eligibility_summary
Adults ≥18 with ITP ≥3 months, platelets <30×10^9/L, failed steroids and ≥1 second-line (rituximab/TPO-RA). Prior emergency ITP therapy ≥2 weeks earlier. Consent, normal liver/renal, ECOG ≤2, NYHA ≤2. Stable maintenance dose ≥4 weeks, stop other immunosuppressants ≥4 weeks, rituximab >3 months, splenectomy >6 months. Autoantibody positivity not required. Exclude: prior anti-CD38, uncontrolled organ disease/infections (HBV/HCV/CMV/EBV/syphilis), HIV, severe bleeding, cardiac/thrombotic disease, transplants, unresolved toxicity, psychiatric illness, antiplatelets, pregnancy/lactation.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Trial: NCT05694767 (Phase 2, single-arm). Intervention: CM313, an intravenous anti-human CD38 monoclonal antibody (immunotherapy, type: IgG mAb), 16 mg/kg weekly for 8 doses. Mechanism of action: CM313 binds CD38 on plasma cells, depleting long-lived autoreactive plasma cells that produce anti-platelet autoantibodies. By reducing pathogenic autoantibody production, it aims to decrease antibody-mediated platelet destruction and indirectly improve platelet production. Targeted cells/pathways: CD38+ long-lived plasma cells (LLPCs) in the humoral immune pathway responsible for antiplatelet autoantibody generation. Rationale: Addresses ITP refractory to B‑cell–directed therapy (e.g., rituximab) by eliminating plasma cells, a persistent source of pathogenic antibodies. Population: Adult primary ITP patients refractory/relapsed after first-line steroids and at least one second-line therapy (rituximab and/or TPO-RAs).