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    10-Hydroxy-2-decenoic acid
    10-Hydroxy-2-decenoic acid
    CAS No. 765-01-5 Price $60 / 20mg
    Catalog No.CFN90512Purity>=98%
    Molecular Weight186.24Type of CompoundMonoterpenoids
    FormulaC10H18O3Physical DescriptionOil
    Download     COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: 10-Hydroxy-2-decenoic acid is a potential HDACI which inhibits the proliferation of FLS cells by PI3K-AKT pathway; it exerts an inhibitory effect on VEGF-induced angiogenesis, partly by inhibiting both cell proliferation and migration. 10-Hydroxy-2-decenoic acid activates AMPK, and insulin independently enhances glucose uptake following translocation of Glut4 to PM; it also can prevent UVA-induced damage and inhibit MMP-1 and MMP-3 expressions.
    Targets: AMPK | GLUT | Calcium Channel | ROS | MMP(e.g.TIMP) | JNK | p38MAPK | HDAC | PI3K | Akt | VEGFR
    In vitro:
    J Eur Acad Dermatol Venereol. 2013 Oct;27(10):1269-77.
    10-Hydroxy-2-decenoic acid prevents ultraviolet A-induced damage and matrix metalloproteinases expression in human dermal fibroblasts.[Pubmed: 23030720]
    10-Hydroxy-2-decenoic acid (10-HDA) is a major fatty acid component of royal jelly, which has been reported to have a variety of beneficial pharmacological characteristics. However, the effects of 10-HDA on skin photoageing and its potential mechanism of action are unclear. We investigated the protective effects of 10-HDA on ultraviolet (UV) A-induced damage in human dermal fibroblasts (HDFs). We then explored the inhibitory effects of 10-HDA on UVA-induced matrix metalloproteinases (MMPs) expression and elucidated the signalling pathways controlling MMPs inhibition.
    Primary human dermal fibroblasts were exposed to UVA. Cell proliferation, cellular senescent state and collagen content were analysed using CCK-8, senescence-associated β-galactosidase staining and Sircol collagen assay, respectively. Fluorometric assays were performed to detect the formation of reactive oxygen species (ROS) in the cells. The mRNA levels of MMP-1, MMP-3 and type I (α1) collagen were determined by quantitative real-time PCR. Western blot was applied to detect the expression of MMP-1, MMP-3, JNK and p38 MAPK. HDFs treated with 10-HDA were significantly protected from UVA-induced cytotoxicity, ROS, cellular senescence and stimulated collagen production. Moreover, 10-HDA suppressed the UVA-induced expression of MMP-1 and MMP-3 at both the transcriptional and protein levels. Treatment with 10-HDA also reduced the UVA-induced activation of the JNK and p38 MAPK pathways.
    The data obtained in this study provide evidence that 10-HDA could prevent UVA-induced damage and inhibit MMP-1 and MMP-3 expressions. Therefore, 10-HDA may be a potential agent for the prevention and treatment of skin photoageing.
    Evid Based Complement Alternat Med. 2009 Dec;6(4):489-94.
    10-Hydroxy-2-decenoic acid, a major fatty acid from royal jelly, inhibits VEGF-induced angiogenesis in human umbilical vein endothelial cells.[Pubmed: 18955252]
    10-Hydroxy-2-decenoic acid (10HDA), a major fatty acid component of RJ, is known to have various pharmacological effects; its antitumor activity being especially noteworthy. However, the mechanism underlying this effect is unclear.
    We examined the effect of 10-Hydroxy-2-decenoic acid on VEGF-induced proliferation, migration and tube formation in human umbilical vein endothelial cells (HUVECs). Our findings showed that, 10-Hydroxy-2-decenoic acid at 20 microM or more significantly inhibited such proliferation, migration and tube formation. Similarly, 10 microM GM6001, a matrix metalloprotease inhibitor, prevented VEGF-induced migration and tube formation.
    These findings indicate that 10-Hydroxy-2-decenoic acid exerts an inhibitory effect on VEGF-induced angiogenesis, partly by inhibiting both cell proliferation and migration.
    10-Hydroxy-2-decenoic acid Description
    Source: From Royal jelly.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 5.3694 mL 26.8471 mL 53.6942 mL 107.3883 mL 134.2354 mL
    5 mM 1.0739 mL 5.3694 mL 10.7388 mL 21.4777 mL 26.8471 mL
    10 mM 0.5369 mL 2.6847 mL 5.3694 mL 10.7388 mL 13.4235 mL
    50 mM 0.1074 mL 0.5369 mL 1.0739 mL 2.1478 mL 2.6847 mL
    100 mM 0.0537 mL 0.2685 mL 0.5369 mL 1.0739 mL 1.3424 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Mol Nutr Food Res. 2013 Oct;57(10):1794-802.
    10-Hydroxy-2-decenoic acid, a unique medium-chain fatty acid, activates 5'-AMP-activated protein kinase in L6 myotubes and mice.[Pubmed: 23754629]
    10-Hydroxy-2-decenoic acid (10H2DA) is one of the unique medium-chain fatty acids (MCFAs) specifically found in royal jelly. We hypothesize that 10-Hydroxy-2-decenoic acid has multiple biological functions and may aid in 5'-AMP-activated protein kinase (AMPK) activation and affect the glucose transport system in skeletal muscle.
    We examined whether various MCFAs present in royal jelly activated AMPKα. Treatment of L6 myotubes with various MCFAs showed that 10-Hydroxy-2-decenoic acid administration resulted in a significant increase in phosphorylated AMPKα. 10-Hydroxy-2-decenoic acid activates AMPK independently of insulin and significantly increased glucose uptake into L6 myotubes following translocation of glucose transporter 4 (Glut4) to the plasma membrane (PM).Oral administration of 10-Hydroxy-2-decenoic acid significantly stimulated phosphorylation of AMPK and Glut4 translocation to the PM in mouse skeletal muscle.
    These findings indicate that (i) 10-Hydroxy-2-decenoic acid activates AMPK, and insulin independently enhances glucose uptake following translocation of Glut4 to PM, (ii) activation of AMPKα by 10-Hydroxy-2-decenoic acid is mediated via extracellular Ca2⁺-dependent Ca2⁺/calmodulin-dependent kinase kinase β, without alteration in the AMP:ATP ratio, and liver kinase B1 was not involved in the activation.
    Cell Research:
    Int Immunopharmacol. 2015 Jun 4.
    10-Hydroxy-2-decenoic acid inhibiting the proliferation of fibroblast-like synoviocytes by PI3K-AKT pathway.[Pubmed: 26050632]
    To reveal the mechanism of 10-Hydroxy-2-decenoic acid inhibiting the proliferation of fibroblast-like synoviocytes (FLSs) of RA patients.
    Cell proliferation, HDAC activity and histone acetylation level of FLS cells treated with 10-Hydroxy-2-decenoic acid were detected by MTT assay, Colorimetric HDAC Activity Assay and Western-blot. Different genes in FLS cells from RA patients were primary cultured and treated with 10-Hydroxy-2-decenoic acid. They were then screened by Human Transcriptome 1.0 ST microarrays and verified by real-time PCR. The results showed dose-dependent and time-dependent decreases in cell viability and HDAC activity in FLSs treated with 10-Hydroxy-2-decenoic acid, and time-dependent induction in the acetylation of H3 and H4 at the same time.
    These results imply that 10-Hydroxy-2-decenoic acid is a potential HDACI which inhibits the proliferation of FLS cells by PI3K-AKT pathway.