4,6,12-Tetradecatriene8,10-diyne-1,3-diacetate
4,6,12-Tetradecatriene8,10-diyne-1,3-diacetate is a polyacetylene compound found in the rhizomes of Atractylodes lancea. 4,6,12-Tetradecatriene8,10-diyne-1,3-diacetate inhibits human pancreatic lipase, with an IC50 of 55.67 μM and 16.7 μg/mL. 4,6,12-Tetradecatriene8,10-diyne-1,3-diacetate can block the digestion of triglycerides by inhibiting the activity of human pancreatic lipase. 4,6,12-Tetradecatriene8,10-diyne-1,3-diacetate can be used in research on obesity.
For research use only. We do not sell to patients.
- CAS No.: 23414-61-1
- Formula: C18H20O4
- Molecular Weight:300.35
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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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
4,6,12-Tetradecatriene8,10-diyne-1,3-diacetate (compound 5) (10 min pre-incubation; 30 min substrate reaction at 37°C) inhibits recombinant human pancreatic lipase with an IC50 of 55.67 μM and 16.7 μg/mL[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. 23414-61-1
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Molecular Weight 300.35
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Formula C18H20O4
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SMILES
C/C=C/C#CC#C/C=C/C=C/C(OC(C)=O)CCOC(C)=O
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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)
4,6,12-Tetradecatriene8,10-diyne-1,3-diacetate Related Classifications
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