HighTide Therapeutics Presents New Data Supporting HTD1801's Renoprotective Potential at ERA 2026

HighTide Therapeutics, Inc. (2511.HK) presented new findings on the renoprotective effects of its lead candidate HTD1801 at the 63rd European Renal Association (ERA) Congress in Glasgow, UK. The data, delivered in an oral presentation, provide mechanistic insights into how HTD1801 may protect kidney function and slow disease progression in patients with chronic kidney disease (CKD) and related conditions.

HTD1801 is a first-in-class anti-inflammatory metabolic modulator (AIMM) that targets the AMPK-NLRP3 axis. In completed Phase III trials (SYMPHONY-1 and 2), the drug 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 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 clinical observations suggest that HTD1801 may differentiate from existing therapies and could potentially delay or prevent disease progression.

The 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 mechanistic basis underlying these clinical observations. In glucose- and palmitic acid-induced podocyte injury models, HTD1801 significantly preserved podocyte viability and inhibited apoptosis. The drug 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 important because CKD affects millions worldwide and current treatments often only slow progression rather than halt or reverse kidney damage. HTD1801’s dual mechanism of action—activation of AMPK and inhibition of the NLRP3 inflammasome—targets key pathways in metabolic dysfunction and inflammation, which are central to CKM diseases. By demonstrating renoprotective effects at the cellular level, HTD1801 offers promise as a foundational therapy for CKD.

HighTide Therapeutics is advancing HTD1801 as a potential disease-modifying therapy for CKD and other renal diseases. For more information about the company and its pipeline, visit www.hightidetx.com.