5-OH-HxMF
5-OH-HxMF is a hydroxylated polymethoxyflavone that has anti-inflammatory, anticancer, neurotrophic and neuroprotective activities.
For research use only. We do not sell to patients.
- CAS No.: 1176-88-1
- Formula: C21H22O9
- Molecular Weight:418.39
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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
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HL-60 | IC50 |
4.16 μM
Compound: IV, 5-demethylheptaMF
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Antiproliferative activity against HL60 after 24 hrs
Antiproliferative activity against HL60 after 24 hrs
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[PMID: 17391969] |
| KB | IC50 |
6 μg/mL
Compound: 5
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Cytotoxicity against human KB cells
Cytotoxicity against human KB cells
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[PMID: 7964782] |
| Monocyte | IC50 |
10 μM
Compound: 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone
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Inhibition of TNFalpha expression in LPS-stimulated human monocytes treated 30 mins before LPS challenge measured after 14 hrs by ELISA
Inhibition of TNFalpha expression in LPS-stimulated human monocytes treated 30 mins before LPS challenge measured after 14 hrs by ELISA
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[PMID: 10096854] |
In Vitro
5-OH-HxMF (5-20 µM; 48 h) effectively induces PC12 neurite outgrowth accompanied with the expression of neuronal differentiation marker protein growth-associated protein-43(GAP-43)[1].
5-OH-HxMF (20 µM; 0-120 min) causes the enhancement of cyclic AMP response element binding protein (CREB) phosphorylation, c-fos gene expression and CRE-mediated transcription[1].
5-OH-HxMF significantly reduces the production of nitric oxide and prostaglandin E2 and downregulates inducible nitric oxide synthase (iNOS) and COX-2 expression in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. 5-OH-HxMF inhibits the release of pro-inflammatory cytokines, such as tumor necrosis factor-α and IL-1β, and decreases the transcriptional levels. 5-OH-HxMF significantly inhibits the LPS-induced NF-κB translocation from the cytosol to the nucleus, which is associated with the abrogation of inhibitory IκBα degradation and subsequent decreases in nuclear p65 levels[2].
5-OH-HxMF inhibits cell growth and induces apoptosis in human leukemia cells[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:PC12 cells
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Concentration:5 µM, 10 µM, 20 µM
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Incubation Time:48 h
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Result:Significantly evoked a dose-dependent increase on neurite outgrowth.
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Cell Line:PC12 cells
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Concentration:5 µM, 10 µM, 20 µM
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Incubation Time:24 h
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Result:Promoted GAP-43 expression in PC12 cells.
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Cell Line:PC12 cells
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Concentration:20 µM
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Incubation Time:0 min, 30 min, 60 min or 120 min
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Result:Stimulated phosphorylation of CREB in PC12 cells.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Female ICR mice treated with 12-O-tetradecanoylphorbol-13-acetate (TPA)[3].
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Dosage:1 and 3 μmol in 200 μL acetone
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Administration:Topically treated; twice a week; for 20 weeks
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Result:Significantly inhibited TPA-induced mouse skin inflammation by decreasing inflammatory parameters.
Chemical Information
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CAS No. 1176-88-1
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Molecular Weight 418.39
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Formula C21H22O9
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SMILES
O=C1C(OC)=C(OC2=C1C(O)=C(C(OC)=C2OC)OC)C3=CC=C(C(OC)=C3)OC
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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
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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
Purity & Documentation
References
[1]. Hui-Chi Lai, et al. Neurotrophic effect of citrus 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone: promotion of neurite outgrowth via cAMP/PKA/CREB pathway in PC12 cells. PLoS One. 2011;6(11):e28280. [Content Brief]
[2]. Min Jeong Kim, et al. Anti-inflammatory effects of 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone via NF-κB inactivation in lipopolysaccharide-stimulated RAW 264.7 macrophage. Mol Med Rep. 2014 Apr;9(4):1197-203. [Content Brief]
[3]. Ching-Shu Lai, et al. Inhibitory effect of citrus 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone on 12-O-tetradecanoylphorbol 13-acetate-induced skin inflammation and tumor promotion in mice. Carcinogenesis. 2007 Dec;28(12):2581-8. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
5-OH-HxMF Related Classifications
HY-121711 Related Classifications
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