The Challenge
Chronic aldosterone excess drives severe tissue fibrosis, inflammation, and maladaptive remodeling. It is a key culprit behind high-stakes cardiometabolic conditions, including resistant hypertension, chronic heart failure (CHF), and chronic kidney disease (CKD).
Chronic aldosterone excess drives severe tissue fibrosis, inflammation, and maladaptive remodeling. It is a key culprit behind high-stakes cardiometabolic conditions, including resistant hypertension, chronic heart failure (CHF), and chronic kidney disease (CKD).
The Therapeutic Gap
Current standard-of-care therapies (MRAs and RAAS antagonists) fall short. They offer incomplete protection against aldosterone excess, often trigger a compensatory spike in aldosterone levels, and fail to fully eliminate the risk of adverse cardiovascular events or death.
Current standard-of-care therapies (MRAs and RAAS antagonists) fall short. They offer incomplete protection against aldosterone excess, often trigger a compensatory spike in aldosterone levels, and fail to fully eliminate the risk of adverse cardiovascular events or death.
Our Innovation
We are developing a best-in-class, highly selective CYP11B2 (aldosterone synthase) inhibitor. By shutting down aldosterone production directly at the source, our drug candidate delivers superior efficacy and an optimized, unique PK/PD profile, completely bypassing the clinical pitfalls of existing therapies.
We are developing a best-in-class, highly selective CYP11B2 (aldosterone synthase) inhibitor. By shutting down aldosterone production directly at the source, our drug candidate delivers superior efficacy and an optimized, unique PK/PD profile, completely bypassing the clinical pitfalls of existing therapies.