White crystalline powder
Ginkgo biloba L./Ginkgo biloba (ginkgo) and minor cashew nut shellBiological Use / Importance: Possesses antitubercular activity
Simple Phenolic Compounds
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
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.
Methanol; Dichloromethane; Petroleum ether; Ethyl Acetate
492.1±40.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:22910-60-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Ginkgolic acid (15:1) is a major toxic component in extracts obtained from Ginkgo biloba (EGb) that has allergic and genotoxic effects. This study is the first to explore the hepatotoxicity of ginkgolic acid (15:1) using a NMR (nuclear magnetic resonance)-based metabolomics approach in combination with biochemistry assays. Mice were orally administered two doses of ginkgolic acid (15:1), and mouse livers and serum were then collected for NMR recordings and biochemical assays. The levels of activity of alanine aminotransferase (ALT) and glutamic aspartate transaminase (AST) observed in the ginkgolic acid (15:1)-treated mice suggested that it had induced severe liver damage. An orthogonal signal correction partial least-squares discriminant analysis (OSC-PLSDA) performed to determine the metabolomic profile of mouse liver tissues indicated that many metabolic disturbances, especially oxidative stress and purine metabolism, were induced by ginkgolic acid (15:1). A correlation network analysis combined with information related to structural similarities further confirmed that purine metabolism was disturbed by ginkgolic acid (15:1). This mechanism might represent the link between the antitumour activity and the liver injury-inducing effect of ginkgolic acid (15:1). A SUS (Shared and Unique Structure) plot suggested that a two-dose treatment of ginkgolic acid (15:1) had generally the same effect on metabolic variations but that its effects were dose-dependent, revealing some of the common features of ginkgolic acid (15:1) dosing. This integrated metabolomics approach helped us to characterise ginkgolic acid (15:1)-induced liver damage in mice.
Ginkgolic acid (15:1); Metabolomics; Mice; NMR.
1 H NMR-based Metabolomics Study of Liver Damage Induced by Ginkgolic Acid (15:1) in Mice
Lei Jiang 1 , Zhi-Hong Si 1 , Ming-Hui Li 1 , He Zhao 1 , Yong-Hong Fu 1 , Yue-Xiao Xing 1 , Wei Hong 1 , Ling-Yu Ruan 1 , Pu-Min Li 1 , Jun-Song Wang 2
2017 Mar 20
Ginkgolic acids (GAs), primarily found in the leaves, nuts, and testa of ginkgo biloba, have been identified with suspected allergenic, genotoxic and cytotoxic properties. However, little information is available about GAs toxicity in kidneys and the underlying mechanism has not been thoroughly elucidated so far. Instead of GAs extract, the renal cytotoxicity of GA (15 : 1), which was isolated from the testa of Ginkgo biloba, was assessed in vitro by using MDCK cells. The action of GA (15 : 1) on cell viability was evaluated by the MTT and neutral red uptake assays. Compared with the control, the cytotoxicity of GA (15 : 1) on MDCK cells displayed a time- and dose-dependent manner, suggesting the cells mitochondria and lysosomes were damaged. It was confirmed that GA (15 : 1) resulted in the loss of cells mitochondrial trans-membrane potential (ΔΨm). In propidium iodide (PI) staining analysis, GA (15 : 1) induced cell cycle arrest at the G0/G1 and G2/M phases, influencing on the DNA synthesis and cell mitosis. Characteristics of necrotic cell death were observed in MDCK cells at the experimental conditions, as a result of DNA agarose gel electrophoresis and morphological observation of MDCK cells. In conclusion, these findings might provide useful information for a better understanding of the GA (15 : 1) induced renal toxicity.
Ginkgolic acid (15:1); Metabolomics; Mice; NMR.
Mechanism for Ginkgolic Acid (15 : 1)-induced MDCK Cell Necrosis: Mitochondria and Lysosomes Damages and Cell Cycle Arrest
Qing-Qing Yao 1 , Zhen-Hua Liu 1 , Ming-Cheng Xu 1 , Hai-Hong Hu 1 , Hui Zhou 1 , Hui-Di Jiang 1 , Lu-Shan Yu 1 , Su Zeng 2
1. In this article, metabolites of ginkgolic acid (GA) (15:1) in rats plasma, bile, urine and faeces after oral administration have been investigated for the first time by high-performance liquid chromatography coupled to tandem mass spectrometry (HPLC-MS/MS) with the aid of on-line hydrogen/deuterium (H/D) exchange technique and β-glucuronidase hydrolysis experiments. 2. After oral administration of GA (15:1, M0) to rats at a dose of 10 mg/kg, it was found that metabolites M1-M5 together with parent compound (M0) existed in rat plasma; parent compound (M0) and metabolites M2-M5 were observed in rat bile, and parent compound (M0) with metabolites M1 and M2 were discovered in rat faeces, and there was no parent compound and metabolite detectable in rat urine. 3. Two oxidative metabolites of GA (15:1, M0) were identified as 2-hydroxy-6-(pentadec-8-enyl-10-hydroxy) benzoic acid (M1) and 2-hydroxy-6-(pentadec-8-enyl-11-hydroxy-13-carbonyl) benzoic acid (M2), respectively. Metabolites M3, M4 and M5 were identified as the mono-glucuronic acid conjugates of parent compound (M0), M1 and M2, respectively. 4. The results indicated that M1 and M2 with parent compound (M0) were mainly eliminated in faeces and three glucuronide metabolites (M3, M4 and M5) excreted in bile as the predominant forms after oral administration of GA (15:1) to rats.
Identification of Ginkgolic Acid (15:1) Metabolites in Rats Following Oral Administration by High-Performance Liquid Chromatography Coupled to Tandem Mass Spectrometry
Hongjun Xia 1 , Zhenhua Liu, Haihong Hu, Hui Zhou, Su Zeng