eligibility_summary
Adults ≥18, CFS<7, new RPGN from AAV within 45 days (eGFR 10–50 plus proteinuria/hematuria), ANCA+ (MPO/PR3), weight ≤130 kg, consent and renal biopsy (recent or by Week 6), not pregnant/lactating, contraception/donation rules apply. Exclude: prior RPGN, anti-GBM+, active/chronic infection incl. TB, HBV/HCV/HIV, prohibited meds/excess steroids/avacopan, recent trials/vaccines, major comorbidity, autoimmune dermatoses, SLE-AAV/EGPA, poor venous access, unrecovered from surgery, substance abuse, recent cancer, hypoxic alveolar hemorrhage, recent dialysis/plasma exchange, hypersensitivity.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
NCT06047171 (RENAL-F02) tests ALE.F02 plus standard therapy vs placebo in ANCA-associated vasculitis with rapidly progressive glomerulonephritis. Interventions and mechanisms: 1) ALE.F02: biological drug, anti–Claudin-1 (CLDN1) monoclonal antibody that selectively binds the non–tight-junction–exposed form of CLDN1, aiming to protect kidney tissue (nephrons). 2) Rituximab: monoclonal antibody against CD20, depletes pre-B and mature B cells to reduce ANCA production. 3) Glucocorticoids: steroid hormones activating the glucocorticoid receptor, broad anti-inflammatory/immunosuppressive effects. 4) Cyclophosphamide: alkylating agent, cytotoxic immunosuppression. 5) Placebo. Targeted cells/pathways: CLDN1-expressing cells in renal tissue (tight-junction CLDN1 pathway), B lymphocytes via CD20, immune/inflammatory signaling via glucocorticoid receptor, and proliferating immune cells via DNA alkylation, overall aimed at attenuating ANCA-mediated small-vessel renal injury.