Cord blood–derived natural killer (NK) cells genetically engineered to express a CD19-directed chimeric antigen receptor for antigen-specific recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies.
Cord blood–derived NK cells are engineered to express a CD19-specific chimeric antigen receptor, enabling antigen-dependent recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies. In this construct, IL-15 supports NK activation, proliferation, and persistence, while IL-10 modulates inflammatory responses to enhance antitumor activity and potentially reduce toxicity.
YES
DIRECT
CAR-engineered NK cells recognize CD19 on target cells and directly kill them via NK-cell cytotoxicity (perforin/granzyme release and death-receptor pathways), with IL-15 supporting activation and persistence.
An intravenous chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, blocking TNFR1/2 signaling and NF-κB–driven inflammation; can induce apoptosis of activated T cells/monocytes and promote mucosal healing. Regimen: 10 mg/kg at week 0, then 5 mg/kg at weeks 2, 4, and 8; maintenance every 6 weeks from week 12.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, neutralizing TNF and preventing engagement of TNFR1/2. This blocks downstream NF-κB–driven inflammatory signaling, reduces proinflammatory cytokines and adhesion molecule expression, and can trigger apoptosis of activated T cells/monocytes, promoting mucosal healing.
NO
INDIRECT
Infliximab neutralizes soluble TNF-α, blocking TNFR signaling and inflammation; it does not directly bind or kill cells via the soluble target. Reported apoptosis occurs when binding transmembrane TNF on immune cells, not the soluble form.
An intravenous chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, blocking TNFR1/2 signaling and NF-κB–driven inflammation; can induce apoptosis of activated T cells/monocytes and promote mucosal healing. Regimen: 10 mg/kg at week 0, then 5 mg/kg at weeks 2, 4, and 8; maintenance every 6 weeks from week 12.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, neutralizing TNF and preventing engagement of TNFR1/2. This blocks downstream NF-κB–driven inflammatory signaling, reduces proinflammatory cytokines and adhesion molecule expression, and can trigger apoptosis of activated T cells/monocytes, promoting mucosal healing.
YES
DIRECT
Binding to transmembrane TNF on activated immune cells triggers Fc-mediated ADCC and complement-dependent cytotoxicity, and tmTNF cross-linking induces reverse-signaling apoptosis.
Humanized IgG1 monoclonal antibody that binds HER2 extracellular domain II to block HER2 heterodimerization (especially with HER3), inhibiting downstream signaling (PI3K/AKT/MAPK) and promoting tumor cell death; also mediates antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Binds HER2 on target cells and recruits FcγR-expressing immune effectors (e.g., NK cells) to mediate ADCC; HER2 signaling blockade may also induce apoptosis.
Humanized IgG1 monoclonal antibody binding HER2 (domain IV); inhibits signaling and mediates ADCC; administered IV or SC.
Humanized IgG1 monoclonal antibody that binds HER2 (domain IV), inhibits HER2 signaling and proliferation, promotes receptor internalization and prevents extracellular domain shedding, and mediates Fc-dependent ADCC against HER2-overexpressing tumor cells.
YES
DIRECT
Binds HER2 and engages Fc receptors on effector cells to trigger antibody-dependent cell-mediated cytotoxicity (ADCC) and phagocytosis; HER2 signaling blockade can also promote apoptosis.