Baxdrostat achieved a 9.8 mmHg placebo-adjusted reduction in systolic blood pressure at 12 weeks, with absolute reductions exceeding 15 mmHg in some patients. How clinically meaningful is this outcome for individuals with hard-to-control hypertension already on multiple therapies?

Baxdrostat targets aldosterone synthase, addressing one of the hormonal drivers of resistant hypertension. How does this novel mechanism compare with existing antihypertensive classes in tackling uncontrolled blood pressure?

The trial demonstrated durable SBP reductions during the randomised withdrawal phase and exploratory ambulatory monitoring showed significant 24-hour and nighttime blood pressure control. How important are these findings for improving cardiovascular outcomes long term?

Results were consistent across both uncontrolled and treatment-resistant patient subgroups. Could baxdrostat emerge as a potential treatment backbone for resistant hypertension, or will its use be broader across difficult-to-treat cases?

Baxdrostat was well tolerated with low hyperkalemia rates (~1.1%) compared to placebo and no unanticipated safety findings. How does this profile affect its potential adoption compared to mineralocorticoid receptor antagonists and other aldosterone-targeting agents?

Given that lowering systolic blood pressure by 10 mmHg can reduce cardiovascular event risk by ~20%, how significant could baxdrostat’s effect be for long-term outcomes like heart attack, stroke, and kidney disease progression?

With AstraZeneca planning regulatory filings and ongoing Phase 3 programs exploring baxdrostat in chronic kidney disease and heart failure prevention, how do you envision its positioning within the broader cardiovascular and renal landscape?

Baxdrostat is also being studied in combination with dapagliflozin and other agents. Do you expect its greatest impact to be as a monotherapy for resistant hypertension or as part of multidrug strategies addressing overlapping CVRM pathways?