Abstract: FR-PO0506
Baxdrostat Effects in CKD with Uncontrolled Hypertension: Biomarker Analysis Results from the Phase 2 FigHTN Trial
Session Information
- CKM: Clinical - Trials, Epidemiology, and Biomarkers
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Cardiovascular-Kidney-Metabolic Health
- 602 Cardiovascular-Kidney-Metabolic Health: Clinical
Authors
- Whatling (née Reznichenko), Anna, Late-Stage Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden
- Chertow, Glenn M., Departments of Medicine, Epidemiology and Population Health, and Health Policy Division of Nephrology, Stanford University School of Medicine, Stanford, California, United States
- Zaozerska, Nataliia, Late-Stage Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Warsaw, Poland
- Myte, Robin, Biometrics, Late-Stage Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden
- Heerspink, Hiddo Jan L., Department of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Centre Groningen, Groningen, Netherlands
- Little, Dustin J., Late-Stage Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, Maryland, United States
- Dwyer, Jamie P., Division of Nephrology & Hypertension, University of Utah, Salt Lake City, Utah, United States
Background
Baxdrostat is a selective aldosterone synthase inhibitor in development with dapagliflozin for the treatment of patients with chronic kidney disease (CKD) and hypertension (HTN). In the phase 2 FigHTN trial, baxdrostat demonstrated clinically relevant reductions in systolic blood pressure (SBP) and urinary albumin-to-creatinine ratio (UACR) vs placebo among participants with CKD and uncontrolled HTN. To further characterize the effect of baxdrostat, we performed biomarker analyses evaluating urinary levels of kidney injury molecule-1 (KIM-1), lipocalin-2 (NGAL), and cystatin C (cysC).
Methods
Adults with estimated glomerular filtration rate (eGFR) 25–75 mL/min/1.73 m2, UACR ≥100 mg/g, and SBP ≥140 mmHg (without type 2 diabetes) or ≥130 mmHg (with type 2 diabetes) were randomized (1:1:1) to baxdrostat low-dose (0.5 mg up-titrated to 1 mg), high-dose (2 mg up-titrated to 4 mg), or placebo for 26 weeks (double-blind). 24-hour urine samples were collected at baseline, Week 16, and Week 26. Biomarker concentrations were measured centrally using specific immunoassays. Change from baseline in log-transformed values normalized to creatinine were analyzed using mixed models for repeated measures.
Results
Overall, 195 participants were randomized (mean age 66, mean baseline eGFR 44 mL/min/1.73 m2, mean baseline SBP 151.2 mm Hg, mean/median UACR 1172/714 mg/g). eGFR was numerically reduced with initial baxdrostat treatment vs placebo from baseline to Week 26 (–2.3 mL/min/1.73m2 [95% CI: –5.1, 0.5]). In total, 186 participants were included in the biomarker analysis (baseline: baxdrostat pooled set n=124, placebo n=62; Week 26: baxdrostat n=97, placebo n=44). At baseline, biomarker levels were similar between baxdrostat and placebo groups. From baseline to Week 26, placebo-corrected least-square mean changes (95% CI) in biomarkers were –10.8% (–23.4, 3.8) for KIM1, –10.2% (–29.9, 15.2) for NGAL, and –13.2% (–31.1, 9.4) for cysC.
Conclusion
Urinary levels of KIM1, NGAL, and cysC levels were numerically reduced from baseline to Week 26 with baxdrostat vs placebo. These data suggest that the initial eGFR reduction is attributable to a reversible hemodynamic effect rather than structural kidney damage. Phase 3 trials investigating effects of baxdrostat with dapagliflozin on CKD progression and cardio-kidney protection are ongoing.
Funding
- Commercial Support – AstraZeneca