Renin is produced in the kidneys, where it serves as gatekeeper to the biochemical cascade that ultimately results in production of the hormone angiotensin II. Under normal conditions, the kidneys control blood volume, blood pressure, and the electrolyte composition of body fluids, through the tightly regulated production of renin and therefore of angiotensin II.

The overproduction of angiotensin II produces a range of deleterious effects. Disorders of this system are a major factor in high blood pressure, heart disease and kidney failure. Drugs that block the renin-angiotensin system comprise an important category of cardiovascular drugs used today. These drugs – angiotensin converting enzyme (ACE) inhibitors, and angiotensin receptor blockers, or ARBs – are approved medicines for high blood pressure, kidney disease and heart failure, and are among the most commercially successful classes of pharmaceuticals.

A compensatory increase in other enzymes, such as chymase, can bypass the effects of an ACE inhibitor; furthermore, ARBs do not block all angiotensin receptors. Therefore, it is predicted that an orally-active renin inhibitor may provide a more specific and more complete inhibition of the renin-angiotensin system than either an ACE inhibitor or an ARB alone.