor targeting CD133. CAR engagement of CD133 on myeloid progenitors/blasts triggers MHC-independent T-cell activation, leading to perforin/granzyme-mediated cytotoxicity and cytokine-driven tumor cell clearance.
CD133-directed CAR T cells engage CD133 on target cells, triggering MHC-independent T-cell activation and perforin/granzyme-mediated cytolysis, with additional cytokine-driven killing.
Reference product (Erbitux); a recombinant chimeric anti-EGFR IgG1 monoclonal antibody that binds EGFR, blocks ligand binding and receptor activation, induces receptor internalization, inhibits downstream signaling (RAS–RAF–MEK–ERK, PI3K–AKT), and mediates ADCC.
Cetuximab is a chimeric IgG1 monoclonal antibody against EGFR (ErbB1/HER1). It binds the extracellular domain of EGFR, blocks ligand (EGF/TGF-alpha) binding, prevents receptor activation and dimerization, promotes receptor internalization, and inhibits downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling, reducing proliferation and survival of EGFR-expressing tumor cells; its IgG1 Fc can also mediate ADCC.
Cetuximab binds EGFR on target cells and engages Fcγ receptor–bearing effectors (e.g., NK cells) to mediate ADCC, with possible CDC; signaling blockade is largely cytostatic.
HER2-directed antibody–drug conjugate: trastuzumab linked via a cleavable linker to the topoisomerase I inhibitor deruxtecan. Binds HER2, is internalized, releases deruxtecan to induce DNA damage and apoptosis; also blocks HER2 signaling and mediates ADCC, with a bystander effect.
HER2-targeted antibody–drug conjugate: trastuzumab binds HER2 and is internalized; a cleavable linker releases the membrane-permeable topoisomerase I inhibitor deruxtecan (DXd) in tumor cells, inducing DNA damage and apoptosis. The trastuzumab moiety also inhibits HER2 signaling and mediates ADCC, enabling a bystander cytotoxic effect.
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan inside the cell, causing DNA damage and apoptosis; Fc-mediated ADCC also contributes, with a membrane-permeable payload enabling bystander killing.
Humanized anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2) that binds the receptor’s extracellular domain, inhibits HER2-driven signaling and proliferation, and recruits immune effector cells to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing immune effectors (e.g., NK cells) to trigger antibody-dependent cellular cytotoxicity (ADCC), killing HER2-expressing cells.
Nectin-4-targeted antibody-drug conjugate (ASG-22CE) that delivers the microtubule-disrupting agent MMAE to tumor cells, causing apoptosis.
Nectin-4–targeted monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE; binding to Nectin-4 on tumor cells triggers internalization and linker cleavage, releasing MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4–expressing cancer cells.
ADC binds Nectin-4 on the cell surface, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptosis of the Nectin-4–expressing cell.