eligibility_summary
Inclusion: consent, 18–75, HLA‑A02:03+, AFP+ HCC/solid tumor post ≥1 line, AFP IHC+ or serum ≥400 ng/mL, BCLC B/C, Child‑Pugh ≤7, ECOG 0–1, ≥4‑mo survival, measurable lesion, adequate labs/organ fxn, contraception, HCG−. Exclusion: unresolved tox >G1, CV/CNS dz, autoimmune on immunosupp, drug allergy, encephalopathy, transplant, recent GI bleed, coagulopathy, infxn/fever, sympt. CNS mets, HIV/syphilis/active HCV, HBV‑DNA ≥2000 IU/mL, pregnant/lactating, uncontrolled DM, lung dz or liver failure.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Interventions: HRYZ-T102, an autologous AFP-specific TCR-engineered T cell therapy (TCR-T), given IV after lymphodepleting chemotherapy with fludarabine (purine analog antimetabolite) and cyclophosphamide (alkylating agent). Mechanisms: TCR-T cells express a high-affinity T-cell receptor that recognizes an AFP-derived peptide presented by HLA-A02:03 on tumor cells, inducing MHC-restricted T-cell activation and cytotoxic killing (perforin/granzyme, cytokines). Fludarabine/cyclophosphamide deplete host lymphocytes (including Tregs) to enhance engraftment, expansion, and persistence of infused cells. Targets: AFP-positive hepatocellular carcinoma and other AFP+ solid tumors, key pathways/cells include AFP antigen presentation via HLA-A02:03, TCR signaling in CD8+ T cells, and tumor cell apoptosis/lysis.