PROMETIC’S PBI-4050 SHOWN TO REDUCE LIVER DAMAGE AND FIBROSIS IN HIGH-FAT DIET INDUCED OBESITY AND METABOLIC SYNDROME MOUSE MODEL
- Strong correlation of results with phase 2 clinical data in metabolic syndrome with type 2 diabetes patients
- New data presented at ILC 2017 EASL conference
' LAVAL, QUEBEC, CANADA, – April 20, 2017 – Prometic Life Sciences Inc. (TSX: PLI) (OTCQX: PFSCF) (“Prometic” or the “Corporation”) today presented new results at the International Liver Congress (“ILC”) 2017 of the European Association for the Study of the Liver (“EASL”) in Amsterdam on the positive effects of PBI-4050 on reduction of non-alcoholic steatohepatitis (NASH) in a mouse model of obesity and metabolic syndrome.
According to Dr. Lyne Gagnon, Vice-President of R&D Pre-clinical of ProMetic “This extensive preclinical study enabled us to further characterize the effects of PBI-4050 on metabolic regulation and white adipose tissue and liver fibrosis induced in a high fat diet model. As such, PBI-4050 effectively reduced liver damage and fibrosis, improved insulin resistance (HOMA-IR) and the pancreatic ß-cells function (HOMA-ß). Furthermore, pro-fibrotic and fibrotic gene expression in liver and in white adipose tissue were reduced with PBI-4050 treatment”, added Dr. Gagnon.
“These results strongly correlate with those seen in our Phase 2 clinical trials in diabetes associated with metabolic syndrome and Alström syndrome”, stated John Moran, Prometic’s Chief Medical Officer. “Prometic is advancing PBI-4547 in the clinical stage in H2 2017, a PBI-4050 analogue that is showing even better results in NASH models at a much lower dose. This provides us with the ability to eventually position different drug candidates for different indications”, added Dr. Moran.
Overall, 38 percent of U.S. adults and 17 percent of teenagers are obese. The Trust for America's Health projects that 44 percent of Americans will be obese by 2030. Obesity is associated with an increased risk of non-alcoholic fatty liver disease. Steatosis, the hallmark feature of NAFLD, occurs when the rate of hepatic fatty acid uptake from plasma and de novo fatty acid synthesis is greater than the rate of fatty acid oxidation and export (as triglyceride within very low-density lipoprotein). Therefore, an excessive amount of intrahepatic triglyceride represents an imbalance between complex interactions of metabolic events. The presence of steatosis is associated with a constellation of adverse alterations in glucose, fatty acid, and lipoprotein metabolism. It is likely that abnormalities in fatty acid metabolism, in conjunction with adipose tissue, hepatic, and systemic inflammation, are key factors involved in the development of insulin resistance, dyslipidemia, and other cardiometabolic risk factors associated with NASH.
Poster presentation at the conference:
Dr Grouix, Thursday April 20, 2017, 8:00 AM – 6:00 PM:
PBI-4050 reduces liver damage and fibrosis in a High-Fat diet mouse model of obesity and metabolic syndrome
More about NAFLD/NASH:
NAFLD is a condition defined by excessive fat accumulation in the form of triglycerides (steatosis) in the liver. A subgroup of NAFLD patients displays liver cell injury and inflammation in addition to excessive fat (steatohepatitis). The latter condition, designated NASH, is virtually indistinguishable histologically from alcoholic steatohepatitis (ASH).
More about PBI-4050
PBI-4050 is an orally active lead drug candidate with excellent safety and efficacy profiles confirmed in several in vivo experiments targeting fibrosis. Fibrosis is a very complex process by which continuing inflammation causes vital organs to lose their function as normal tissue is replaced by fibrotic scar tissue. The proof of concept data generated to date confirms our lead drug candidates’ anti-fibrotic activity in several key organs including the kidneys, the heart, the lungs and the liver. Twenty-six million subjects in the U.S. alone are believed to suffer from chronic kidney diseases (“CKD”). Subjects with severe CKD stages (3 and 4) suffer from a progressive loss of their renal function leading to end-stage renal disease and the need for dialysis or kidney transplant. Cardiovascular complications are the most common cause of death in dialysis patients.'
Jim
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