Ginkgolic acid C15:1CAS# 22910-60-7 |
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| Cas No. | 22910-60-7 | SDF | Download SDF |
| PubChem ID | 5281858 | Appearance | Beige powder |
| Formula | C22H34O3 | M.Wt | 346.50 |
| Type of Compound | Phenols | Storage | Desiccate at -20°C |
| Synonyms | Ginkgolic acid (15:1); Ginkgolic acid I; Romanicardic acid | ||
| Solubility | DMSO : ≥ 100 mg/mL (288.60 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 2-hydroxy-6-[(Z)-pentadec-8-enyl]benzoic acid | ||
| SMILES | CCCCCCC=CCCCCCCCC1=C(C(=CC=C1)O)C(=O)O | ||
| Standard InChIKey | YXHVCZZLWZYHSA-FPLPWBNLSA-N | ||
| Standard InChI | InChI=1S/C22H34O3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-16-19-17-15-18-20(23)21(19)22(24)25/h7-8,15,17-18,23H,2-6,9-14,16H2,1H3,(H,24,25)/b8-7- | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Ginkgolic acid C15:1 has antibacterial, antiparasitic, and anti-cancer activities, it can suppress lung cancer invasion and migration through the inhibition of PI3K/Akt/mTOR signaling pathway. |
| Targets | PI3K | Akt | mTOR | TGF-β/Smad | Antifection |
| In vitro | Ginkgolic acids and Ginkgo biloba extract inhibit Escherichia coli O157:H7 and Staphylococcus aureus biofilm formation.[Pubmed: 24457153]Int J Food Microbiol. 2014 Mar 17;174:47-55.Infection by enterohemorrhagic Escherichia coli O157:H7 (EHEC) is a worldwide problem, and there is no effective therapy. Biofilm formation is closely related to EHEC infection and is also a mechanism of antimicrobial resistance. The antibacterial activity and mechanism of ginkgolic acid C15:1.[Pubmed: 28088196]BMC Biotechnol. 2017; 17: 5.The present study investigated the antibacterial activity and underlying mechanisms of Ginkgolic acid C15:1(GA (C15:1)) monomer using green fluorescent protein (GFP)-labeled bacteria strains.
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| In vivo | In vivo assessment of anthelmintic efficacy of ginkgolic acids (C13:0, C15:1) on removal of Pseudodactylogyrus in European eel.[Reference: WebLink]Aquaculture, 2009, 297(1-4):38-43.Pseudodactylogyrus is a significant monogenean parasite of the gills of aquacultured European eels, and can cause severe gill pathology.
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| Kinase Assay | Ginkgolic Acid Inhibits Invasion and Migration and TGF-β-Induced EMT of Lung Cancer Cells Through PI3K/Akt/mTOR Inactivation.[Pubmed: 27177359]J Cell Physiol. 2017 Feb;232(2):346-354.Epithelial-to-mesenchymal transition (EMT) is a critical cellular phenomenon regulating tumor metastases.
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Ginkgolic acid C15:1 Dilution Calculator
Ginkgolic acid C15:1 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.886 mL | 14.43 mL | 28.86 mL | 57.7201 mL | 72.1501 mL |
| 5 mM | 0.5772 mL | 2.886 mL | 5.772 mL | 11.544 mL | 14.43 mL |
| 10 mM | 0.2886 mL | 1.443 mL | 2.886 mL | 5.772 mL | 7.215 mL |
| 50 mM | 0.0577 mL | 0.2886 mL | 0.5772 mL | 1.1544 mL | 1.443 mL |
| 100 mM | 0.0289 mL | 0.1443 mL | 0.2886 mL | 0.5772 mL | 0.7215 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Ginkgolic Acid is a natural compound with suspected cytotoxic, allergenic, mutagenic and carcinogenic properties, and it can inhibit protein SUMOylation both in vitro and in vivo without affecting in vivo ubiquitination.
In Vitro:Ginkgolic acid inhibits the in vitro SUMOylation of RanGAP1-C2 with the IC50 values of 3.0 μM. The level of SUMOylated p53 is markedly reduced by the ginkgolic acid treatment. Importantly, ginkgolic acid does not affect protein ubiquitination in cells. Ginkgolic acid inhibits the binding between E1 and GA-BODIPY in a dose-dependent manner[1]. Ginkgolic acid (31.2 μg/mL) inhibits HIV protease activity by 60%, compared with the negative control, and the effect is concentration-dependent. Ginkgolic acid treatment (50 and 100 μg/mL) effectively inhibits HIV infection in human PBMC cells. Ginkgolic acid at the concentrations up to 150 μg/mL does not cause any significant cytotoxicity in Jurkat cells[2]. GA only inhibits the growth of tumorogenic cell lines in a both dose- and time-dependent manner. Tumor cells are treated with GA for 72 h, 70.53±4.54% Hep-2 and 63.5±7.2% Tca8113 cells are retarded at GO/G1 phase, and the percentage of apoptosis is 40.4±1.58 and 38.4±1.7%, respectively. GA-treated activated caspase-3 downregulates the expression of anti-apoptotic Bcl-2 protein and upregulates the expression of pro-apoptotic Bax protein, eventually leading to a decrease in the Bcl-2/Bax ratio in tumor cellsin human PBMC cells. Ginkgolic acid at the concentrations up to 150 μg/mL does not cause any significant cytotoxicity in Jurkat cells[3].
References:
[1]. Fukuda I, et al. Ginkgolic acid inhibits protein SUMOylation by blocking formation of the E1-SUMO intermediate. Chem Biol. 2009 Feb 27;16(2):133-40.
[2]. Lü JM, et al. Ginkgolic acid inhibits HIV protease activity and HIV infection in vitro. Med Sci Monit. 2012 Aug;18(8):BR293-298.
[3]. Zhou C, et al. Antitumor effects of ginkgolic acid in human cancer cell occur via cell cycle arrest and decrease the Bcl-2/Bax ratio to induce apoptosis. Chemotherapy. 2010;56(5):393-402.
[4]. Qiu F, et al. Pharmacological inhibition of SUMO-1 with ginkgolic acid alleviates cardiac fibrosis induced by myocardial infarction in mice. Toxicol Appl Pharmacol. 2018 Apr 15;345:1-9.
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Ginkgolic acids and Ginkgo biloba extract inhibit Escherichia coli O157:H7 and Staphylococcus aureus biofilm formation.[Pubmed:24457153]
Int J Food Microbiol. 2014 Mar 17;174:47-55.
Infection by enterohemorrhagic Escherichia coli O157:H7 (EHEC) is a worldwide problem, and there is no effective therapy. Biofilm formation is closely related to EHEC infection and is also a mechanism of antimicrobial resistance. Antibiofilm screening of 560 purified phytochemicals against EHEC showed that ginkgolic acids C15:1 and C17:1 at 5mug/ml and Ginkgo biloba extract at 100mug/ml significantly inhibited EHEC biofilm formation on the surfaces of polystyrene and glass, and on nylon membranes. Importantly, at their working concentrations, ginkgolic acids and G. biloba extract did not affect bacterial growth. Transcriptional analyses showed that Ginkgolic acid C15:1 repressed curli genes and prophage genes in EHEC, and these findings were in-line with reduced fimbriae production and biofilm reductions. Interestingly, ginkgolic acids and G. biloba extract did not inhibit the biofilm formation of a commensal E. coli K-12 strain. In addition, ginkgolic acids and G. biloba extract inhibited the biofilm formation of three Staphylococcus aureus strains. The findings of this study suggest that plant secondary metabolites represent an important resource for biofilm inhibitors.
Molluscicidal activity against Oncomelania hupensis of Ginkgo biloba.[Pubmed:18334286]
Fitoterapia. 2008 Jun;79(4):250-4.
In search for molluscicidal active components, petroleum ether, ethyl acetate, ethanol, and water extracts from Ginkgo sarcotesta were evaluated against the snail Oncomelania hupensis. The bioassay-oriented showed that the activity concentrates in the petroleum ether extract (LD(50) 7.81 ppm). Ginkgolic acids, isolated from the petroleum ether extract, exhibited strong molluscicidal activity (LD(50) 1.49 ppm), gingkgolic acid C15:1 having the strongest molluscicidal activity.
The antibacterial activity and mechanism of ginkgolic acid C15:1.[Pubmed:28088196]
BMC Biotechnol. 2017 Jan 14;17(1):5.
BACKGROUND: The present study investigated the antibacterial activity and underlying mechanisms of ginkgolic acid (GA) C15:1 monomer using green fluorescent protein (GFP)-labeled bacteria strains. RESULTS: GA presented significant antibacterial activity against Gram-positive bacteria but generally did not affect the growth of Gram-negative bacteria. The studies of the antibacterial mechanism indicated that large amounts of GA (C15:1) could penetrate GFP-labeled Bacillus amyloliquefaciens in a short period of time, and as a result, led to the quenching of GFP in bacteria. In vitro results demonstrated that GA (C15:1) could inhibit the activity of multiple proteins including DNA polymerase. In vivo results showed that GA (C15:1) could significantly inhibit the biosynthesis of DNA, RNA and B. amyloliquefaciens proteins. CONCLUSION: We speculated that GA (C15:1) achieved its antibacterial effect through inhibiting the protein activity of B. amyloliquefaciens. GA (C15:1) could not penetrate Gram-negative bacteria in large amounts, and the lipid soluble components in the bacterial cell wall could intercept GA (C15:1), which was one of the primary reasons that GA (C15:1) did not have a significant antibacterial effect on Gram-negative bacteria.
Ginkgolic Acid Inhibits Invasion and Migration and TGF-beta-Induced EMT of Lung Cancer Cells Through PI3K/Akt/mTOR Inactivation.[Pubmed:27177359]
J Cell Physiol. 2017 Feb;232(2):346-354.
Epithelial-to-mesenchymal transition (EMT) is a critical cellular phenomenon regulating tumor metastases. In the present study, we investigated whether ginkgolic acid can affect EMT in lung cancer cells and the related underlying mechanism(s) of its actions. We found that Ginkgolic acid C15:1 (GA C15:1) inhibited cell proliferation, invasion, and migration in both A549 and H1299 lung cancer cells. GA C15:1 also suppressed the expression of EMT related genes (Fibronectin, Vimentin, N-cadherin, MMP-9, MMP-2, Twist and Snail) and suppressed TGF-beta-induced EMT as assessed by reduced expression of mesenchymal markers (Fibronectin, Vimentin, N-cadherin), MMP-9, MMP-2, Twist and Snail. However, GA C15:1 did not affect the expression of various epithelial marker proteins (Occludin and E-cadherin) in both A549 and H1299 cells. TGF-beta-induced morphologic changes from epithelial to mesenchymal cells and induction of invasion and migration were reversed by GA C15:1. Finally, GA C15:1 not only abrogated basal PI3K/Akt/mTOR signaling cascade, but also reduced TGF-beta-induced phosphorylation of PI3K/Akt/mTOR pathway in lung cancer cells. Overall, these findings suggest that GA C15:1 suppresses lung cancer invasion and migration through the inhibition of PI3K/Akt/mTOR signaling pathway and provide a source of potential therapeutic compounds to control the metastatic dissemination of tumor cells. J. Cell. Physiol. 232: 346-354, 2017. (c) 2016 Wiley Periodicals, Inc.
