Chimeric IgG1 monoclonal antibody against TNF-α; binds soluble and transmembrane TNF-α to block TNFR1/2 signaling (e.g., NF-κB/MAPK), reduce pro-inflammatory cytokines and adhesion molecules, and induce apoptosis of TNF-expressing activated T cells and macrophages; may mediate ADCC/CDC. Administered subcutaneously after switching from prior IV infliximab.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, neutralizing TNF and blocking TNFR1/2 signaling (e.g., NF-κB/MAPK), thereby reducing pro‑inflammatory cytokines and adhesion molecules; can induce apoptosis of TNF-expressing activated immune cells and may mediate ADCC/CDC.
NO
INDIRECT
No direct cell killing via the soluble TNF-α target; the antibody neutralizes soluble TNF-α and blocks TNFR signaling. Cytotoxic effects (ADCC/CDC/apoptosis) occur only when binding membrane TNF-α, not the soluble form.
Chimeric IgG1 monoclonal antibody against TNF-α; binds soluble and transmembrane TNF-α to block TNFR1/2 signaling (e.g., NF-κB/MAPK), reduce pro-inflammatory cytokines and adhesion molecules, and induce apoptosis of TNF-expressing activated T cells and macrophages; may mediate ADCC/CDC. Administered subcutaneously after switching from prior IV infliximab.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, neutralizing TNF and blocking TNFR1/2 signaling (e.g., NF-κB/MAPK), thereby reducing pro‑inflammatory cytokines and adhesion molecules; can induce apoptosis of TNF-expressing activated immune cells and may mediate ADCC/CDC.
YES
DIRECT
IgG1 anti–TNF-α binds transmembrane TNF on activated immune cells, triggering reverse signaling–mediated apoptosis and engaging Fc effector functions (ADCC by NK cells and CDC) to kill the target-expressing cells.
Human IgG1 bispecific T‑cell–engaging monoclonal antibody that binds CD20 on B cells and CD3 on T cells to redirect cytotoxic T cells against malignant B cells.
CD20×CD3 bispecific IgG1 antibody that simultaneously binds CD20 on B cells and CD3 on T cells, physically bridging them to activate cytotoxic T cells and induce perforin/granzyme-mediated lysis and apoptosis of CD20-positive malignant B cells.
YES
DIRECT
Glofitamab bridges CD3 on T cells to CD20 on B cells, activating cytotoxic T cells to kill CD20+ cells via perforin/granzyme-mediated lysis and apoptosis.
Human IgG1 bispecific T‑cell–engaging monoclonal antibody that binds CD20 on B cells and CD3 on T cells to redirect cytotoxic T cells against malignant B cells.
CD20×CD3 bispecific IgG1 antibody that simultaneously binds CD20 on B cells and CD3 on T cells, physically bridging them to activate cytotoxic T cells and induce perforin/granzyme-mediated lysis and apoptosis of CD20-positive malignant B cells.
NO
INDIRECT
The antibody bridges CD3ε on T cells to CD20 on B cells, activating T cells to kill CD20+ B cells via perforin/granzyme-mediated cytolysis; CD3ε+ T cells are effectors, not targets.
Anti‑CD79b antibody–drug conjugate that delivers MMAE, a microtubule inhibitor, to B‑cell lymphomas.
Anti-CD79b monoclonal antibody–drug conjugate that binds CD79b on B cells, is internalized, and releases MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of malignant B cells.
YES
DIRECT
The anti-CD79b antibody-drug conjugate binds CD79b, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cell.