eligibility_summary
Adults 18–75 with CD19+ B-cell NHL (DLBCL, PMBCL, TFL, HGBCL, FL, MCL, MZL) relapsed ≥2L or refractory, prior anti‑CD20+anthracycline (MCL also bendamustine+BTKi). ECOG 0–2, LVEF ≥50%, adequate organs/blood, measurable disease, tissue/biopsy available, survival >3 mo, contraception, ≤G1 prior toxicity. Excludes CNS disease, allo/organ transplant, active malignancy, autoimmune on immunosuppression, infection, recent RT/immuno/cell therapy/trial, pregnancy, major surgery, effusions, allergy, inability to consent.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Interventions: Autologous TRAC locus–inserted CD19-targeting STAR-T cells (gene-edited cellular therapy), plus lymphodepletion with fludarabine and cyclophosphamide. Mechanisms: Using CRISPR/Cas9, the endogenous TRAC is disrupted and a CD19-STAR receptor is knocked in under the TRAC promoter. The STAR receptor grafts the FMC63 anti-CD19 scFv onto TCR α/β constant regions, enabling HLA-independent antigen recognition but signaling through the native TCR–CD3 complex, intracellular OX40 costimulation supports activation, survival, and proliferation. TRAC insertion minimizes random integration and GVHD risk. Fludarabine (purine analog antimetabolite) and cyclophosphamide (alkylating agent) induce lymphodepletion to enhance T-cell expansion. Targets: CD19+ malignant B cells, signaling via TCR–CD3 and OX40 pathways, endogenous TCR ablated to prevent alloreactivity.