Antibody-drug conjugate targeting a tumor-associated cell-surface antigen; internalizes and releases a cytotoxic payload (e.g., topoisomerase I or microtubule-targeting warhead) to kill cancer cells.
IgG1 monoclonal antibody targeting nectin‑4 binds tumor cells, is internalized, and via a cleavable linker releases a topoisomerase I inhibitor payload that blocks DNA topoisomerase I, inhibiting DNA replication and inducing cell-cycle arrest and apoptosis in nectin‑4–expressing cancers.
The ADC binds nectin-4 on tumor cells, is internalized, and a cleavable linker releases a topoisomerase I inhibitor that blocks DNA replication, leading to cell-cycle arrest and apoptosis of nectin-4–expressing cells.
A humanized anti-CD2 monoclonal antibody that binds CD2 on T lymphocytes and NK cells, leading to depletion/modulation of these cells and blockade of CD2–CD58 costimulatory/adhesion signaling to reduce autoreactive T-cell activation.
Humanized anti-CD2 monoclonal antibody that binds CD2 on T lymphocytes and NK cells, depleting/modulating these cells and blocking CD2–CD58 costimulatory/adhesion signaling to reduce autoreactive T-cell activation.
Unconjugated anti-CD2 IgG binds CD2 on T and NK cells; its Fc recruits immune effectors and complement, causing ADCC and CDC-mediated depletion of CD2+ cells.
Humanized anti-CD19 IgG1 monoclonal antibody (IV) that depletes CD19+ B cells and plasmablasts via ADCC/CDC to reduce pathogenic AQP4-IgG autoantibodies in NMOSD.
Humanized, afucosylated anti-CD19 IgG1 monoclonal antibody that binds CD19 on B-lineage cells (including plasmablasts) and depletes them via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing production of pathogenic AQP4-IgG autoantibodies in NMOSD.
Binds CD19 on B-lineage cells and induces Fc-mediated ADCC (e.g., NK cells/macrophages) and complement-dependent cytotoxicity, leading to lysis of CD19+ cells.
Recombinant immunotoxin (D2C7-(scdsFv)-PE38KDEL) targeting EGFR/EGFRvIII; an antibody fragment fused to Pseudomonas exotoxin A that is delivered intracerebrally by convection-enhanced delivery, internalizes into tumor cells, and inactivates EF2 to block protein synthesis and induce tumor cell death.
Recombinant immunotoxin in which an EGFR/EGFRvIII-targeting scFv (D2C7) is fused to Pseudomonas exotoxin A (PE38KDEL). After binding EGFR/EGFRvIII on tumor cells and internalization, the PE domain ADP-ribosylates and inactivates elongation factor 2 (EF2), blocking protein synthesis and inducing tumor cell death; the KDEL motif enhances intracellular retention. Delivered intracerebrally by convection-enhanced delivery.
The EGFR-targeted immunotoxin binds EGFR on the cell surface, is internalized, and its Pseudomonas exotoxin A moiety ADP-ribosylates and inactivates EF2, blocking protein synthesis and inducing apoptotic cell death.
Recombinant immunotoxin (D2C7-(scdsFv)-PE38KDEL) targeting EGFR/EGFRvIII; an antibody fragment fused to Pseudomonas exotoxin A that is delivered intracerebrally by convection-enhanced delivery, internalizes into tumor cells, and inactivates EF2 to block protein synthesis and induce tumor cell death.
Recombinant immunotoxin in which an EGFR/EGFRvIII-targeting scFv (D2C7) is fused to Pseudomonas exotoxin A (PE38KDEL). After binding EGFR/EGFRvIII on tumor cells and internalization, the PE domain ADP-ribosylates and inactivates elongation factor 2 (EF2), blocking protein synthesis and inducing tumor cell death; the KDEL motif enhances intracellular retention. Delivered intracerebrally by convection-enhanced delivery.
The D2C7 scFv binds EGFRvIII on tumor cells, the PE38 exotoxin is internalized and ADP‑ribosylates EF2, blocking protein synthesis and inducing apoptotic cell death (KDEL enhances intracellular retention).