AstraZeneca announced positive results from the Bax24 Phase III trial on October 10, 2025, evaluating baxdrostat, a highly selective aldosterone synthase inhibitor, in patients with treatment-resistant hypertension (rHTN). The randomized, double-blind, placebo-controlled study met its primary endpoint, demonstrating a statistically significant and clinically meaningful reduction in 24-hour ambulatory systolic blood pressure (SBP) at 12 weeks compared to placebo.
Baxdrostat (2 mg daily) was administered alongside standard care to 218 patients, showing consistent blood pressure control throughout the day, including during the critical morning period when cardiovascular risks peak. The drug’s safety profile was consistent with prior trials, with no major tolerability concerns reported. Hypertension affects 1.4 billion people globally, with approximately 50% of treated U.S. patients failing to achieve blood pressure control, increasing risks of heart attack, stroke, and kidney disease. Baxdrostat’s long half-life (26-30 hours) and selective inhibition of aldosterone, a hormone driving sodium retention and blood pressure elevation, position it as a potential first-in-class therapy.
The trial’s secondary endpoints, including reductions in nighttime and daytime SBP, further underscored baxdrostat’s efficacy. Dr. Bryan Williams, the primary investigator, highlighted the trial’s groundbreaking implications for patients with uncontrolled hypertension. AstraZeneca is advancing regulatory filings globally and will present detailed findings at the American Heart Association Scientific Sessions in November 2025. Baxdrostat is also under investigation as a monotherapy for hypertension and primary aldosteronism, and in combination with dapagliflozin for chronic kidney disease and heart failure prevention.
This development, following AstraZeneca’s acquisition of CinCor Pharma in 2023, reinforces the company’s commitment to addressing unmet needs in cardiovascular, renal, and metabolic diseases through innovative therapies targeting aldosterone-driven mechanisms.
