eligibility_summary
Adults 18–<70 with biopsy‑proven AL amyloidosis involving heart/kidney/liver, relapsed/refractory, dFLC>50 mg/L, ECOG≤2, survival ≥12 wks, adequate marrow/renal/hepatic/coagulation, LVEF≥50%, NT‑proBNP<1800, contraception if fertile. Exclude prior gene therapy, recent live vaccine/investigational drugs, active infections (HBV/HCV/HIV/CMV/syphilis), severe CV disease/uncontrolled HTN, unresolved toxicity, recent/planned major surgery, transplant, pregnancy, CNS disease, bleeding/thrombosis risk.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: FKC288, an autologous dual-target chimeric antigen receptor T-cell (CAR-T) therapy directed at BCMA and CD19. Type: Cellular immunotherapy (gene-modified T cells). Mechanism of action: Patient T cells are collected, engineered ex vivo to express CARs recognizing BCMA (on plasma cells) and CD19 (on B-lineage cells), then reinfused after fludarabine/cyclophosphamide lymphodepletion. Upon antigen binding, CAR-T cells activate and lyse BCMA+/CD19+ cells, aiming to eradicate the clonal plasma/B-cell populations that produce amyloidogenic light chains. Cells/pathways targeted: clonal plasma cells and B cells, BCMA pathway involved in plasma-cell survival, CD19-associated B-cell signaling. Goal: reduce serum free light chains and reverse organ involvement in relapsed/refractory systemic AL amyloidosis.