Archived Content
Diabetes Drug Discovery and Beyond
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The Diabetes Drug Discovery and Beyond meeting will not only cover progress on promising pre-clinical and early clinical phase diabetes drug candidates. But this year, we will also highlight emerging therapeutic targets that probe how the underlying defects in metabolic diseases are connected. Some presentations will cover obesity, other metabolic disorders and cardiovascular disease in the context of diabetes and energy homeostasis.
TUESDAY, OCTOBER 2
Targets for New Diabetes Therapies
1:30 pm Chairperson’s Remarks
Claire Steppan, Ph.D., Associate Research Fellow, Diabetes, Pfizer
1:40 FEATURED SPEAKER
Targeting Diabetes via Glucocorticoid Modulation: The Identification of Advanced 11b-HSD-1 Inhibitors
 Jeffrey A. Robl, Ph.D., Executive Director, Metabolic Diseases R&D, Bristol-Myers Squibb
Preventing excess glucocorticoid tone in metabolically active tissues such as the liver and adipose may be beneficial in addressing glucose homeostasis and hyperglycemia in patients with type 2 diabetes. We have optimized a series of triazolopyridine based inhibitors resulting in the advancement of BMS-770767 to phase 2 clinical trials. The discovery of BMS-770767 will be presented as well as a description of its development properties, pharmacokinetics, and pre-clinical pharmacology profile.
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2:10 Dyslipidemia Targets and Diabetes
Rebecca Taub, M.D., CEO, Madrigal Pharmaceuticals
This talk will defining diabetic dyslipidemia and discuss how elevated VLDL, triglycerides and fatty liver might contribute to diabetic CV disease. Novel dyslipidemia mechanisms to treat diabetic dyslipidemia including THRbeta agonists will also be covered.
2:40 Effects of PF-04620110, a Novel Diacylglycerol Acyl-Transferase 1 (DGAT1) Inhibitor on Healthy-Obese Volunteers and Type 2 Diabetic Subjects
Claire Steppan, Ph.D., Associate Research Fellow, Diabetes, Pfizer
Inhibition of DGAT1, the terminal enzyme in the synthesis of triglycerides (TG), has been proposed for the treatment of type 2 diabetes (T2DM). We sought to examine the effects of a potent and selective DGAT1 inhibitor, PF-04620110, on vitamin A absorption, TG, glucose, insulin and total amide glucagon like peptide-1 (GLP-1) levels in both healthy-obese volunteers and Type 2 Diabetic subjects. The results of these studies will be presented.
3:10 Refreshment Break in the Exhibit Hall with Poster Viewing
3:45 Pharmacological Manipulation of Diacyl Glycerol Acyl Transferase 1 Using Pre-Clinical Models
Shirly Pinto, Ph.D., CVD - Atherosclerosis Team Lead, Merck Research Laboratories
4:15 Targeting the Ileal Brake with an Oral Mimetic of RYGB
Jerome J. Schentag, PharmD, Professor of Pharmaceutical Sciences, University at Buffalo
Reports of putative cures of T2D by RYGB surgery has led to a search for oral
mimetics of these beneficial properties. T2D is controlled even before weight loss occurs, and even more surprisingly, it now seems clear that beneficial effects occur after RYGB even in patients without obesity. As an oral mimetic of RYGB surgery, Brake™ specifically targets the ileal Brake. When taken once daily, oral Brake™ treatment elicits the full range of hormonal mediator outputs and controls hyperglycemia, hyperlipidemia, and obesity. There was resolution of hepatic steatosis and NAFLD as added benefit.
4:45 Beneficial and Adverse Effects of Glucokinase Activators on Glucose Metabolism in Rat Liver Cells
Gabriel Baverel, Ph.D., CEO and CSO, Metabolomics, Metabolys, Inc.
Using a metabolic flux approach, we show the potential beneficial and adverse effects of three gluco-kinase activator drug candidates for type2 diabetes. We report the gluco-kinase activators’ effects on glucose utilization and production, glycogen synthesis and degradation, lactic acid and triglyceride accumulation and on the citric acid cycle during glucose metabolism in rat liver cells. Our work illustrates the advantage of metabolic flux analysis for predicting early during the drug development process, both the efficacy and safety of very small amounts of antidiabetic drug candidates.
5:15 Connecting Mitochondrial Dysfunction and Diabetes
James Dykens, CEO, Eyecyte Therapeutics
Mitochondrial dysfunction contributes via bioenergetic and oxidative mechanisms to a host of degenerative and metabolic diseases, including diabetes. Mitochondrial Ca2+ dynamics alter insulin release, while production of free radicals yields dysregulation of glycolysis. Importantly, xenobiotic therapies for diabetes, e.g., biguanides and thiazolidinediones, directly undermine mitochondrial function thereby lowering blood glucose, albeit via an untoward mechanism. The latter results from cell culture conditions that model diabetes and anaerobic poise, not normal aerobic physiology.
5:45 End of Day
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