AS1842856 

AS1842856 (GMP) is AS1842856 (HY-100596) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. AS1842856, a specific Foxo1 inhibitor (IC₅₀=30 nM), potently suppresses autophagy^[1]. AS1842856 reduces Foxo1 activity and, to a lesser extent, inhibits Foxo1 protein expression by simply binding to Foxo1^[2].

AS1842856 potently inhibits human Foxo1 transactivation and reduces glucose production through the inhibition of glucose-6 phosphatase and phosphoenolpyruvate carboxykinase mRNA levels in a rat hepatic cell line^[1]. After AS1842856 treatment, there is no significant difference in the protein expression of p-FoxO1 and FoxO1 compared with the control group, but the expression of p-Akt is decreased compared with the control group^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Oral administration of AS1842856 (GMP) to diabetic db/db mice leads to a drastic decrease in fasting plasma glucose level via the inhibition of hepatic gluconeogenic genes, whereas administration to normal mice has no effect on the fasting plasma glucose level. Treatment with AS1842856 (GMP) also suppresses an increase in plasma glucose level caused by pyruvate injection in both normal and db/db mice^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

347.38

C₁₈H₂₂FN₃O₃

836620-48-5

O=C(C1=CN(CC)C2=C(C(N)=C(F)C(NC3CCCCC3)=C2)C1=O)O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Nagashima T, et al. Discovery of novel forkhead box O1 inhibitors for treating type 2 diabetes: improvement of fasting glycemia in diabetic db/db mice. Mol Pharmacol. 2010 Nov;78(5):961-70.  [Content Brief]

  [2]. He J, et al. The resistant effect of SIRT1 in oxidative stress-induced senescence of rat nucleus pulposus cell is regulated by Akt-FoxO1 pathway. Biosci Rep. 2019 May 10;39(5). pii: BSR20190112.  [Content Brief]