Linked Life Data

19137908

Source:http://linkedlifedata.com/resource/pubmed/id/19137908

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pubmed-article:19137908pubmed:abstractTextAVE2268, a substituted glycopyranoside, is an orally active and selective inhibitor of sodium-dependent glucose transporter 2 (SGLT2; IC50 = 13 nmol/L). Investigation of the pharmacological profile of AVE2268 on urinary glucose excretion (UGE) and blood glucose after glucose challenge (po or Intraperitoneal) was performed in mice and rats. AVE2268 caused a dose-dependent increase of UGE in mice (ID30 = 79 +/- 8.1 mg/kg p.o.) and rats (ID30 = 39.8 +/- 4.0 mg/kg p.o.). AVE2268 in mice was more potent to decrease blood glucose ascent when glucose was given intraperitoneally (ID50 = 13.2 +/- 3.9 mg/ kg), compared to orally administered glucose (ID50 = 26.1 +/- 3.9 mg/kg), showing that AVE2268 has no effects on SGLT 1 in the gut in vivo, which is in accordance with ist very low affinity to the SGLT 1 in vitro (IC50 >10,000 nmol/L). During an oral glucose tolerance test, AVE2268 dose-dependently increased UGE, with subsequent decreases of AUC and blood glucose. A highly significant inverse correlation between AUC and UGE was found (p < 0.001). The increase in UGE is linked to the inhibition of SGLT2 only. This profile renders AVE2268 as a new antidiabetic drug for the treatment of type 2 diabetes.lld:pubmed
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pubmed-article:19137908pubmed:articleTitleEffects of AVE2268, a substituted glycopyranoside, on urinary glucose excretion and blood glucose in mice and rats.lld:pubmed
pubmed-article:19137908pubmed:affiliationResearch & Development, TD Metabolism, Sanofi-Aventis, Frankfurt/Main, Germany. martin.bickel@gmx.delld:pubmed
pubmed-article:19137908pubmed:publicationTypeJournal Articlelld:pubmed