Key result
Baxdrostat lowers systolic BP by ~7 mmHg vs. placebo in resistant hypertension.
Why the study?
Baxdrostat selectively inhibits aldosterone synthase to target excess aldosterone in resistant hypertension, but a comprehensive synthesis of randomized evidence incorporating recent 2026 trial data was lacking.
Does baxdrostat reduce systolic and diastolic blood pressure in adults with resistant hypertension compared to placebo?
Meta-Analysis (n=1,996)
Does baxdrostat reduce systolic and diastolic blood pressure in adults with resistant hypertension compared to placebo?
Across five RCTs in patients with resistant hypertension, selective aldosterone synthase inhibition with baxdrostat significantly lowers systolic and diastolic blood pressure with a manageable increase in mild-to-moderate hyperkalemia.
Answers are grounded in this paper and cite their sources.
Supports baxdrostat as add-on therapy in resistant hypertension; extends RCT evidence for selective aldosterone synthase inhibition.
Background: Resistant hypertension (RH), defined as persistently elevated blood pressure despite treatment with three or more antihypertensive agents including a diuretic, affects a substantial proportion of hypertensive patients and is associated with high cardiovascular morbidity and mortality. Excess aldosterone activity is a key pathophysiologic driver. Baxdrostat, a highly selective aldosterone synthase inhibitor, suppresses aldosterone production while sparing cortisol, providing a targeted mechanism for RH management. A comprehensive synthesis of randomized evidence, incorporating recent 2026 trial data, has been lacking. Methods: This systematic review and meta-analysis followed a preregistered PROSPERO protocol (CRD420251038564) and PRISMA 2020 guidelines. PubMed, Embase, Cochrane CENTRAL, and Scopus were searched through December 2025 for randomized controlled trials (RCTs) comparing baxdrostat to placebo in adults with RH. Co-primary efficacy endpoints were changes in systolic (SBP) and diastolic blood pressure (DBP) from baseline. The primary safety outcome was hyperkalemia (serum potassium ≥5.5 mmol/L). Random-effects models were used for pooling. Risk of bias was assessed using Cochrane RoB 2, and evidence certainty was evaluated with GRADE. Results: Five RCTs (BrigHTN, HALO, BaxHTN, Bax24, and Dwyer et al.) totaling 1,996 patients were included. Baxdrostat significantly reduced SBP (mean difference [MD] –6.98 mmHg ; 95% CI –9.78 to –4.18; I 2 =93%; P<0.00001) and DBP (MD –3.58 mmHg ; 95% CI –4.40 to –2.75; I 2 =51%; P<0.00001). Hyperkalemia risk was increased (risk ratio [RR] 3.77 ; 95% CI 2.29-6.21; I 2 =0%; P<0.00001; 103 events with baxdrostat vs. 19 with placebo). Most hyperkalemia cases were mild-to-moderate and manageable. No significant differences occurred in overall or serious adverse events. Conclusions: This meta-analysis of five RCTs (N=1,996) shows baxdrostat significantly reduces SBP and DBP in resistant hypertension via selective aldosterone synthase inhibition, sparing cortisol. Hyperkalemia risk is elevated but manageable, supporting its role as a promising novel therapeutic option.
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Kumar et al. (2026) conducted a meta-analysis in Resistant hypertension (n=1,996). Baxdrostat vs. Placebo was evaluated on Co-primary efficacy endpoints: changes in systolic blood pressure (SBP) and diastolic blood pressure (DBP) from baseline (MD -6.98 mmHg, 95% CI -9.78 to -4.18, p=<0.00001). Baxdrostat significantly reduced systolic BP (MD -6.98 mmHg; 95% CI -9.78 to -4.18; P<0.00001) and diastolic BP (MD -3.58 mmHg; 95% CI -4.40 to -2.75) vs placebo in resistant hypertension.
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