Hypercohin K
Hypercohin K is a polycyclic polyprenylated acylphloroglucinol isolated from Hypericum henryi, containing a rare spiro-fused cyclopropane ring in its structure. Hypercohin K exhibits anti-inflammatory, antitumor, and AChE-enhancing activities. Hypercohin K reduces intracellular lipid accumulation by regulating lipid metabolism genes, and can inhibit NO production to exert anti-inflammatory effects. Hypercohin K can be used in research on non-alcoholic steatohepatitis and tumors.
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- CAS. Nr.: 1809058-37-4
- Formel: C33H40O4
- Molecular Weight:500.68
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
IC50 & Target
[2]|
AChE |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HL-60 | IC50 |
18.2 μM
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Cytotoxic activity against human HL-60 cells assessed as inhibition of cell growth.
Cytotoxic activity against human HL-60 cells assessed as inhibition of cell growth.
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j.tetlet.2015.08.033 |
| SMMC-7721 | IC50 |
18.1 μM
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Cytotoxic activity against human SMMC-7721 cells assessed as inhibition of cell growth.
Cytotoxic activity against human SMMC-7721 cells assessed as inhibition of cell growth.
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j.tetlet.2015.08.033 |
| A549 | IC50 |
23.3 μM
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Cytotoxic activity against human A-549 cells assessed as inhibition of cell growth.
Cytotoxic activity against human A-549 cells assessed as inhibition of cell growth.
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j.tetlet.2015.08.033 |
| MCF7 | IC50 |
23.5 μM
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Cytotoxic activity against human MCF-7 cells assessed as inhibition of cell growth.
Cytotoxic activity against human MCF-7 cells assessed as inhibition of cell growth.
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j.tetlet.2015.08.033 |
| RAW264.7 | IC50 |
10.29 μM
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Inhibition of nitric oxide production in LPS-induced mouse RAW264.7 macrophage cells pretreated for 1 hr followed by 24 hrs co-culture with LPS.
Inhibition of nitric oxide production in LPS-induced mouse RAW264.7 macrophage cells pretreated for 1 hr followed by 24 hrs co-culture with LPS.
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42119714 |
In Vitro
Hypercohin K exhibits cytotoxicity against HL-60 with an IC50 of 18.2 μM, SMMC-7721 with an IC50 of 18.1 μM, A-549 with an IC50 of 23.3 μM, and MCF-7 with an IC50 of 23.5 μM[2].
Hypercohin K (5-10 μM; 48 h) demonstrates significant in vitro anti-NASH activity by decreasing intracellular lipid accumulation and regulating the expression of lipid metabolism-related genes in FFA-induced L02 cells[3].
Hypercohin K (3.125-25 μM; 1 h pretreatment, followed by 24 h co-culture with LPS) inhibits nitric oxide production in LPS-induced RAW264.7 cells with an IC50 of 10.29 μM[4].
Hypercohin K (50 μM) increases AChE activity in the acetylcholinesterase inhibition assay[2].
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:FFA-induced L02 cell line
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Concentration:10 μM
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Incubation Time:48 h
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Result:Downregulated the expression of CD36 and FASN genes and increased the expression of PPARα and ACOX1 genes.
Chemical Information
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CAS. Nr. 1809058-37-4
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Molecular Weight 500.68
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Formel C33H40O4
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SMILES
O=C1[C@@]23[C@@](C2)(C(C)(C)OC3=C(C(=O)C4=CC=CC=C4)C(=O)[C@]1(C/C=C(/CCC=C(C)C)\C)CC=C(C)C)[H]
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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3T3-L1 preadipocyte-to-adipocyte differentiation
3T3-L1 preadipocytes are induced to differentiate after growth arrest using adipogenic media containing insulin, dexamethasone, and IBMX; differentiation is assessed by lipid-droplet accumulation, triglyceride increase, Oil Red O staining, and adipocyte-marker induction such as PPARγ and C/EBPα.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Lipid Droplets: Oil Red O/Sudan Dye Lipid Staining
Lipid droplets are intracellular organelles with a neutral-lipid core that stores triacylglycerols and sterol esters, and Oil Red O or Sudan dyes detect these hydrophobic lipid deposits by partitioning into retained lipids in fresh or frozen specimens. Oil Red O stains neutral triglycerides and lipids in frozen tissue sections or air-dried cytologic preparations, while Sudan Black B has also been used as a histochemical fat stain for lipid-rich tissue structures.
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Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Hypercohin K Related Classifications
HY-N21706 Related Classifications
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