GLASGOW and HONG KONG – HighTide Therapeutics, Inc. (2511.HK), a biopharmaceutical company focused on cardiovascular–kidney–metabolic (CKM) diseases, 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 mechanistic studies, suggest that HTD1801 may delay or prevent progression of chronic kidney disease (CKD) and related renal conditions.
HTD1801 is a first-in-class anti-inflammatory metabolic modulator (AIMM) that targets the AMPK-NLRP3 axis. In the Phase III SYMPHONY-1 and SYMPHONY-2 trials, patients with Type 2 Diabetes Mellitus (T2DM) and baseline eGFR of 60–90 mL/min/1.73m² experienced a mean increase of +3.08 mL/min/1.73m² in eGFR after 52 weeks of treatment (95% CI: 0.46–5.70), without evidence of hyperfiltration or fluid retention. These clinical results indicate that HTD1801 may offer renal benefits distinct 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 biological basis for these observations. In glucose- and palmitic acid-induced podocyte injury models, HTD1801 preserved podocyte viability and inhibited apoptosis. It also restored expression of key podocyte structural proteins nephrin and podocin, while reducing levels of the inflammatory marker phosphorylated NF-kB 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.
“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.”
The findings are significant because CKD affects millions worldwide and is a major contributor to morbidity and mortality. Current treatments often slow but do not halt disease progression. HTD1801’s dual mechanism of action – activating AMP Kinase and inhibiting the NLRP3 inflammasome – targets two complementary pathways that mitigate metabolic dysfunction. This approach may offer a foundational therapy for CKM disease management, addressing residual risks that persist with standard care.
For more information about HighTide Therapeutics and HTD1801, visit www.hightidetx.com. View the original release on www.newmediawire.com.
