Date: 2014-03-10
Type of information: Initiation of preclinical development
phase: 1
Announcement: initiation of the study
Company: Betagenon (Sweden) Baltic Bio(Sweden)
Product: O304
Action
mechanism: AMPK regulates fat metabolism and insulin sensitivity in liver, glucose disposal in muscle and glucose sensing in ?-cells. In a humanized animal model of type 2 diabetes, AMPK activator O304 reduces fatty liver and peripheral insulin resistance and improves impaired ?-cell function, hallmarks of type 2 diabetes. O304 also increases glucose-stimulated insulin secretion in human islets. Thus, O304 is expected to reduce fatty liver and to improve glucose homeostasis intype 2 diabetes.
O304 also enhances endurance both in aged sedentary normal mice and in obese diabetic mice by improving vascular function. O304 increases peripheral blood flow and the formation of arterioles in muscle. O304 also reduces blood pressure and platelet activation. Thus, by improving vascular function, O304 is predicted to show efficacy in peripheral arterial disease and to reduce vascular complications associated with type 2 diabetes.
Diet-induced increase in plasma levels of IGF-1 are correlated to increased type 2 diabetes mortality, and to increased incidence of certain cancers. AMPK activation inhibits proliferation of tumour cells by both direct and indirect mechanisms. O304 reduces plasma levels of both IGF-1 and insulin, and inhibits lipid synthesis and mTOR signalling, which in combination inhibit tumour cell proliferation.
Disease: NASH (non-alcoholic steatohepatitis)
type 2 diabetes
peripheral arterial disease
Therapeutic area: Metabolic diseases - Liver diseases - Cardiovascular diseases
Country: Sweden
Trial details:
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