eligibility_summary
Eligible: adults >18 with advanced solid tumors (NSCLC, pancreatic, colorectal, others) after standard therapy failure, KRAS G12V/G12D with matching HLA, ECOG ≤2, survival >3 mo, measurable lesion, adequate organ/marrow, contraception. Exclude: brain mets or draining effusion, active TB/HBV/HCV/HIV, pregnancy, uncontrolled comorbidities, major lung/cardiac disease or immunosuppression, transplant, psych/substance, allergy to HSA, cyclophosphamide, fludarabine, IL-2, bleeding/thrombosis risk.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: Autologous KRAS G12V/G12D-specific TCR-engineered T cells (biologic, adoptive cell therapy) given after lymphodepletion, optional second infusion. Mechanism: Patient T cells are genetically modified to express an HLA-A–restricted T-cell receptor recognizing mutant KRAS neoantigens on tumor cells, enabling MHC-restricted cytotoxic killing (perforin/granzyme, cytokines). Conditioning drugs: Cyclophosphamide (alkylating chemotherapy) and fludarabine (purine analog antimetabolite) create lymphodepletion to enhance T-cell engraftment/expansion. Supportive drug: recombinant human IL-2 (cytokine therapy) promotes proliferation/survival of transferred T cells. Targets: Tumor cells bearing KRAS G12V/G12D, antigen presentation via HLA-A, immune pathways of TCR activation/expansion, tumor microenvironment and cytokine dynamics (CRS/neurotoxicity) monitored.