eligibility_summary
Adults 18–75 with unresectable/advanced solid tumors lacking options, HLA-A11:01+, KRAS G12V (NW-301V) or G12D (NW-301D), ECOG 0–1, measurable disease, adequate organ function. Exclude: recent chemo/biologics/immunosuppressants near apheresis/lymphodepletion, allergy to cyclophosphamide/fludarabine or components, severe/active autoimmune disease, symptomatic CNS or leptomeningeal mets, active infection or HIV/HBV/HCV/syphilis, pregnant/breastfeeding.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Interventions and mechanisms: Two autologous TCR-engineered T cell therapies. NW-301V targets KRAS G12V, NW-301D targets KRAS G12D. Type: adoptive cellular gene therapy (TCR-T). Mechanism: patient T cells are transduced with a high-affinity TCR that recognizes KRAS G12V or G12D neoantigen peptides presented by HLA-A11:01 on tumor cells. After lymphodepletion (cyclophosphamide + fludarabine) and low-dose IL-2 support, infused T cells expand, engage peptide–MHC I, and mediate cytotoxic killing (perforin/granzyme). Cells/pathways targeted: HLA-A11:01–positive advanced solid tumor cells bearing KRAS G12V or G12D mutations, oncogenic RAS/MAPK pathway–driven tumors. Immune pathways engaged: TCR signaling, MHC I antigen presentation, CD8+ T cell cytotoxicity, and IL-2–driven proliferation.