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NEW YORK, Jan. 12, 2014 (GLOBE NEWSWIRE) -- Intercept Pharmaceuticals, Inc. (Nasdaq:ICPT) (Intercept) today provided additional information regarding the FLINT clinical trial of obeticholic acid (OCA) in nonalcoholic steatohepatitis (NASH), based on a written statement distributed after market close on January 10, 2014 by the National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK), a part of the National Institutes of Health.
The NIDDK confirmed in its statement that:
Its decision to halt the 72-week therapeutic phase of FLINT was based on interim efficacy results showing that "OCA has a significant beneficial effect on liver damage due to NASH."
As specified in the protocol, a 24-week follow up period is now commencing and all FLINT patients will stop taking OCA or placebo no later than January 20, 2014.
Both the FLINT investigators and patients enrolled in the trial will remain blinded until completion of the follow up phase. All the trial data will then be thoroughly analyzed and the NIDDK anticipates presenting the results in 4Q 2014.
Lipid abnormalities involving increased total cholesterol and LDL and decreased HDL were seen in OCA-treated patients compared to placebo.
Since lipid abnormalities are common in NASH, all of the patients will be followed for the 24-week period to help determine whether lipids return to pre-treatment levels.
While the NIDDK did not provide any information concerning the magnitude of lipid effects, Intercept believes that the reported lipid changes in FLINT patients on OCA will likely be similar to the results previously reported in a clinical trial of OCA in diabetic patients with nonalcoholic fatty liver disease (NAFLD) that were presented at the 2009 meeting of the American Association for the Study of Liver Disease (AASLD) by Dr. Arun Sanyal and subsequently described in a paper published in the journal
Gastroenterology in 2013 (Mudaliar et al.). The efficacy results from this earlier trial (insulin sensitization, weight loss and liver enzyme improvements), together with the safety and tolerability profile of OCA, established the basis for its selection as the therapeutic candidate in FLINT in 2010.
"OCA is an FXR agonist and we have known for a long time that it is involved in many aspects of lipid metabolism," said Mark Pruzanski, M.D., Intercept's Chief Executive Officer. "An important part of the rationale for advancing our drug in NASH is that by activating FXR in the liver, we believe that it reduces the excess lipid load which is a causal factor in the disease. In addition, there is preclinical evidence that by activating FXR systemically, OCA is able to shunt excess lipids away from collecting in arteries and other organs which could also be beneficial. It is in any case clear that the lipid changes seen in OCA-treated patients are part of a complex set of mechanisms and we are already conducting further studies to gain a more complete understanding of the clinical implications."