Adenosine is one of the commonly occurring nucleosides and, when phosphorylated, forms ATP (adenosine triphosphate), the primary energy source for human cells.  Adenosine in its unphosphorylated form interacts with one of four G-protein-coupled receptors which regulate adenylate cyclase activity.

Hepatorenal syndrome is a condition whereby deterioration in liver function is accompanied by deterioration in renal function.  Afferent nerves arising in the liver can be activated by increased adenosine levels, and this stimulates the hepatorenal reflex which results in decreased renal fluid and electrolyte output, especially sodium.  Adenosine accumulates in the liver due to portal vein hypertension that causes shunting, or because inflammation and/or hypoxia in the cirrhotic liver allows ATP to break down to adenosine.

The result of decrease renal output is the accumulation of acitic fluid in the abdomen that can reach twenty liters in volume.  Patients with severe liver damage thus experience liver failure and renal failure at the same time, and this leads to death within a few months.  It has been shown in animal experiments that a selective antagonist of the A₁ receptor restored salt and water excretion ability in the kidney.

To date, a number of A₁ receptor antagonists have been developed, but none have had the required pharmacokinetic properties for treating this condition.