1. Epigenetics PI3K/Akt/mTOR Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Apoptosis
  2. AMPK Reactive Oxygen Species (ROS) Heme Oxygenase (HO) Apoptosis
  3. AMPK activator 20

AMPK activator 20 is an α1-selective AMPK activator. AMPK activator 20 inhibits Helicobacter pylori-induced ROS production. AMPK activator 20 induces AMPK-dependent expression of Heme oxygenase-1. AMPK activator 20 suppresses Helicobacter pylori-induced Apoptosis. AMPK activator 20 exerts protective activity against Helicobacter pylori-induced cytotoxicity via an AMPK-dependent pathway. AMPK activator 20 is applicable to research related to Helicobacter pylori infection and gastric diseases.

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AMPK activator 20

AMPK activator 20 Chemical Structure

CAS No. : 1243184-62-4

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Description

AMPK activator 20 is an α1-selective AMPK activator. AMPK activator 20 inhibits Helicobacter pylori-induced ROS production. AMPK activator 20 induces AMPK-dependent expression of Heme oxygenase-1. AMPK activator 20 suppresses Helicobacter pylori-induced Apoptosis. AMPK activator 20 exerts protective activity against Helicobacter pylori-induced cytotoxicity via an AMPK-dependent pathway. AMPK activator 20 is applicable to research related to Helicobacter pylori infection and gastric diseases[1].

IC50 & Target[1]

AMPKα1

 

AMPKα2

 

HO-1

 

Cellular Effect
Cell Line Type Value Description References
Hepatocyte EC50
20 nM
Compound: 13
Inhibition of de novo lipogenesis in rat hepatocytes assessed as 14C-acetic acid incorporation treated 1 hr before substrate administration and measured after 1 hr by scintillation counter
Inhibition of de novo lipogenesis in rat hepatocytes assessed as 14C-acetic acid incorporation treated 1 hr before substrate administration and measured after 1 hr by scintillation counter
[PMID: 24900234]
In Vitro

AMPK activator 20 (Compound C13) (1-30 μM; 1 h) activates AMPK in a dose-dependent manner via the α1 subunit, and induces phosphorylation of AMPKα1 and its downstream target ACC in GES-1 cells and primary gastric epithelial cells[1].
AMPK activator 20 (10-30 μM; 30 min pretreatment) attenuates H. pylori-induced apoptosis, restores cell viability in GES-1 cells and primary human gastric epithelial cells, and does not affect the basal health status of cells[1].
AMPK activator 20 (10 μM; 30 min pretreatment) requires activation of AMPK via the α1 subunit to mediate protective effects against H. pylori-induced apoptosis in GES-1 cells and primary gastric epithelial cells; inhibition of AMPKα1 or AMPK kinase activity abolishes this protective effect[1].
AMPK activator 20 (1-30 μM; 30 min pretreatment) inhibits H. pylori-induced ROS production and subsequent apoptosis in GES-1 cells and primary gastric epithelial cells via activating AMPKα1-mediated HO-1 expression; inhibition of AMPK or HO-1 abolishes these effects[1].

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

Western Blot Analysis[1]

Cell Line: GES-1 human gastric epithelial cells, primary human gastric epithelial cells (GECs)
Concentration: 1 μM, 10 μM, 30 μM
Incubation Time: 1 h
Result: Dose-dependently increased phosphorylation of AMPKα1 (with 10 μM and 30 μM showing the highest levels) and ACC in GES-1 cells with scramble shRNA.
Completely prevented AMPK activator 20-induced phosphorylation of AMPKα1 and ACC in GES-1 cells with AMPKα1 knockdown.
Showed no effect on AMPKα1 and ACC phosphorylation in GES-1 cells with AMPKα2 knockdown.
Strongly increased phosphorylation of AMPKα1 and ACC in primary human GECs with scramble shRNA.
Abolished AMPK activator 20-induced phosphorylation of AMPKα1 and ACC in primary human GECs with AMPKα1 knockdown.

Apoptosis Analysis[1]

Cell Line: GES-1 human gastric epithelial cells, primary human gastric epithelial cells (GECs)
Concentration: 1 μM, 10 μM, 30 μM
Incubation Time: 30 min pretreatment; 24 h H. pylori infection
Result: Dose-dependently inhibited H. pylori-induced apoptosis in GES-1 cells across Annexin V FACS, Histone-DNA ELISA, and TUNEL staining assays.
Restored cell survival in H. pylori-infected GES-1 cells measured via MTT assay.
Inhibited H. pylori-induced apoptosis in primary human GECs.
Reversed viability reduction in H. pylori-infected primary human GECs.
Showed no significant effect on baseline apoptosis or cell survival at 1-30 μM alone.

Western Blot Analysis[1]

Cell Line: GES-1 human gastric epithelial cells, primary human gastric epithelial cells (GECs)
Concentration: 10 μM, 10 μM Compound C
Incubation Time: 30 min pretreatment; 3 h H. pylori infection (Western blot); 24 h H. pylori infection (apoptosis assays)
Result: Further enhanced H. pylori-induced moderate AMPKα1 and ACC phosphorylation in GES-1 cells and primary human GECs.
Completely abolished AMPK activator 20's protective effect against H. pylori-induced apoptosis in GES-1 cells and primary human GECs when AMPK was inhibited via Compound C or AMPKα1 knockdown.
Showed no impact on AMPK activator 20's anti-apoptotic activity in GES-1 cells with AMPKα2 knockdown.
Molecular Weight

431.33

Formula

C17H22NO10P

CAS No.
SMILES

O=C1ON=C(C=2OC(=CC2)P(=O)(OCOC(=O)C(C)C)OCOC(=O)C(C)C)C1

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

Purity & Documentation
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AMPK activator 20
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HY-120913
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