Date: 2017-04-21
Type of
information: Presentation of results at a congress
phase:
Announcement: presentation of results at The International Liver Congress 2017
Company: Gilead Sciences (USA - CA)
Product: GS-0976 ( NDI-010976)
Action
mechanism: acetyl-coenzyme A carboxylase inhibitor. GS-0976 ( NDI-010976) is an investigational inhibitor of Acetyl-CoA carboxylase (ACC). This program has been developed by Nimbus Apollo. Gilead Sciences has acquired this company in April 2016.
Disease: NASH (non-alcoholic steatohepatitis)
Therapeutic
area: Hepatic diseases - Liver diseases
Country:
Trial
details:
Latest
news:
- • On April 21, 2017, Gilead Sciences announced results from an open-label, proof-of-concept study evaluating GS-0976, an investigational inhibitor of Acetyl-CoA carboxylase (ACC), in patients with nonalcoholic steatohepatitis. 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). The late-breaking data were presented during a general session at The International Liver Congress 2017 in Amsterdam (#GS-009).
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, from 15.7 percent to 9.0 percent (p=0.006), as measured by magnetic resonance imaging-proton density fat fraction (MRI-PDFF). Median liver stiffness, a noninvasive marker of fibrosis, declined from 3.4 to 3.1 kPa 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.
All adverse events were Grade 1 or 2 in severity. No patients prematurely discontinued study medication.
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).
Is
general: Yes
