Avenanthramide B
Based on 1 publication(s) in Google Scholar
Avenanthramide B is an oat phytoalexin, a porcine liver esterase inhibitor, and an amyloglucosidase inhibitor, with an IC50 of 4.4 mg/mL against Aspergillus niger amyloglucosidase. Avenanthramide B increases the activation status of Akt1 and the expression level of eNOS, elevates the levels of NO and cGMP, and reduces the level of superoxide anions. Avenanthramide B acts on amyloglucosidase via a competitive mixed mechanism, functions as a fluorescence quencher, and exerts bidirectional regulatory effects on protein thermal stability. Avenanthramide B serves as a substrate for oat leaf peroxidase. Avenanthramide B can be used in research related to type 2 diabetes.
For research use only. We do not sell to patients.
- CAS No.: 108605-69-2
- Formula: C17H15NO6
- Molecular Weight:329.31
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
Publications Citing Use of MedChemExpress (MCE) Avenanthramide B
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Biological Activity
Description
IC50 & Target
[2]|
Akt1 |
In Vitro
Avenanthramide B (1 µM; 24 h) significantly increases intracellular NO levels and cGMP production, reduces superoxide anion generation, enhances Akt1 activation, and upregulates the protein expression level of eNOS in HUVEC cells[2].
Avenanthramide B (50 µM; 10 min) significantly inhibits the activity of porcine liver esterase[1].
Avenanthramide B (31.3-1000 μg/mL) inhibits amyloglucosidase derived from Aspergillus niger via a competitive-dominant mixed-type mechanism, with an IC50 value of 4.4 mg/mL[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HUVEC
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Concentration:1 µM
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Incubation Time:24 h
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Result:Significantly increased cGMP levels compared to vehicle control.
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Cell Line:HUVEC
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Concentration:1 µM
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Incubation Time:2 h
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Result:Significantly increased the Akt1 phosphorylation/total protein ratio compared to vehicle control, indicating enhanced Akt1 activation.
Significantly increased eNOS protein expression compared to vehicle control.
Chemical Information
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CAS No. 108605-69-2
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Appearance Solid
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Molecular Weight 329.31
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Formula C17H15NO6
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SMILES
C(O)(=O)C1=C(NC(/C=C/C2=CC(OC)=C(O)C=C2)=O)C=CC(O)=C1
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
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Journal Impact Factor
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Most Recent
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
[1]. Lim H, et al. Compared Inhibitory Activities of Tamoxifen and Avenanthramide B on Liver Esterase and Correlation Based on the Superimposed Structure Between Porcine and Human Liver Esterase. International journal of molecular sciences. 2024 Dec 11;25(24):13291. [Content Brief]
[2]. Serreli G, et al. Ferulic Acid Derivatives and Avenanthramides Modulate Endothelial Function through Maintenance of Nitric Oxide Balance in HUVEC Cells. Nutrients. 2021 Jun 12;13(6):2026. [Content Brief]
[3]. Feng W, et al. Unraveling the inhibition mechanism of avenanthramides on amyloglucosidase: Probing by multi-spectroscopic techniques, enzyme kinetics, and molecular docking simulations. Food chemistry. 2026 Apr 30;509:148552. [Content Brief]
[4]. Okazaki Y, et al. New dimeric compounds of avenanthramide phytoalexin in oats. The Journal of organic chemistry. 2007 May 11;72(10):3830-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)