Aldosterone excess may lead to accelerated chronic kidney disease (CKD) progression, elevated blood pressure (BP), and an increased risk of cardiovascular events.1,2 The mechanisms of kidney and cardiovascular injury by aldosterone include fibrosis, inflammation, and dysfunctional remodeling.3 Renin-angiotensin system (RAS) inhibitors and nonsteroidal mineralocorticoid receptor antagonists are beneficial for treatment of CKD but may not fully block harmful effects of aldosterone. This may be achieved by targeting aldosterone synthase (AS; CYP11B2), the enzyme that mediates the final steps in aldosterone synthesis.