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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
D2C7-IT binds EGFR/EGFRvIII on tumor cells, is internalized, and its PE toxin ADP-ribosylates EF2 to block protein synthesis and kill the cell. EF2 is not the recognition target; EF2-expressing cells are killed only if they first bind the drug via EGFR/EGFRvIII.