1. Epigenetics PI3K/Akt/mTOR Metabolic Enzyme/Protease Stem Cell/Wnt Membrane Transporter/Ion Channel MAPK/ERK Pathway Immunology/Inflammation NF-κB
  2. AMPK PEPCK GSK-3 GLUT Akt p38 MAPK Reactive Oxygen Species (ROS)
  3. Pterosin A

Pterosin A  (Synonyms: (2S)-Pterosin A)

Cat. No.: HY-N7912 Purity: 94.07%
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Pterosin A ((2S)-Pterosin A) is a sesquiterpene compound. Pterosin A is an orally active AMPK activator with anti-diabetic effect. Pterosin A can promote glucose uptake, increase serum insulin, and improve hyperglycemia and glucose intolerance. Pterosin A can prevent insulin-secreting cells death and reduce ROS production. Pterosin A can be used for the research of metabolic disease, such as diabetes.

For research use only. We do not sell to patients.

Pterosin A

Pterosin A Chemical Structure

CAS No. : 35910-16-8

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Based on 1 publication(s) in Google Scholar

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Description

Pterosin A ((2S)-Pterosin A) is a sesquiterpene compound. Pterosin A is an orally active AMPK activator with anti-diabetic effect. Pterosin A can promote glucose uptake, increase serum insulin, and improve hyperglycemia and glucose intolerance. Pterosin A can prevent insulin-secreting cells death and reduce ROS production. Pterosin A can be used for the research of metabolic disease, such as diabetes[1][2].

IC50 & Target[1]

GLUT4

 

p-GSK-3

 

In Vitro

Pterosin A (50 μg/mL, 0.5-4 h) enhances glucose uptake and AMPK phosphorylation in muscle cells[1].
Pterosin A (50-150 μg/mL, 0.5-4 h) inhibits PEPCK expression, triggers the phosphorylations of AMPK, ACC, and GSK-3, decreases glycogen synthase phosphorylation, and increases the intracellular glycogen level in liver cells[1].
Pterosin A (10-100 μM, 18 h) inhibits H2O2-induced ROS production in RINm5f β-cells[2].
Pterosin A (10-100 μM, 24 h) reduces lipotoxicity-induced cell death in RINm5f β-cells[2].

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

Western Blot Analysis[1]

Cell Line: Liver cells
Concentration: 50 and 150 μg/mL
Incubation Time: 0.5, 1, 2 and 4 h
Result: Increased p-AMPK and P-ACC and p-GSK3-α/β levels.
In Vivo

Pterosin A (10-100 mg/kg, p.o., daily for 4 weeks) improves hyperglycemia and glucose intolerance in diabetic mica[1].

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

Animal Model: Streptozotocin (HY-13753), high-fat diet-fed and db/db diabetic mice models[1]
Dosage: 10, 30 and 100 mg/kg
Administration: Orally administration, daily for 4 weeks
Result: Reversed the increased serum insulin and insulin resistance in dexamethasone-IR mice.
Reversed the reduced muscle GLUT-4 translocation and the increased liver phosphoenolpyruvate carboxyl kinase (PEPCK) expression.
Reversed the decreased phosphorylations of AMP-activated protein kinase (AMPK) and Akt in muscles.
Reversed increased p38 phosphorylation in livers.
Molecular Weight

248.32

Formula

C15H20O3

CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C1C(C(C[C@](C)1CO)=CC(C)=C2CCO)=C2C

Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Purity & Documentation
References
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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