HighTide Therapeutics Unveils New Data Supporting HTD1801's Renoprotective Effects at ERA 2026
New findings from HighTide Therapeutics show that its lead candidate HTD1801 protects kidney function by targeting podocyte inflammation and apoptosis, offering potential as a disease-modifying therapy for chronic kidney disease.
HighTide Therapeutics, Inc. (2511.HK) presented new preclinical and clinical data at the 63rd European Renal Association (ERA) Congress in Glasgow, UK, demonstrating the renoprotective potential of its lead candidate HTD1801. The findings, delivered in an oral presentation on June 4, 2026, highlight the drug's ability to preserve podocyte viability and reduce glomerular injury, offering insights into its mechanism of action for treating 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 completed 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 clinical results suggest HTD1801 may differentiate from existing therapies by potentially delaying or preventing disease progression.
The new 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 significantly 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.”
HTD1801 is an orally delivered AIMM that 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 comprehensive benefits including improved insulin sensitivity, glycemic control, lipid lowering, renal protection, weight reduction, hepatic improvement, and anti-inflammatory effects. These findings support HTD1801's potential as a foundational therapy in cardiovascular–kidney–metabolic (CKM) disease management. For more information, visit www.hightidetx.com.
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