A Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to tumor cells, causing DNA damage and a bystander effect.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38; binds Trop-2 on tumor cells, is internalized and cleaved to release SN-38, a topoisomerase I inhibitor that stabilizes topoisomerase I–DNA complexes, causing DNA damage, replication arrest, apoptosis, and a bystander effect.
YES
DIRECT
SN-38 released from the ADC binds and inhibits topoisomerase I, stabilizing topo I–DNA complexes and causing DNA damage and apoptosis (after delivery via Trop-2 targeting or bystander diffusion).
A humanized IgG1 monoclonal antibody targeting HER2/ERBB2 that inhibits HER2 signaling and dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody that binds HER2/ERBB2 on tumor cells, blocking receptor dimerization and downstream signaling (e.g., MAPK and PI3K–AKT), and mediating antibody-dependent cellular cytotoxicity (ADCC) via Fcγ receptor–bearing immune cells.
YES
DIRECT
Trastuzumab binds HER2 and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate ADCC, killing HER2-expressing cells.
A Trop-2–directed antibody–drug conjugate (IMMU-132; SG; hziy) composed of a humanized anti–Trop-2 IgG linked via a hydrolyzable linker to SN-38, the active metabolite of irinotecan; delivers SN-38 to Trop-2–expressing tumor cells to inhibit topoisomerase I and induce DNA damage/apoptosis with a bystander effect.
Trop-2–targeted humanized IgG linked via a hydrolyzable linker to SN-38 (irinotecan’s active metabolite). After binding Trop-2 and internalization, SN-38 is released to inhibit topoisomerase I, stabilizing topo I–DNA complexes and causing DNA breaks, leading to cell-cycle arrest and apoptosis; the membrane-permeable payload enables a bystander effect.
YES
DIRECT
The ADC binds TROP-2, is internalized, and releases SN-38 that inhibits topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis (with a bystander effect).
A Trop-2–directed antibody–drug conjugate (IMMU-132; SG; hziy) composed of a humanized anti–Trop-2 IgG linked via a hydrolyzable linker to SN-38, the active metabolite of irinotecan; delivers SN-38 to Trop-2–expressing tumor cells to inhibit topoisomerase I and induce DNA damage/apoptosis with a bystander effect.
Trop-2–targeted humanized IgG linked via a hydrolyzable linker to SN-38 (irinotecan’s active metabolite). After binding Trop-2 and internalization, SN-38 is released to inhibit topoisomerase I, stabilizing topo I–DNA complexes and causing DNA breaks, leading to cell-cycle arrest and apoptosis; the membrane-permeable payload enables a bystander effect.
NO
INDIRECT
The ADC binds Trop-2 on tumor cells, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis; topoisomerase I is the intracellular enzymatic target of the payload, not the binding antigen used to target cells.
Anti-EGFR IgG1 monoclonal antibody that blocks upstream receptor signaling.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor dimerization/activation, thereby suppressing downstream MAPK and PI3K-AKT signaling and inhibiting tumor cell proliferation; its IgG1 Fc can also mediate ADCC.
YES
DIRECT
Cetuximab binds EGFR and its IgG1 Fc engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC (and possibly CDC), killing EGFR+ cells; it also blocks EGFR signaling to inhibit proliferation.