ORCID Profile
0000-0002-0357-1672
Current Organisation
Relay Therapeutics
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Publisher: Informa UK Limited
Date: 15-07-2013
DOI: 10.4161/CC.25268
Publisher: American Association for the Advancement of Science (AAAS)
Date: 08-03-2013
Abstract: Intense attention has focused on the SIRT1 deacetylase as a possible target for anti-aging drugs. But unexpected complications in assays of SIRT1 activity have made it unclear whether compounds thought to be sirtuin-activating compounds (STACs) are really direct regulators of the enzyme. Further exploration of these effects by Hubbard et al. (p. 1216 see the Perspective by Yuan and Marmorstein ) revealed that interaction of SIRT1 with certain substrates allows activation of SIRT1 by STACs and identified critical amino acids in SIRT1 required for these effects. Mouse myoblasts reconstituted with SIRT1 mutated at this amino acid lost their responsiveness to STACs.
Publisher: Springer Science and Business Media LLC
Date: 29-11-2007
DOI: 10.1038/NATURE06261
Publisher: American Chemical Society (ACS)
Date: 06-02-2009
DOI: 10.1021/JM8012954
Abstract: A series of imidazo[1,2-b]thiazole derivatives is shown to activate the NAD(+)-dependent deacetylase SIRT1, a potential new therapeutic target to treat various metabolic disorders. This series of compounds was derived from a high throughput screening hit bearing an oxazolopyridine core. Water-solubilizing groups could be installed conveniently at either the C-2 or C-3 position of the imidazo[1,2-b]thiazole ring. The SIRT1 enzyme activity could be adjusted by modifying the amide portion of these imidazo[1,2-b]thiazole derivatives. The most potent analogue within this series, namely, compound 29, has demonstrated oral antidiabetic activity in the ob/ob mouse model, the diet-induced obesity (DIO) mouse model, and the Zucker fa/fa rat model.
No related grants have been discovered for Jeremy Disch.