Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and a significant contributor to the global burden of kidney failure, requiring dialysis or transplant. HSK39297 is a once-daily, oral, highly potent, selective small-molecule inhibitor of complement factor B (CFB) developed for the treatment of IgAN. Herein, we report efficacy and safety data up to Week 12 from the ongoing Phase II trial of HSK39297.
This study is a multicenter, randomized, double-blind, placebo-controlled Phase II trial (NCT06670352). Patients with biopsy-confirmed primary IgAN, estimated glomerular filtration rate (eGFR) ≥30 mL/min per 1.73 m², and persistent proteinuria (urine protein≥0.75g/24h or first morning void (FMV) UPCR≥0.8g/g at screening) despite optimal supportive therapy, were randomized (1:1:1:1) to receive HSK39297 50mg BID, 100mg BID, 200mg QD, or placebo for 24 weeks. The primary endpoint was the ratio of 24-hour urine protein-to-creatinine (24h-UPCR) at Week 12 relative to baseline. Other efficacy, safety and biomarker parameters were also assessed.
Eighty-seven patients were randomized to the HSK39297 50mg BID (n=21), 100mg BID (n=21), 200mg QD (n=24) and placebo (n=21) groups. Baseline characteristics were generally well balanced across treatment arms. The ratio of 24h-UPCR (g/g) at Week 12 relative to baseline for the HSK39297 50mg BID, 100mg BID, and 200mg QD groups were -52.3%, -52.5%, and -48.2%, respectively, compared to -5.3% in the placebo group (Figure 1). The reductions relative to placebo were -49.6%, -49.8%, and -45.3% (P＜0.0001, ＜0.0001, and =0.0001, respectively). Additionally, all other urine protein related endpoints were met (Figure 2). The eGFR remained stable over time.The inhibitory effect on AP activity increased with higher doses of HSK39297. Based on trough concentration data, the change from baseline in AP activity in the 50 mg BID, 100 mg BID, and 200 mg QD groups was approximately -64%, -85%, and -79%, respectively (Figure 3).The safety profile of HSK39297 was like placebo, most treatment-emergent adverse events (TEAEs) were mild or moderate. In the overall HSK39297 treatment group, TEAEs with an incidence ≥5% included upper respiratory tract infection (9.1% vs. placebo 0%). No adverse events leading to treatment discontinuation or serious adverse events were reported in the investigational drug group.
Consistent with its mechanism of action, HSK39297 once-daily treatment demonstrated a clinically meaningful and highly statistically significant reduction in proteinuria compared to placebo at 12 weeks in patients with IgAN. These findings suggest that HSK39297 may reduce the risk of IgAN progression. The results strengthen the therapeutic rationale for selective CFB inhibitors and further support the evaluation of HSK39297 in Phase III clinical trials for the treatment of IgAN.
