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TMCNet:  ENDECE Neural to Present Findings for Remyelination at 2013 Keystone Symposia on Multiple Sclerosis

[November 28, 2012]

ENDECE Neural to Present Findings for Remyelination at 2013 Keystone Symposia on Multiple Sclerosis

MEQUON, Wis., Nov. 28, 2012 /PRNewswire via COMTEX/ -- ENDECE Neural, LLC (www.EndeceNeural.com) announced today that Dr. Steven Nye, Vice President of Discovery, will be presenting at the 2013 Keystone Symposia on Multiple Sclerosis to be held in January, in Big Sky, Montana, USA.


Dr. Nye's presentation, "Estrogen analogs dramatically up-regulate intracellular signaling pathways for remyelination (1)," will review the mechanism behind the novel ENDECE Neural compounds that induce remyelination in rodent animal models of Multiple Sclerosis (MS).

"Unlike current MS therapeutics, which target immune response and inflammation to slow relapses, ENDECE Neural is developing the first drug compounds to induce remyelination of demyelinated axons, and potentially reverse disease progression," states Dr. Nye.

Abstract below:Estrogen analogs dramatically up-regulate intracellular signaling pathways for remyelination.

A new series of nuclear receptor ligands was synthesized for treating multiple sclerosis and other neurodegenerative disorders. The ligands are analogs of 17beta-estradiol (E2) that bind to the estrogen receptors (ERs) and induce distinct intracellular responses which can determine cell fate. Based on molecular modeling studies, modifications to the core structure of E2 were made with different C-6 alkoxyalkyl moieties and/or substitution of the C-18 methyl group. The E2 alterations caused pronounced changes in subtype selectivity for ER-alpha or ER-beta, along with varying degrees of ER dimerization and ER activation. Microarray studies revealed that several of the E2 analogs cause a dramatic up-regulation of genes in signaling pathways related to OPC differentiation and myelin sheath production. While all three E2 analogs are ER agonists, NDC-1308 was the most potent at causing mouse OPC differentiation concomitant with myelin basic protein expression in vitro. The findings presented here relate the structure of the E2 analogs to biological function. We conclude that cellular responses for neuronal repair/remyelination may be controlled to some extent by making key alterations to the core structure of endogenous ER ligands.

(1) Steven H. Nye, ENDECE, LLC, Mequon, WI, USA 53092; Wei Xu, University of Wisconsin, McArdle Laboratory for Cancer Research, Madison, WI, USA 53706; Michael Bittner, Translational Genomics Research Institute, Scottsdale, AZ, USA 85004; Robert E. Babine, Rebexsess Discovery Chemistry, Encinitas, CA, USA 92024; James G. Yarger, ENDECE, LLC, Mequon, WI, USA 53092.

About ENDECE Neural, LLC (an ENDECE Company)ENDECE Neural is the wholly owned subsidiary of ENDECE, LLC. ENDECE Neural was founded in 2011 to focus on the development of what could be the first drug capable of inducing remyelination of damaged nerve axons, and potentially restoring muscle control, mobility and independence to the lives of Multiple Sclerosis patients. ENDECE Neural maintains an exclusive license for the IP from its parent company.

SOURCE ENDECE Neural, LLC

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