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.
For research use only. We do not sell to patients.
- CAS No.: 1243184-62-4
- Formula: C17H22NO10P
- Molecular Weight:431.33
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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All AMPK Isoforms
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Biological Activity
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AMPKα1 |
AMPKα2 |
HO-1 |
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Hepatocyte | EC50 |
20 nM
Compound: 13
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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
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[PMID: 24900234] |
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.
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Cell Line:GES-1 human gastric epithelial cells, primary human gastric epithelial cells (GECs)
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Concentration:1 μM, 10 μM, 30 μM
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Incubation Time:1 h
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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.
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Cell Line:GES-1 human gastric epithelial cells, primary human gastric epithelial cells (GECs)
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Concentration:1 μM, 10 μM, 30 μM
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Incubation Time:30 min pretreatment; 24 h H. pylori infection
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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.
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Cell Line:GES-1 human gastric epithelial cells, primary human gastric epithelial cells (GECs)
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Concentration:10 μM, 10 μM Compound C
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Incubation Time:30 min pretreatment; 3 h H. pylori infection (Western blot); 24 h H. pylori infection (apoptosis assays)
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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.
Chemical Information
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CAS No. 1243184-62-4
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Molecular Weight 431.33
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Formula C17H22NO10P
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SMILES
O=C1ON=C(C=2OC(=CC2)P(=O)(OCOC(=O)C(C)C)OCOC(=O)C(C)C)C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
AMPK activator 20 Related Classifications
HY-120913 Related Classifications
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- AMPK activator 20
- 1243184-62-4
- AMPK activator20
- AMPK activator-20
- AMPK
- Reactive Oxygen Species (ROS)
- Heme Oxygenase (HO)
- Apoptosis
- acetyl-CoA carboxylase
- reactive oxygen species
- apoptosis
- AMPK kinase
- GES-1 cells
- gastric epithelial cells
- primary human gastric epithelial cells
- AMP-activated protein kinase α1 subunit
- Helicobacter pylori
- heme oxygenase-1
- Inhibitor
- inhibitor
- inhibit