An antibody–drug conjugate (Trodelvy) consisting of a humanized anti–TROP-2 monoclonal antibody (sacituzumab) linked to SN-38 (govitecan), a topoisomerase I inhibitor. It binds TROP-2 on tumor cells, is internalized, and releases SN-38 intracellularly, causing Topo I inhibition, DNA damage, and tumor cell death.
Humanized anti-TROP-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis.
The ADC binds TROP-2 on target cells, is internalized, and releases SN-38, a topoisomerase I inhibitor, causing DNA damage and apoptosis.
A HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death, with potential bystander and immunogenic effects.
Trastuzumab-based HER2-targeted antibody-drug conjugate (trastuzumab rezetecan). After binding HER2 on tumor cells and internalization, a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor (rezetecan), which stabilizes topo I–DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis; may produce bystander killing and immunogenic effects.
The ADC binds HER2 on target cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that stabilizes topo I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis (with potential bystander effect).
An investigational antibody–drug conjugate (ADC) administered intravenously every 2 weeks; a tumor-targeting monoclonal antibody binds a tumor-associated surface antigen, is internalized, and releases a cytotoxic payload inside cancer cells to induce targeted cell death.
A tumor-targeting monoclonal antibody binds a tumor-associated surface antigen, is internalized by cancer cells, and releases a linked cytotoxic payload intracellularly to induce targeted cell death.
ADC binds the tumor-associated surface antigen, is internalized, and releases an intracellular cytotoxic payload that kills the antigen-positive cell (e.g., via DNA damage or microtubule disruption leading to apoptosis).
Anti‑HER2 antibody–drug conjugate (RC48) that delivers the microtubule inhibitor MMAE via a cleavable linker; binds HER2 on urothelial tumor cells, is internalized, releases MMAE to disrupt microtubules (G2/M arrest → apoptosis), with potential bystander effect and Fc‑mediated ADCC.
Anti-HER2 antibody–drug conjugate (RC48). The anti-HER2 IgG binds HER2 on tumor cells, is internalized, and a cleavable linker releases MMAE, which inhibits tubulin polymerization to induce G2/M arrest and apoptosis; may also mediate bystander killing and Fc-dependent ADCC.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE that inhibits tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC and bystander effects may also contribute.
Oral, small-molecule, highly selective HER2 tyrosine kinase inhibitor with CNS penetration; blocks HER2 phosphorylation and downstream PI3K/AKT/MAPK signaling.
Oral, selective HER2 (ErbB2) tyrosine kinase inhibitor that blocks HER2 autophosphorylation and downstream PI3K/AKT/MAPK signaling, leading to inhibition of proliferation and survival of HER2-overexpressing tumor cells; possesses CNS penetration supporting activity against brain metastases.
Small-molecule HER2 TKI that blocks HER2 autophosphorylation and PI3K/AKT/MAPK survival signaling, causing cell-cycle arrest and apoptosis of HER2-expressing tumor cells (not immune-mediated).