Ginkgolic acid C15:1

Names

[ Name ]:
Ginkgolic acid C15:1

[Synonym ]:
MFCD03093717
15:1 anacardic acid
Ginkgolic acid
Ginkgolic acid 15:1
Romanicardic acid
(Z)-2-Hydroxy-6-(pentadec-8-en-1-yl)benzoic acid
Ginkgolic acid (15:1)
2-Hydroxy-6-(pentadec-8-en-1-yl)benzoic acid
(Z)-6-[8-pentadecenyl]salicylic acid
2-hydroxy-6-pentadec-8(Z)-enylbenzoic acid
6-[(8Z)-Pentadecenyl]-salicylic acid,Ginkgolic acid I
Ginkgoic acid
2-hydroxy-6-(8-pentadecenyl) salicylic acid
Anacardic acid monoene
6-(8-pentadecenyl)salicylic acid
2-Hydroxy-6-[(8Z)-pentadec-8-en-1-yl]benzoic acid
Ginkgolic acid I
Gingkolic Acid
2-Hydroxy-6-[(8Z)-8-pentadecen-1-yl]benzoic acid
6-(8Z-pentadecenyl)salicylic acid
Ginkgolic acid (C15:1)
6-<8(Z)-pentadecenyl>salicylic acid
Benzoic acid, 2-hydroxy-6-(8-pentadecenyl)-, (Z)-
Benzoic acid, 2-hydroxy-6-[(8Z)-8-pentadecen-1-yl]-
Ginkgolic Acid C15:1
(Z)-2-Hydroxy-6-(8-pentadecenyl)benzoic acid

Biological Activity

[Description]:

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.

[Related Catalog]:

Signaling Pathways >> Metabolic Enzyme/Protease >> E1/E2/E3 Enzyme

Research Areas >> Cancer

Natural Products >> Phenols

[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].

[Cell Assay]

Jurkat cells (106 cells/mL) are cultured in the RPMI medium with or without different concentrations of ginkgolic acid for 48 hours to test the cytotoxicity of ginkgolic acid. The cytotoxicity of ginkgolic acid is determined using a tetrazolium compound (MTS) and an electron coupling reagent (PMS). MTS is chemically reduced by cells into formazan, which is soluble in the tissue culture medium. The measurement of the absorbance of the formazan can be carried out using 96 well microplates at 492 nm. Since the production of formazan is proportional to the number of living cells, the intensity of the produced color is a good indication of the viability of the cells.

[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.

[Related Small Molecules]

PYR-41 | NSC232003 | CC122 | SZL P1-41 | TAK-243(MLN7243) | 2-Chloro-N-(3,4-dimethoxybenzyl)acetamide | PRT 4165 | SKPin C1 | TZ9 | CC 0651 | 2-D08 | PYZD 4409 | CC-885 | COH000

Chemical & Physical Properties

[ Density]:
1.0±0.1 g/cm3

[ Boiling Point ]:
492.1±40.0 °C at 760 mmHg

[ Melting Point ]:
136-137ºC

[ Molecular Formula ]:
C₂₂H₃₄O₃

[ Molecular Weight ]:
346.504

[ Flash Point ]:
265.5±23.8 °C

[ Exact Mass ]:
346.250793

[ PSA ]:
57.53000

[ LogP ]:
9.44

[ Vapour Pressure ]:
0.0±1.3 mmHg at 25°C

[ Index of Refraction ]:
1.527

Safety Information

[ Symbol ]:

GHS07

[ Signal Word ]:
Warning

[ Hazard Statements ]:
H315-H319-H335

[ Precautionary Statements ]:
P261-P305 + P351 + P338

[ Personal Protective Equipment ]:
dust mask type N95 (US);Eyeshields;Gloves

[ Hazard Codes ]:
Xi:Irritant;

[ Risk Phrases ]:
R36/37/38

[ Safety Phrases ]:
S26

[ RIDADR ]:
NONH for all modes of transport

Precursor & DownStream

Precursor

DownStream

Articles

Design and evaluation of anacardic acid derivatives as anticavity agents.

Eur. J. Med. Chem. 43 , 1315-20, (2008)

On the basis of antibacterial anacardic acids, 6-pentadecenylsalicylic acids, isolated from the cashew apple, Anacardium occidentale L. (Anacardiaceae), a series of 6-alk(en)ylsalicylic acids were syn...

Cytotoxicity of ginkgolic acid in HepG2 cells and primary rat hepatocytes.

Toxicol. Lett. 187(3) , 131-6, (2009)

Ginkgolic acids and related alkylphenols (e.g. cardanols and cardols) have been recognized as hazardous compounds with suspected cytotoxic, allergenic, mutagenic and carcinogenic properties. To determ...

Identification of TRIML2, a novel p53 target, that enhances p53 SUMOylation and regulates the transactivation of proapoptotic genes.

Mol. Cancer Res. 13(2) , 250-62, (2015)

The tumor-suppressor protein p53, encoded by TP53, inhibits tumorigenesis by inducing cell-cycle arrest, senescence, and apoptosis. Several genetic polymorphisms exist in TP53, including a proline to ...