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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.
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Abstract titles should be brief and reflect the content of the abstract.
Alternative complement pathway overactivation is seen in IgAN and is believed to contribute to glomerular inflammation and disease progression. Iptacopan is a highly potent, oral, factor B inhibitor of the alternative complement pathway. At the Month (M)9 interim analysis (n=250) of APPLAUSE-IgAN, iptacopan resulted in a 24‑hour urine protein–creatinine ratio (24h‑UPCR) reduction of 38.3% vs placebo (pbo) and a promising safety profile. We report the final results of APPLAUSE-IgAN.
APPLAUSE-IgAN was a double-blind, Phase III trial in adults with biopsy-proven IgAN and 24h‑UPCR ≥1 g/g despite optimized supportive care (NCT04578834). Patients (pts) had an estimated glomerular filtration rate (eGFR) ≥30 mL/min/1.73 m2 and were randomized 1:1 to iptacopan 200 mg bid or matching pbo. The primary endpoint at this final analysis was the annualized total eGFR slope estimated over 24 months. Secondary endpoints were time to first composite kidney failure endpoint event (sustained ≥30% eGFR decline vs baseline, sustained eGFR <15 mL/min/1.73 m2, maintenance dialysis, kidney transplant, or death from kidney failure), proportion of pts reaching 24h-UPCR <1 g/g at M9, change from baseline in Functional Assessment of Chronic Illness Therapy (FACIT)–Fatigue to M9, and safety.
In this trial, 238 and 239 pts received iptacopan and pbo, respectively. Mean baseline eGFR (standard deviation) was 63.4 (25.5) and 65.6 (26.5) mL/min/1.73 m2, and baseline median 24h-UPCR (interquartile range) was 1.7 (1.3, 2.4) and 1.8 (1.5, 2.6) g/g in the iptacopan and pbo arms, respectively. Iptacopan-treated pts had a statistically significant slower eGFR decline vs pbo (Figure). The annualized total eGFR slope (95% confidence interval [CI]) was −3.10 (−3.80, −2.40) with iptacopan and −6.12 (−6.83, −5.41) mL/min/1.73 m2/year with pbo, resulting in a treatment difference of 3.02 mL/min/1.73 m2/year in favor of iptacopan (95% CI 2.02, 4.01; P<0.0001). The composite kidney failure endpoint was reached by 21.4% (51/238) of pts on iptacopan vs 33.5% (80/239) on pbo (hazard ratio 0.57 [95% CI 0.40, 0.81]; P=0.0015). The proportion of pts reaching 24h-UPCR <1 g/g at M9 (95% CI) was 43.9% (38.0, 49.8) with iptacopan vs 17.5% (12.7, 22.4) with pbo (odds ratio 4.45 [95% CI 2.79, 7.09]; P<0.0001). The change from baseline to M9 in FACIT-Fatigue was similar between arms (iptacopan: 1.07 [95% CI 0.23, 1.91]; pbo: 0.31 [−0.54, 1.16]; mean difference: 0.76 [−0.43, 1.95]; P=0.11). Treatment-emergent adverse events (TEAEs) occurred in 87.0% (207/238) of pts on iptacopan and 89.1% (213/239) on pbo; the majority of TEAEs were mild or moderate in severity. Infections possibly caused by encapsulated bacteria occurred in 10 and eight pts on iptacopan and pbo, respectively. TEAEs led to treatment discontinuation in 11 pts in each arm, and there were no deaths.
In APPLAUSE-IgAN, iptacopan demonstrated a statistically significant and clinically important slowing in the rate of kidney function decline, as shown by the annualized total eGFR slope estimated over 24 months and by the lower percentage of pts reaching the composite kidney failure endpoint compared with pbo. Iptacopan also reduced proteinuria, was well tolerated, and had similar rates of TEAEs to pbo. The results demonstrate the clinical benefit of sustained alternative complement pathway inhibition with iptacopan in pts with IgAN.
