Subcutaneous bispecific IgG1 T-cell engager (CD3×CD20) that redirects cytotoxic T cells to kill CD20+ B cells.
Bispecific IgG1 antibody that binds CD3 on T cells and CD20 on B cells, cross-linking them to activate cytotoxic T cells and induce perforin/granzyme-mediated killing of CD20-positive B-cell tumor cells.
YES
DIRECT
Epcoritamab binds CD3 on T cells and CD20 on target B cells, crosslinking them to activate cytotoxic T cells that kill CD20+ cells via perforin/granzyme-mediated lysis.
Subcutaneous bispecific IgG1 T-cell engager (CD3×CD20) that redirects cytotoxic T cells to kill CD20+ B cells.
Bispecific IgG1 antibody that binds CD3 on T cells and CD20 on B cells, cross-linking them to activate cytotoxic T cells and induce perforin/granzyme-mediated killing of CD20-positive B-cell tumor cells.
NO
INDIRECT
Epcoritamab binds CD3 on T cells to activate and redirect them to CD20+ B cells, which are killed via perforin/granzyme. CD3+ T cells are not targeted for killing.
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement-mediated cytotoxicity (CDC), and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and depletes CD20+ B cells primarily via Fc‑mediated antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces killing via Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis signaling.
Anti–TNF-α chimeric IgG1 monoclonal antibody that neutralizes soluble and transmembrane TNF-α, blocking TNFR→NF-κB signaling, reducing inflammatory cytokines/adhesion molecules, and inducing apoptosis of activated T cells/macrophages to dampen Th1/Th17-driven gut inflammation.
Chimeric IgG1 monoclonal antibody against TNF-α that neutralizes soluble and transmembrane TNF-α, blocking TNFR→NF-κB signaling, decreasing proinflammatory cytokines and adhesion molecules, and inducing apoptosis of activated T cells and macrophages to suppress Th1/Th17-driven inflammation.
YES
DIRECT
By binding transmembrane TNF-α on activated immune cells, infliximab’s IgG1 Fc triggers ADCC and complement-dependent cytotoxicity and can induce reverse-signaling apoptosis in tmTNF-α–expressing cells.
Oral small-molecule BCL-2 inhibitor that promotes apoptosis in BCL-2–dependent myeloid blasts.
Selective oral BH3-mimetic that binds the hydrophobic groove of the anti-apoptotic protein BCL-2, blocking its function and restoring mitochondrial apoptosis in BCL-2–dependent tumor cells; relatively spares BCL-XL to limit thrombocytopenia.
YES
DIRECT
BH3-mimetic binds and inhibits BCL-2, releasing pro-apoptotic effectors (e.g., BAX/BAK) to trigger mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and apoptosis in BCL-2–dependent cells.