eligibility_summary
Patients with unresectable/metastatic colorectal adenocarcinoma, KRAS/NRAS (G12/G13) and BRAF V600 wild type, measurable disease (RECIST 1.1), ECOG 0–1, progressed after 1 prior fluoropyrimidine+oxaliplatin line (anti‑VEGF allowed), agree to provide tumor tissue. Exclude ILD/pneumonitis, hypersensitivity to amivantamab/cetuximab/bevacizumab/FOLFIRI, interfering second cancer, untreated dMMR/MSI‑H, HER2+, prior irinotecan or EGFR/MET therapy.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Trial: Phase 3, RAS/RAF wild-type recurrent/metastatic colorectal cancer, Amivantamab+FOLFIRI vs Cetuximab or Bevacizumab+FOLFIRI. Interventions and mechanisms: • Amivantamab (biologic, bispecific IgG1 mAb) targets EGFR and MET, blocks ligand binding and signaling, promotes receptor internalization/degradation, and mediates ADCC. • Cetuximab (biologic, chimeric IgG1 anti‑EGFR mAb) inhibits EGFR signaling and can induce ADCC. • Bevacizumab (biologic, humanized IgG1 anti‑VEGF‑A mAb) neutralizes VEGF‑A to inhibit angiogenesis. • 5‑Fluorouracil (drug, antimetabolite) inhibits thymidylate synthase and incorporates into RNA/DNA. • Leucovorin (folinic acid) stabilizes the 5‑FU–TS complex, enhancing 5‑FU activity. • Irinotecan (drug, prodrug to SN‑38) inhibits topoisomerase I, causing DNA damage. Targeted cells/pathways: tumor epithelial cells with EGFR/MET (RAS/MAPK and PI3K/AKT), endothelial/angiogenic pathway via VEGF‑VEGFR, DNA synthesis/repair (TS, Topo I), and immune effector-mediated ADCC.