eligibility_summary
Adults 18–75 with advanced solid tumors, measurable disease, failed/untolerated standard therapy, HLA‑A11:01+ & KRAS G12V+, ECOG 0–1, >6‑mo life expectancy, and adequate cardiac/organ function, contraception required. Exclude recent anti‑cancer therapy, prior KRAS G12V‑targeted or gene/cell therapy, drug allergy, unresolved ≥G2 AEs, major CV/QTc issues, active infection/autoimmune disease, immunosuppression, symptomatic brain mets, bleeding/thrombosis, effusions, live vaccine, transplants, uncontrolled illness, substance abuse, pregnancy/breastfeeding.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: RE002, an autologous, gene-edited TCR-T cell therapy (biological/cellular therapy) engineered to express an HLA-A11:01–restricted TCR specific for the KRAS G12D neoantigen. Single infusion with 3+3 dose escalation (4×10^9, 8×10^9, 1.6×10^10 cells), optional second infusion. Preconditioning: cyclophosphamide (alkylating agent) and fludarabine (purine analog) for lymphodepletion to enhance T‑cell engraftment and reduce suppressive immune cells. Mechanism: RE002 T cells recognize KRAS G12D peptide presented on MHC I of tumor cells and mediate antigen-specific cytotoxicity. Targets: KRAS G12D–mutant solid tumor cells via HLA-A11:01 peptide–MHC complexes, immune effector pathway is TCR signaling and CD8+ T-cell cytotoxicity.