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Cambridge, MA, United States

Patent
Elixir Pharmaceuticals Inc. | Date: 2013-05-24

Compound of formula (I) and methods of treating disorders by administering a compound of formula (I) are described herein. Examples of disorders include neoplastic disorders, fat-cell related disorders, neurodegenerative disorders, and metabolic disorders.


Trademark
Elixir Pharmaceuticals Inc. | Date: 2008-04-08

Pharmaceutical preparations for use in reducing the occurence of diabetes and complications of diabetes.


Trademark
Elixir Pharmaceuticals Inc. | Date: 2008-04-27

Pharmaceutical preparations for the treatment of diabetes; Pharmaceutical preparations for the treatment of metabolic syndrome.


Trademark
Elixir Pharmaceuticals Inc. | Date: 2008-04-27

Pharmaceutical preparations for the treatment of diabetes; Pharmaceutical preparations for the treatment of metabolic syndrome.


Huber J.L.,Elixir Pharmaceuticals Inc. | McBurney M.W.,Ottawa Health Research Institute | Distefano P.S.,Elixir Pharmaceuticals Inc. | McDonagh T.,Elixir Pharmaceuticals Inc. | McDonagh T.,Adnexus Therapeutics A BMS Company
Future Medicinal Chemistry | Year: 2010

Background: SRT1720 and SRT2183 were described recently as activators of the NAD+-dependent deacetylase, SIRT1. These molecules enhanced metabolic function when administered to rodents at doses of 100-500 mg/kg/day, purportedly by activating SIRT1 enzymatic activity in various tissues; however, considerable controversy surrounds these claims. Results: We find that these molecules do not activate SIRT1 deacetylase activity when tested in a variety of enzymatic assay formats and conditions. The compounds effectively decrease acetylated p53 in cells treated with DNA damaging agents but do so in cells that lack SIRT1, calling into question their designation as direct activators of SIRT1. In contrast, we find that the compounds inhibit p300 histone acetyltransferase activity in vitro, suggesting a possible mechanism for their effects in vivo. Conclusion: Structural features of these molecules may account for false-positive activation using fluorescence-based assays. © 2010 Future Science Ltd. Source

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