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ERA 2026: HighTide Therapeutics Presents New Findings Supporting HTD1801's Renoprotective Potential in Oral Presentation

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HONG KONG, Jun 5, 2026 - (ACN Newswire) - HighTide Therapeutics, Inc. (2511.HK), an innovative biopharmaceutical company specializing in the development of multifunctional, multi-targeted therapies for cardiovascular–kidney–metabolic (CKM) diseases, today presented new findings on the renoprotective effects of its lead candidate HTD1801 in an oral presentation at the 63rd European Renal Association (ERA) Congress in Glasgow, UK.

HTD1801 is a first-in-class anti-inflammatory metabolic modulator (AIMM) targeting the AMPK-NLRP3 axis. In the completed Phase III trials (SYMPHONY-1 and 2), HTD1801 demonstrated significant improvement in renal function in patients with Type 2 Diabetes Mellitus (T2DM) and baseline eGFR of 60–90 mL/min/1.73m².  Treatment of these patients with HTD1801 resulted in a mean increase of +3.08 mL/min/1.73m² in eGFR after 52 weeks (95% CI: 0.46–5.70), without evidence of hyperfiltration or fluid retention. These findings suggest that HTD1801 may differentiate from existing therapies, with the potential to delay or prevent disease progression.

This study was conducted by HighTide Therapeutics in collaboration with the research team led by Academician Jiandong Jiang at the Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences, and further explored the mechanistic basis underlying these clinical observations. In glucose- and palmitic acid-induced podocyte injury models, HTD1801 significantly preserved podocyte viability and inhibited apoptosis. HTD1801 also restored expression of the key podocyte structural proteins nephrin and podocin, while reducing the levels of the inflammatory marker phosphorylated NF-κB and the apoptosis executioner caspase-3. In a diabetic nephropathy (DN) model, HTD1801 demonstrated dose-dependent improvements in renal architecture, reduced tubular injury scores, attenuated renal inflammatory and fibrotic changes, and drove a robust decrease in 24-hour urinary microalbumin.

The study systematically demonstrated that HTD1801 suppresses podocyte inflammation and apoptosis while stabilizing glomerular structure, providing the latest findings supporting its renoprotective potential. These findings provide important scientific rationale for the development of HTD1801 as a potential disease-modifying therapy for chronic kidney disease (CKD) and other renal diseases.

Abstract Title: HTD1801 Attenuates Podocyte Apoptosis and Glomerular Injury: Mechanistic Insights into RenoprotectionPresentation Number: 2243Presentation Date/Time: Thursday, June 4, 2026, 8:15 a.m. BSTFormat: Oral PresentationSpeaker: Dr. Filip Surmont, Chief Medical Officer of HighTide Therapeutics

“This study provides the first evidence into the renoprotective effects of HTD1801 at the podocyte and glomerular levels. The convergence of clinical and preclinical data further supports the disease-modifying potential of HTD1801 and its ability to target fundamental pathophysiologic processes in CKD or other renal diseases,” said Dr. Filip Surmont, Chief Medical Officer of HighTide Therapeutics. “We will continue advancing the clinical development of HTD1801 across CKD and related indications to provide more treatment options for patients worldwide.”

About HTD1801

HTD1801 is a first-in-class new molecular entity that targets the residual risks underlying cardiovascular–kidney–metabolic (CKM) diseases. It is an orally delivered, anti-inflammatory metabolic modulator (AIMM) that, as a single molecule, exerts a unique dual mechanism of action through activation of AMP Kinase and inhibition of the NLRP3 inflammasome, two complementary pathways that mitigate metabolic dysfunction. Multiple global clinical studies have demonstrated the comprehensive benefits of HTD1801, including improved insulin sensitivity, glycemic control, lipid lowering, renal protection, weight reduction, hepatic improvement, and anti-inflammatory effects. Collectively, these findings support the potential of HTD1801 to serve as a foundational therapy in CKM disease management.  




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