Euphominoid C
Euphominoid C is a competitive α-glucosidase inhibitor (IC50 = 52.50 μM) and a mixed-type β-glucuronidase inhibitor (IC50 = 45.87 μM). Euphominoid C exhibits reversible binding modes against both enzymes. Euphominoid C can be used for the research of diabetes.
For research use only. We do not sell to patients.
- CAS No.: 2113766-69-9
- Formula: C20H32O2
- Molecular Weight:304.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
α‑glucosidase 52.5 μM (IC50) |
β-glucuronidase 45.87 μM (IC50) |
In Vitro
Euphominoid C (compound 11) (100-45.87 μM) significantly inhibits Escherichia coli β-glucuronidase with an IC50 value of 45.87 μM, acting through a mixed-type inhibition mode[1].
Euphominoid C effectively inhibits α-glucosidase through a competitive mechanism, with an IC50 of 52.50 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2113766-69-9
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Molecular Weight 304.47
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Formula C20H32O2
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SMILES
C[C@@]12C3=C([C@](CO)(C)[C@@H](O)CC3)CC[C@]1(C[C@](C=C)(C)CC2)[H]
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Structure Classification
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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.
Protocols
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Euphominoid C Related Classifications
HY-N21640A Related Classifications
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