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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Alport syndrome is a rare genetic disease resulting from collagen IV abnormalities and is marked by interstitial fibrosis and declining kidney function. Fibrosis prevention may preserve kidney function. We report safety and preliminary efficacy findings with setanaxib, an enzyme-driven hydrogen peroxide-depleting agent with anti-fibrotic properties, in patients with Alport syndrome.
In this Phase 2a trial (NCT06274489), 20 patients (12–40 years) with genetically confirmed Alport syndrome, UPCR ≥0.8 g/g, eGFR ≥30 mL/min/1.73 m2 and at risk of disease progression despite background therapy were randomized 2:1 to receive oral setanaxib (800 mg BID [18–40 years]/800 + 400 mg/day [12–17 years]; n=13) or placebo (n=7) plus background therapy for 24 weeks. Primary endpoints were serious adverse events (SAEs) and AEs of special interest (AESIs); secondary endpoints included changes in UPCR and eGFR from baseline. After 24 weeks, patients were followed for 4 weeks on background therapy alone. Of the background therapies allowed, 16 patients were on ACEis (11 setanaxib, 5 placebo), 11 on SGLT2is (7 setanaxib, 4 placebo) and 10 on both (7 setanaxib, 3 placebo).
One randomized patient in the placebo group withdrew consent before treatment start. AEs occurred at similar frequencies in both treatment groups. Primary endpoints were met: 1 setanaxib group patient had an SAE of acute cholecystitis that was not deemed treatment related by the investigator, and no AESIs were reported. The setanaxib group had a 15% mean UPCR reduction at 24 weeks versus placebo. Two (15.4%) setanaxib group patients had a UPCR reduction of ≥25% from baseline at 24 weeks, versus none in the placebo group. An ad hoc analysis showed that 5 (38.5%) setanaxib group patients had a UPCR reduction of ≥10% versus baseline, compared with 1 (16.7%) placebo group patient. The setanaxib group also had a 27% mean UPCR reduction at 4 weeks post dosing versus placebo. There was a 5% mean reduction in eGFR with setanaxib versus placebo at 24 weeks and a 4% reduction at 4 weeks post dosing.
In patients with Alport syndrome, setanaxib plus background therapy had an acceptable safety profile with a trend towards UPCR reduction after 24 weeks of dosing and at 4 weeks post dosing versus background therapy alone.
This abstract was also submitted for the American Society of Nephrology Kidney Week 2025 congress.