Bispecific IgG1 monoclonal antibody (MCLA-158) targeting EGFR and LGR5; inhibits EGFR-driven MAPK/PI3K signaling and uses Fc-mediated cytotoxicity/phagocytosis to deplete LGR5+ tumor stem-like cells.
Bispecific IgG1 monoclonal antibody that binds EGFR and LGR5 to block EGFR-driven MAPK/PI3K and LGR5/Wnt signaling, inhibiting tumor proliferation; its Fc domain mediates ADCC/ADCP to deplete LGR5+ cancer stem–like cells.
NO
INDIRECT
Petosemtamab binds EGFR to inhibit EGFR signaling (MAPK/PI3K), reducing proliferation. Its Fc-mediated ADCC/ADCP is directed toward LGR5+ cells; EGFR binding is not used as the cytotoxic trigger unless cells also co-express LGR5.
Bispecific IgG1 monoclonal antibody (MCLA-158) targeting EGFR and LGR5; inhibits EGFR-driven MAPK/PI3K signaling and uses Fc-mediated cytotoxicity/phagocytosis to deplete LGR5+ tumor stem-like cells.
Bispecific IgG1 monoclonal antibody that binds EGFR and LGR5 to block EGFR-driven MAPK/PI3K and LGR5/Wnt signaling, inhibiting tumor proliferation; its Fc domain mediates ADCC/ADCP to deplete LGR5+ cancer stem–like cells.
YES
DIRECT
Petosemtamab binds LGR5 on tumor cells and its IgG1 Fc engages FcγR-expressing effector cells, inducing ADCC (NK cells) and ADCP (macrophages) to deplete LGR5+ cells.
EGFR-targeting monoclonal antibody that inhibits EGFR signaling.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream signaling (RAS–MAPK, PI3K–AKT) and tumor cell proliferation; may also engage immune effector functions such as ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and engages Fcγ receptor–bearing immune cells to mediate antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC); it also blocks EGFR signaling.
Autologous CD19-directed CAR T cells (19-28z CAR with CD28 and CD3ζ signaling domains) engineered to secrete IL-12; includes a truncated EGFR (EGFRt) tag for tracking and potential cetuximab-mediated depletion.
Autologous T cells engineered with an anti-CD19 CAR containing CD28 and CD3zeta signaling domains recognize CD19 on B-cell malignancies, become activated, proliferate, and kill targets via cytotoxic effector mechanisms. The cells are further engineered to secrete IL-12, which enhances Th1/IFN-gamma responses, activates NK cells, and augments cytotoxic T-cell activity to strengthen antitumor immunity. A truncated EGFR (EGFRt) tag enables in vivo tracking and optional depletion of the cells via cetuximab-mediated ADCC as a safety switch.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 via the CAR (CD28/CD3ζ signaling), activate, and kill the engaged cells through cytotoxic T-cell mechanisms (perforin/granzyme and Fas–FasL). IL-12 secretion enhances this activity.
Patient-specific cancer vaccine delivering tumor neoantigens to antigen-presenting cells to prime and expand tumor-specific CD8+ and CD4+ T cells.
Patient-specific neoantigen peptides are delivered to antigen-presenting cells for MHC I/II presentation, priming and expanding tumor-specific CD8+ and CD4+ T cells to generate targeted antitumor immunity.
YES
INDIRECT
The vaccine primes and expands neoantigen-specific CD8+ T cells, which recognize MHC I–presented neoantigen epitopes on tumor cells and kill them via perforin/granzyme and Fas–FasL pathways.