Autologous, gene-modified chimeric antigen receptor (CAR) T cells produced with a non-viral vector, engineered to target mesothelin and MUC1 on tumor cells and to auto-secrete multifunctional antibodies to enhance antitumor immunity within the tumor microenvironment; evaluated in a dose-escalation regimen (5×10^5, 1×10^6, 5×10^6 cells/kg).
Autologous T cells engineered with a non-viral vector to express chimeric antigen receptors recognizing mesothelin and MUC1 on tumor cells, triggering CAR-mediated T-cell activation and cytolytic killing via CD3ζ and costimulatory signaling; additionally engineered to secrete multifunctional antibodies within the tumor microenvironment to enhance antitumor immunity (e.g., overcoming immunosuppression/checkpoints) and amplify T-cell activity.
CAR T cells recognize MUC1 via the CAR, activating CD3ζ/costimulatory signaling and inducing T-cell cytolysis (perforin–granzyme and/or Fas-mediated apoptosis) of MUC1-expressing cells.
Type II anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC/ADCP and direct cell death.
Glycoengineered type II humanized anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and, via enhanced FcγRIIIa engagement, promotes antibody-dependent cellular cytotoxicity and phagocytosis, as well as direct caspase-independent cell death, resulting in depletion of CD20+ B cells.
Binds CD20 on B cells; Fc engages Fc-gamma RIIIa on NK cells/macrophages to drive ADCC/ADCP, and the antibody also induces direct caspase-independent cell death of CD20+ cells.
Autologous, fully human anti-CD19 chimeric antigen receptor T-cell therapy; patient T cells are engineered to express an anti-CD19 CAR to selectively eliminate CD19+ B-lineage cells and plasmablasts, reducing pathogenic autoimmunity in systemic sclerosis.
Autologous CD4/CD8 T cells are engineered with a fully human anti‑CD19 chimeric antigen receptor (scFv–CD8α hinge/transmembrane–CD28 costimulatory–CD3ζ signaling). After infusion, the CAR T cells recognize CD19 on B-lineage cells and plasmablasts, become activated, and mediate perforin/granzyme-dependent cytotoxicity, depleting CD19+ cells and reducing autoantibody production and pathogenic B-cell activity in systemic sclerosis.
Anti-CD19 CAR T cells recognize CD19 on target cells and directly kill them via T-cell cytotoxic mechanisms, primarily perforin/granzyme-mediated lysis after immune synapse formation.
Intravenous anti‑EGFR/c‑MET bispecific monoclonal antibody that blocks ligand‑driven EGFR and MET receptor signaling and can engage Fc‑mediated cytotoxicity (ADCC/ADCP).
Bispecific monoclonal antibody targeting EGFR and c-MET that inhibits ligand-driven receptor signaling to suppress downstream MAPK and PI3K–AKT pathways (including MET-driven bypass resistance) and leverages an intact Fc to induce ADCC/ADCP against EGFR/MET-expressing tumor cells.
Binds EGFR on tumor cells and uses its intact Fc to recruit immune effectors (e.g., NK cells/macrophages) to mediate ADCC/ADCP, killing EGFR-expressing cells.
Intravenous anti‑EGFR/c‑MET bispecific monoclonal antibody that blocks ligand‑driven EGFR and MET receptor signaling and can engage Fc‑mediated cytotoxicity (ADCC/ADCP).
Bispecific monoclonal antibody targeting EGFR and c-MET that inhibits ligand-driven receptor signaling to suppress downstream MAPK and PI3K–AKT pathways (including MET-driven bypass resistance) and leverages an intact Fc to induce ADCC/ADCP against EGFR/MET-expressing tumor cells.
Antibody binds MET and uses its intact Fc to recruit immune effector cells, leading to Fc-dependent ADCC and ADCP (e.g., by NK cells and macrophages). Signaling blockade is non-cytotoxic; killing is via Fc-mediated effector functions.