Press Release (ePRNews.com) - San Antonio, Texas - Apr 21, 2017 - Dr. Eric Lawitz, internationally recognized for his work in liver disease, presented a proof-of-concept study at The International Liver Congress™ 2017, presented by the European Association for the Study of Liver (EASL). The study was performed at the American Research Corp at the Texas Liver Institute, a world-renowned facility for liver research and the prevention and treatment of liver disease.
In collaboration with Gilead Sciences, Dr. Lawitz presented the results of an open-label, proof-of-concept study evaluating GS-0976, an investigational inhibitor of Acetyl-CoA carboxylase (ACC), in patients with nonalcoholic steatohepatitis (NASH), commonly referred to as nonalcoholic fatty liver disease. The data, from ten patients treated with GS-0976 20 mg taken orally once daily for 12 weeks, indicated that treatment was associated with statistically significant improvements in liver fat content and noninvasive markers of fibrosis, via inhibition of hepatic de novo lipogenesis (DNL).
Fatty liver disease is a potentially serious condition marked by liver inflammation and too much fat stored in the liver, as the name implies. Fatty liver is estimated to affect up to twenty-five percent of people in the United States in some form, and up to 5-10% of the population in a more severe form.
“The identification of novel strategies for reducing liver fibrosis is a core focus in the development of therapies for patients with NASH,” says Dr. Lawitz, the lead study author and Clinical Professor of Medicine at the University of Texas Health, San Antonio. “We know that elevated DNL is a major contributor to the pathogenesis of NASH, and these data suggest that decreasing DNL through inhibition of ACC can lead to significant reductions in both liver fat content and stiffness, with early decreases in markers of liver fibrosis.”
Based on a novel approach involving the labeling of newly synthesized palmitate by deuterated water administration, patients receiving GS-0976 experienced a median decrease of 29 percent in hepatic DNL from baseline after 12 weeks. At week 12, patients receiving GS-0976 experienced a 43 percent median relative decrease in liver fat content (p=0.006), as measured by magnetic resonance imaging-proton density fat fraction (MRI-PDFF). Median liver stiffness, a noninvasive marker of fibrosis, declined 9 percent at week 12 (p=0.049), as assessed by magnetic resonance elastography (MRE). In addition, patients with reductions in hepatic fat demonstrated improvements in liver biochemistry and serum markers of fibrosis and apoptosis, supporting the biological activity of GS-0976.
Preclinical data from a mouse model of NASH are also being presented at The International Liver Congress demonstrating that GS-0976 reduces hepatic steatosis, liver biochemistry, and the expression of pro-fibrotic and pro-inflammatory genes in the liver (#FRI-352).
GS-0976 is an investigational therapy and has not been determined to be safe or efficacious.
About Texas Liver Institute
The Texas Liver Institute (TLI) is a one-of-a-kind facility, and one of the very few dedicated and freestanding clinical care and research facilities in the world. The most advanced research in viral hepatitis, fatty liver disorders, liver cancer and cirrhosis is being conducted in this facility, which has been recognized internationally for its contributions to the field of liver diseases.
The Texas Liver Institute continues to push the boundaries of new discoveries and advance the field of liver disease into the future through research and education.
About Dr. Eric Lawitz
Dr. Eric Lawitz is Vice President of Scientific and Research Development at the Texas Liver Institute and Clinical Professor of Medicine at the University of Texas Health, San Antonio. He has conducted extensive research in liver disease, authored over 300 publications and presented his work at both national and international medical meetings. He is internationally recognized for his work in liver disease research and education.
Contact: Tina Mulqueen
Phone: (775) 544-5131
E-Mail: [email protected]