Ocera Therapeutics licenses novel treatment for acute hepatic encephalopathy...( LONDON and SAN DIEGO April 2 2009 U...)

LONDON and SAN DIEGO, April 2, 2009 University College London Business PLC (UCLB) and Ocera Therapeutics Inc., a privately held biopharmaceutical company, announced the signing of an exclusive worldwide licensing agreement for UCL-L1V and all assets and technologies related to the compound for the treatment of acute hepatic encephalopathy (AHE).

The compound recently demonstrated that it directly reduces blood levels of ammonia, a highly toxic chemical that builds up during attacks of AHE.

Ocera will develop the licensed compound as its second pipeline compound and refer to it as OCR-002. OCR-002 is a novel injectable for the treatment of AHE in patients with advanced liver cirrhosis and acute liver failure.

The licensing agreement is based on research conducted by the collaborative global research project led by Professor Rajiv Jalan and the Liver Failure Group at the Institute of Hepatology, UCL (University College London). The research includes a study which demonstrated an acute and sustained reduction of systemic ammonia levels as well as decreased intracranial pressure in models of AHE in acute liver failure and cirrhosis. The data was published online in Hepatology in February 2009.

Clinical trials in patients with AHE due to cirrhosis and acute liver failure will be carried out at University College Hospital as well as other centres in 2009 under funding from the Medical Research Council (MRC) in the U.K. Ocera is planning to file an IND in late 2009 and U.S. trials will begin in early 2010.

AHE is a reversible neuropsychiatric abnormality frequently seen as a complication of acute liver failure and cirrhosis. With severe liver impairment, toxic substances such as ammonia that are normally removed by the liver accumulate in the blood and impair the function of brain cells.

Signs of AHE include impaired cognition, uncontrolled movements and decreased levels of consciousness leading to
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