eligibility_summary
Incl: R/M HNSCC (oral/oro/hypo/larynx) after PD‑1 and/or platinum failure, measurable disease, known p16 and PD‑L1, ECOG 0–1, life ≥3 mo, adequate marrow/liver/renal/coag, LVEF ≥50, contraception, consent. Excl: prior 1L cetuximab, ≥G2 neuropathy, need other therapy/surgery, recent chemo/IO/RT, active CNS mets, ulcerated lesions, unresolved tox, recent VTE, uncontrolled illness/bleeding, active HBV/HCV/HIV/infection, live vaccine <30 d, severe lung disease, uncontrolled effusions, pregnancy/breastfeeding.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Trial: Single-arm Phase II in recurrent/metastatic HNSCC after PD‑1/L1 and/or platinum failure. Interventions: AK117 (anti‑CD47) + an anti‑EGFR antibody (cetuximab‑like). Type: Both are monoclonal antibodies. Mechanisms: AK117 blocks the CD47–SIRPα innate immune checkpoint (“don’t‑eat‑me” signal), restoring macrophage phagocytosis and enhancing antigen presentation with downstream T‑cell priming. The anti‑EGFR mAb binds EGFR on tumor cells to inhibit ligand‑driven signaling (RAS/MAPK, PI3K/AKT) and elicits Fc‑dependent cytotoxicity (ADCC by NK cells, ADCP by macrophages). Targets: tumor EGFR, tumor/stromal CD47, effector cells include macrophages, dendritic cells, NK cells, with secondary activation of cytotoxic T cells. Rationale: EGFR‑opsonization plus CD47 blockade synergize to boost myeloid clearance and antitumor immunity.