eligibility_summary
Adults 18–75, ECOG 0–1, advanced CRC with HER2 expression/amplification/mutation after failure/intolerance of ≥2nd-line therapy, ≥1 measurable lesion (RECIST 1.1) with imaging ≤28 days, survival ≥12 wks, adequate marrow/organ function (incl. CrCl ≥50 mL/min), LVEF ≥50%, QTcF <470 ms (women), contraception and consent. Exclude recent major surgery, cardiac disease/uncontrolled HTN, absorption issues, drug allergy, HIV/HBV/HCV, pregnancy/lactation, other antitumor therapy/trials, serious comorbidity.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Interventions: Disitamab vedotin (RC48) plus fruquintinib. Disitamab vedotin is an antibody–drug conjugate (ADC): a humanized anti‑HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE), a microtubule‑disrupting cytotoxic. It binds HER2 on tumor cells, is internalized, and releases MMAE to cause mitotic arrest/apoptosis, the permeable payload confers a bystander killing effect. Fruquintinib is an oral small‑molecule tyrosine kinase inhibitor highly selective for VEGFR‑1/2/3, inhibiting VEGF‑driven angiogenesis. Targets/pathways: HER2 (ERBB2)-expressing or mutated colorectal cancer cells, microtubule dynamics via MMAE, tumor endothelial cells via VEGFR signaling, reducing tumor vascularization. Combination aims to directly kill HER2+ tumor cells and starve tumors by anti‑angiogenic blockade.