ASNRT — Arab Society of Nephrology and Renal Transplantation

النسخة العربية من هذه الصفحة

Efficacy and Safety of Sparsentan in Patients with FSGS: Results from the Pivotal Phase 3 DUPLEX-3 Study

In the phase 3 DUPLEX trial of 371 patients with focal segmental glomerulosclerosis (FSGS), sparsentan — a single-molecule dual endothelin–angiotensin receptor antagonist — produced significantly greater and more durable proteinuria reduction than irbesartan, although the two drugs did not differ significantly on the primary eGFR-slope endpoint at 108 weeks.

Background

FSGS is a podocyte injury pattern that frequently progresses to kidney failure, and effective non-immunosuppressive therapies remain an unmet need. Sparsentan blocks both the endothelin type-A receptor and the angiotensin II type-1 receptor in one molecule, simultaneously targeting two pathways that drive glomerular injury and proteinuria.

Study design

DUPLEX (NCT03493685) was an international, randomized, double-blind, active-controlled phase 3 trial. 371 patients aged 8–75 with biopsy-proven or genetic FSGS were assigned 1:1 to sparsentan 800 mg/day or irbesartan 300 mg/day for 108 weeks. The primary endpoint was eGFR slope; a key surrogate was FSGS partial remission of proteinuria (urine protein-to-creatinine ratio ≤1.5 g/g with a >40% reduction from baseline).

Key findings

At the 36-week interim analysis, 42.0% of sparsentan-treated patients achieved partial remission of proteinuria versus 26.0% with irbesartan (P=0.009), and this antiproteinuric advantage was sustained through 108 weeks. However, there was no significant between-group difference in eGFR slope at week 108. The two drugs had similar safety profiles and adverse-event frequencies.

Clinical implications

Sparsentan delivers a robust, durable antiproteinuric effect beyond standard angiotensin-receptor blockade in FSGS, reinforcing its role where lowering proteinuria is the goal. The absence of a measurable eGFR-slope benefit over 108 weeks highlights how difficult it remains to demonstrate hard kidney-function gains in this heterogeneous disease, and supports proteinuria reduction — linked in DUPLEX to lower kidney-failure risk — as a meaningful treatment target.

Category

Research

Source

NEJM

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