The leaders of Metabolic Solutions Development Company are frequently asked to speak on diabetes, insulin sensitizers and metabolic diseases associated with age-related mitochondrial dysfunction. Supporting materials from select presentations are listed below.

22nd Annual BioCenturty Future Leaders in the Biotech Industry Conference, New York 2015
Presentation includes an overview of the Company’s development plans for its lead compound, MSDC- 0602, which is expected to enter into large Phase 2b clinical trials in 2015 in patients diagnosed with NASH and polycystic kidney disease (PKD), respectively.

March 20, 2015

2:30 PM ET

Listen to Webcast

ADA Presentation, Chicago 2013
Effects of MSDC-0602 and GLP1 on Pancreatic Islets in ZDSD/Pco Rats Challenged with a High Fat Diet

ADA Presentation, Chicago 2013
The Mitochondrial Target of Thiazolidinediones (mTOT): a New Target for Insulin Sensitizers

mTOT Modulators

Data presented to date suggest that the mTOT protein complex functions as a molecular "sensor switch" connecting mitochondrial metabolism to important cellular activities perturbed in age-related metabolic diseases such as type 2 diabetes, including insulin sensitivity. MSDC's novel pharmaceutical agents selectively bind and modulate proteins in the mTOT complex, effecting pyruvate utilization and resulting in improved insulin action, lipid oxidation, preservation of beta cell function, and generation of brown fat.


The Science of Diabetes

Type 2 diabetes is a metabolic disorder affecting the ways in which the body uses various nutrients for growth and energy. The root cause of this disorder is insulin resistance, which is a result of the body's inability to efficiently and effectively convert glucose - a simple sugar made from the food you eat - to energy. Insulin, a hormone produced by the beta cells in the pancreas, aids in the transfer of glucose into the bloodstream, where it is used or metabolized by cells for growth and energy. Diabetes results when changes in metabolism alter both the ability of insulin to work on its target tissues and the ability of the beta cells to make and secrete insulin.


ADA Presentation, Philadelphia 2012
Identification of a Mitochondrial Target of Thiazolidinediones (mTOT) – Poster and Slides

ADA Presentation, Philadelphia 2012
Clinical proof of concept with a prototype mTOT modulating insulin sensitizer – Poster and Slides

EASD Presentation, Lisbon 2011
New Insulin Sensitizers Produce Differentiation of Brown-like Adipose Cells from a Subcutaneous Fat Depot and Increase Secretion of Adiponectin in vitro

ADA Presentation, San Diego 2011
Enhancement of Brown Adipose Tissue Development in vivo by a Novel Insulin Sensitizer

ADA Poster, San Diego 2011
Novel Insulin Sensitizers Enhance Brown Adipose Cell Differentiation by Modulation of the Wnt Signaling Pathway

IDF World Diabetes Congress Poster, Montreal 2009
A PPAR-sparing insulin sensitizer is effective in type 2 diabetic patients without causing weight gain

MD Conference Express: Diabetes, EASD Highlights, September 2008, excerpt
Mitoglitazone and PPAR-sparing insulin sensitizers

EASD Abstract, Rome 2008
PPAR-sparing insulin sensitizers; path for development and clinical evaluation