Autologous anti-CD20 CAR T-cell therapy (also known as ELC-301) engineered to express and secrete Helicobacter pylori neutrophil-activating protein (HP-NAP) upon CD20 engagement, enabling direct killing of CD20+ B cells and recruitment/activation of innate immune cells to enhance anti-tumor immunity.
Autologous anti-CD20 CAR T cells that directly kill CD20+ B cells; upon antigen engagement they secrete Helicobacter pylori neutrophil-activating protein (HP-NAP), recruiting and activating innate immune cells (e.g., neutrophils, monocytes/dendritic cells) and promoting Th1/NK responses to enhance bystander anti-tumor immunity.
YES
DIRECT
Anti-CD20 CAR T cells recognize CD20 and directly kill CD20+ cells via T‑cell cytolysis (perforin/granzyme and death‑receptor pathways); secreted HP‑NAP further recruits innate cells to augment bystander killing.
Autologous anti-CD20 CAR T-cell therapy (also known as ELC-301) engineered to express and secrete Helicobacter pylori neutrophil-activating protein (HP-NAP) upon CD20 engagement, enabling direct killing of CD20+ B cells and recruitment/activation of innate immune cells to enhance anti-tumor immunity.
Autologous anti-CD20 CAR T cells that directly kill CD20+ B cells; upon antigen engagement they secrete Helicobacter pylori neutrophil-activating protein (HP-NAP), recruiting and activating innate immune cells (e.g., neutrophils, monocytes/dendritic cells) and promoting Th1/NK responses to enhance bystander anti-tumor immunity.
NO
INDIRECT
TLR2+ cells are not targeted or killed. HP-NAP secreted by the CAR T cells engages TLR2 on innate immune cells to activate them; cytotoxicity is directed against CD20+ cells via CAR T–mediated killing, with additional bystander effects from activated innate cells.
Bispecific IgG1 monoclonal antibody against EGFR and MET that blocks ligand/receptor signaling, promotes receptor internalization and degradation, and induces Fc-mediated ADCC/ADCP.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and receptor phosphorylation/signaling, promotes receptor internalization and degradation, and engages Fc-mediated ADCC/ADCP to suppress and eliminate EGFR/MET-expressing tumor cells.
YES
DIRECT
Amivantamab binds EGFR on target cells and its IgG1 Fc engages FcγR-bearing effector cells (e.g., NK cells, macrophages) to mediate ADCC and ADCP, killing EGFR-expressing cells; it also blocks signaling/internalizes receptors (antiproliferative).
Bispecific IgG1 monoclonal antibody against EGFR and MET that blocks ligand/receptor signaling, promotes receptor internalization and degradation, and induces Fc-mediated ADCC/ADCP.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and receptor phosphorylation/signaling, promotes receptor internalization and degradation, and engages Fc-mediated ADCC/ADCP to suppress and eliminate EGFR/MET-expressing tumor cells.
YES
DIRECT
Amivantamab binds MET on tumor cells and, via its IgG1 Fc, recruits immune effector cells to mediate ADCC/ADCP, leading to killing of MET-expressing cells; it also inhibits signaling and promotes receptor internalization/degradation.