Our Approach

At Ocelot Bio, our approach in the treatment of liver disease is focused on improving outcomes for patients with end-stage liver disease (ESLD) who are impacted by the serious consequences associated with complications of portal hypertension.

Aiming to achieve a delicate balance to improve ESLD patient outcomes 

At Ocelot Bio, our approach in the treatment of liver disease is focused on improving outcomes for patients with end-stage liver disease (ESLD) who are impacted by the serious – often life-threatening – consequences associated with complications of portal hypertension, such as hepatorenal syndrome with acute kidney injury (HRS-AKI) and ascites. 

ESLD-induced portal hypertension can lead to substantial vasodilation resulting in plasma leakage throughout the abdomen and a significant drop in arterial pressure. This acute drop in arterial pressure triggers a large renal vasoconstriction response which, if left untreated, rapidly leads to renal failure.  If renal failure occurs, patients often need both a liver and kidney transplant – and their probability of survival until transplant is significantly reduced.

OCE-205: Bold Science for Better Outcomes in ESLD

Ocelot Bio’s lead asset is OCE-205, a therapeutic peptide with a differentiated mechanism of action that has potential for improving outcomes for patients with complications of ESLD.

 

OCE-205’s innovation emanates from its design as a mixed agonist-antagonist peptide selective for the vasopressin 1a (V1a) receptor with no vasopressin 2 (v2) receptor activity at drug concentrations well above those used in treating ESLD. By virtue of its mixed V1a agonist/antagonist activity, OCE-205 treatment is designed to relieve portal hypertension while offering a capped maximal efficacy that avoids excessive vasoconstriction seen with full agonists, which often lead to ischemic and other serious adverse events such as respiratory failure. By eliminating V2 activity, OCE-205 treatment is designed to potentially avoid fluid retention and overload. Enhancing V1a receptor activity in this manner offers a proven mechanism of action for the treatment of HRS-AKI and ascites.

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