eligibility_summary
Adults 18–65 with SLE and SLE‑PAH ≤5 yrs, mPAP ≥25, PAWP ≤15, PVR >3 WU, WHO FC II–IV, on stable PAH therapy ≥8 wks (stable ≥4 wks, no change 24 wks). Exclude: recent biologic immunosuppression, severe SLE organ damage, uncontrolled infection, Child‑Pugh B/C or LVEF <45%, 6MWT‑limiting conditions, significant lab abnormalities, SBP <90, non‑SLE PAH, mod/severe obstructive/restrictive lung disease, CTEPH, pregnancy/lactation, cancer <5 yrs, inability to consent, other high risk.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: Rituximab (Hanlikang), an IV chimeric anti‑CD20 monoclonal antibody immunotherapy (1000 mg ×2, 2 weeks apart). Mechanism of action: binds CD20 on pre‑B and mature B cells, depleting them via complement- and antibody‑dependent cytotoxicity and apoptosis. Intended effects: reduce pathogenic autoantibody production, immune complex–driven inflammation, and downstream pulmonary vascular inflammation/remodeling in SLE‑PAH. Targets: CD20+ B cells, downstream pathways include autoantibody/Ig (anti‑U1 RNP, anticardiolipin, IgG subclasses), cytokine networks, and T/B‑cell subset dynamics assessed by multi‑omics (proteomics, RNA‑seq, WES). Background PAH drugs (prostanoids, endothelin receptor antagonists, PDE‑5 inhibitors, sGC stimulators) are maintained but not tested. Primary efficacy endpoint: change in pulmonary vascular resistance at 24 weeks.