Travere Presents New Biomarker Data at ASN Kidney Week Suggesting FILSPARI® (sparsentan) May Modify Underlying Disease Pathophysiology in IgA Nephropathy
FILSPARI achieved greater reductions in biomarkers linked to kidney inflammation and injury than maximum labeled dose irbesartan
Findings provide further evidence of the biological effects of dual endothelin and angiotensin receptor antagonism and support FILSPARI as foundational treatment in IgAN
SAN DIEGO, October 23, 2026--Travere Therapeutics, Inc. (Nasdaq: TVTX) today presented new biomarker data from the Phase 3 PROTECT Study providing evidence that FILSPARI® (sparsentan) may modify the underlying disease pathophysiology in people with IgA nephropathy (IgAN). Data were shared today in an oral presentation at the American Society of Nephrology (ASN) Kidney Week 2026 in Denver, CO.
"These biomarker data provide new insight into how FILSPARI's dual mechanism of action may modify the underlying biology of IgA nephropathy," said Jula Inrig, M.D., chief medical officer of Travere Therapeutics. "When considered alongside the PROTECT results which demonstrated superior proteinuria reduction and a slower rate of kidney function decline compared with maximum labeled dose irbesartan, as well as published real-world evidence showing consistent outcomes in clinical practice, the totality of evidence supports the use of FILSPARI as a non-immunosuppressive, kidney-targeted, foundational first-line treatment for IgA nephropathy."
The Phase 3 PROTECT Study was a global, randomized, multicenter, double-blind, active-controlled clinical trial evaluating the safety and efficacy of FILSPARI, compared to irbesartan in 404 adult patients with IgAN. Of the overall study population, 295 patients participated in the biomarker analysis. Across measured time points through Week 110, FILSPARI led to rapid and sustained reductions in all four urinary biomarkers evaluated.
"These findings extend the exploratory signal observed in SPARTAN and show in a larger, randomized study that dual endothelin and angiotensin receptor antagonism may modulate several biological pathways associated with IgAN pathophysiology," said Chee Kay Cheung, M.B.Ch.B., Ph.D., consultant nephrologist at University Hospitals of Leicester NHS Trust.
At Week 110, least-squares mean percent changes from baseline, normalized to urine creatinine, were greater with FILSPARI than with irbesartan (reported p values are nominal):
sCD163, a marker of macrophage activation, decreased 60.1% with FILSPARI versus 26.0% with irbesartan, representing a 46.1% difference between treatment arms (p<0.001).
BAFF, a marker of B-cell activation and survival, decreased 64.4% with FILSPARI versus 45.2% with irbesartan, representing a 34.9% difference between treatment arms (p=0.02).
C5b-9, a marker of complement pathway activation, decreased 50.2% with FILSPARI versus 7.3% with irbesartan, representing a 46.3% difference between treatment arms (p=0.032).
IL-6, a pro-inflammatory cytokine, decreased 45.4% with FILSPARI versus an 8.7% increase with irbesartan, representing a 49.7% difference between treatment arms (p<0.001).