eligibility_summary
Adults 18–80 with AML or high/intermediate‑risk MDS/CMML that is relapsed/refractory or MRD>0.1% after ≥2 lines (incl HMA+ven), HLA‑A02:01+, KPS>50, adequate organs (EF≥40). ≥7 d from cytotoxic chemo, TKIs stop 3 d prior. Key exclusions: pregnancy/lactation, uncontrolled infection, HBV/HCV or HIV viremia, active GVHD, recent surgery<4 wk or allo SCT/DLI<12 wk, steroids/immunosuppression. Before LD/infusion: afebrile 48 h, no ≥G3 toxicity, off steroids, SpO2>92%, no heart failure/rapid progression.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: PRAME‑TCR‑NK cells—engineered allogeneic cord blood–derived natural killer cells expressing an HLA‑A02:01–restricted T‑cell receptor specific for the cancer‑testis antigen PRAME. Mechanism: TCR‑mediated, antigen‑specific recognition of PRAME peptide–HLA complexes on myeloid blasts, triggering NK cytotoxicity (perforin/granzyme) and potential in vivo expansion/persistence. Conditioning co‑therapies: decitabine (DNA hypomethylating nucleoside analog) to epigenetically upregulate PRAME/HLA class I, fludarabine (purine analog) and cyclophosphamide (alkylator) for lymphodepletion to reduce host immunity and improve NK engraftment, dexamethasone (glucocorticoid) to mitigate inflammatory/toxic reactions. Targets and pathways: PRAME+ AML/MDS/CMML cells, HLA‑A02:01 antigen presentation, TCR/NK activation pathways, host lymphocyte depletion (Flu/Cy).