ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: PO2541

Long-Term Phase 2 Efficacy of the MASP-2 Inhibitor Narsoplimab for Treatment of Severe IgA Nephropathy

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials


  • Lafayette, Richard A., Stanford University, Stanford, California, United States
  • Carroll, Kevin, KJC Statistics Ltd., Cheshire, United Kingdom
  • Barratt, Jonathan, University of Leicester, Leicester, United Kingdom

Group or Team Name

  • On behalf of the ALC Steering Committee

IgA nephropathy (IgAN) is a glomerular disease in which the lectin pathway of complement is activated following mesangial deposition of IgA immune complexes. Narsoplimab (OMS721) inhibits mannan-binding lectin-associated serine protease-2 (MASP-2), the effector enzyme of the lectin pathway.


A staged Phase 2 study (NCT02682407) enrolled adult patients with severe IgAN. Substudy 1 was a single-arm open-label study of 12 weekly IV infusions of narsoplimab and tapered corticosteroids. In substudy 2, corticosteroid-free patients were randomized 1:1 to receive weekly IV narsoplimab or vehicle infusions for 12 weeks followed by open-label extension. The primary endpoint was safety and tolerability of narsoplimab. Key secondary endpoints were 24-hour urine protein excretion (UPE) and estimated glomerular filtration rate (eGFR) assessed by time-weighted average regression analysis after up to 35 months follow-up. Patients from the Leicester Renal Unit IgA Nephropathy Registry with similar disease burden and matched baseline UPE and eGFR values were used as the comparator group.


This high-risk population with advanced IgAN at enrollment had a median disease duration of 6.9 yrs (range 0.4–27.5). Baseline risk factors included hypertension (10/12, 83%), obesity (7/12, 58%; median BMI 32.5 kg/m2; range 24.4–44.3), excessive proteinuria (median UPE of 4.2 g/24 hr; range 1.5–11.9), and kidney dysfunction (median eGFR of 40.8 mL/min/1.73m2; range 25.4–76.5). 12 patients participated in the dosing extension phase and were followed for a median of 22 months. Patients received median 1 course of 12 weekly doses of narsoplimab per year (range 0.7–2.5 courses), with 58% (7/12) receiving ≤1 course per year. eGFR rate of decline was 5.2 (±2.1) mL/min/yr vs 8.6 (±3.7) mL/min/yr in the Leicester IgAN control cohort, suggesting better eGFR stability in the patient population. Over 3 years, eGFR improved in 25% (3/12) of patients. UPE decreased 38% from baseline through the follow-up period. Narsoplimab was well tolerated with no treatment-related serious adverse events reported.


In this Phase 2 study, narsoplimab was well tolerated. Treatment in patients with severe IgAN resulted in proteinuria reduction and better renal protection via eGFR stability relative to a matched comparator group.


  • Commercial Support