HighTide Therapeutics Presents New Data Showing HTD1801’s Renoprotective Effects at ERA 2026

HighTide Therapeutics, Inc. (2511.HK) 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. The data, drawn from completed Phase III trials and preclinical studies, show that HTD1801 significantly improves kidney function and targets fundamental mechanisms of chronic kidney disease (CKD).

In the Phase III trials SYMPHONY-1 and 2, patients with Type 2 Diabetes Mellitus (T2DM) and baseline eGFR of 60–90 mL/min/1.73m² treated with HTD1801 experienced 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 results suggest that HTD1801 may slow or prevent disease progression, differentiating it from existing therapies.

The mechanistic study, conducted in collaboration with the research team led by Academician Jiandong Jiang at the Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences, explored the underlying biology. In glucose- and palmitic acid-induced podocyte injury models, HTD1801 preserved podocyte viability and inhibited apoptosis. It also restored expression of key structural proteins nephrin and podocin while reducing levels of inflammatory marker phosphorylated NF-kB and the apoptosis executioner caspase-3. In a diabetic nephropathy model, HTD1801 dose-dependently improved renal architecture, reduced tubular injury scores, attenuated inflammatory and fibrotic changes, and decreased 24-hour urinary microalbumin.

“This study provides the first evidence into the renoprotective effects of HTD1801 at the podocyte and glomerular levels,” said Dr. Filip Surmont, Chief Medical Officer of HighTide Therapeutics. “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.”

HTD1801 is a first-in-class anti-inflammatory metabolic modulator (AIMM) targeting the AMPK-NLRP3 axis. It is an orally delivered molecule that activates AMP Kinase and inhibits the NLRP3 inflammasome, addressing multiple aspects of cardiovascular–kidney–metabolic (CKM) diseases. The findings presented at ERA add to a growing body of evidence supporting HTD1801’s potential as a foundational therapy in CKM management. HighTide plans to continue advancing HTD1801 across CKD and related indications. For more information, visit www.hightidetx.com.

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