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Ginkgolide C


  • Brand : BIOFRON

  • Catalogue Number : BF-G2014

  • Specification : 98%

  • CAS number : 15291-76-6

  • Formula : C20H24O11

  • Molecular Weight : 440.4

  • PUBCHEM ID : 24721502

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystal

Botanical Source

Ginkgo biloba

Structure Type



Standards;Natural Pytochemical;API




Ginkgolid C/(1R,3R,7S,8S,9R,10S,11R,13S,16S,17R)-8-tert-Butyl-6,9,12,17-tetrahydroxy-16-methyl-2,4,14,19-tetraoxahexacyclo[]nonadecane-5,15,18-trione/(1R,3R,7S,8S,9R,10S,11R,13S,16S,17R)-6,9,12,17-Tetrahydroxy-16-methyl-8-(2-methyl-2-propanyl)-2,4,14,19-tetraoxahexacyclo[]nonadecane-5,15,18-trione/6H-9,4a-(Epoxymethano)-3aH,9H-cyclopenta[c]furo[2,3-b]furo[3',2':3,4]cyclopenta[1,2-d]furan-2,6,13(1H)-trione, 11-(1,1-dimethylethyl)hexahydro-1,4b,8,10-tetrahydroxy-5-methyl-, (3aR,4aR,4bR,5S,7aS,8aR,9S,10R,11S,11aS)-/1,7-DIHYDROXY-GINKGOLIDE A/Gingkolide C/1,3,7,10-Tetrahydroxyginkgolid/GinkgolideC




1.7±0.1 g/cm3


Methanol; Ethyl Acetate

Flash Point

291.4±27.8 °C

Boiling Point

813.8±65.0 °C at 760 mmHg

Melting Point



InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:15291-76-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Ginkgolide C, isolated from Ginkgo biloba, is a diterpene lactone that has multiple biological functions and can improve Alzheimer disease and platelet aggregation. Ginkgolide C also inhibits adipogenesis in 3T3-L1 adipocytes. The present study evaluated whether ginkgolide C reduced lipid accumulation and regulated the molecular mechanism of lipogenesis in oleic acid-induced HepG2 hepatocytes. HepG2 cells were treated with 0.5 mM oleic acid for 48 h to induce a fatty liver cell model. Then, the cells were exposed to various concentrations of ginkgolide C for 24 h. Staining with Oil Red O and the fluorescent dye BODIPY 493/503 revealed that ginkgolide C significantly reduced excessive lipid accumulation in HepG2 cells. Ginkgolide C decreased peroxisome proliferator-activated receptor γ and sterol regulatory element-binding protein 1c to block the expression of fatty acid synthase. Ginkgolide C treatment also promoted the expression of adipose triglyceride lipase and the phosphorylation level of hormone-sensitive lipase to enhance the decomposition of triglycerides. In addition, ginkgolide C stimulated CPT-1 to activate fatty acid β-oxidation, significantly increased sirt1 and phosphorylation of AMP-activated protein kinase (AMPK), and decreased expression of acetyl-CoA carboxylase for suppressed fatty acid synthesis in hepatocytes. Taken together, our results suggest that ginkgolide C reduced lipid accumulation and increased lipolysis through the sirt1/AMPK pathway in oleic acid-induced fatty liver cells.


AMPK; Anti-obesity; Ginkgolide C; Lipogenesis; Lipolysis.


Ginkgolide C Reduced Oleic Acid-Induced Lipid Accumulation in HepG2 Cells


Wen-Chung Huang 1 2 , Ya-Ling Chen 3 , Hui-Chia Liu 3 , Shu-Ju Wu 3 4 , Chian-Jiun Liou 2 5

Publish date

2018 Dec




Ginkgolide C, isolated from Ginkgo biloba leaves, is a diterpene lactone derivative [corrected] reported to have multiple biological functions, from decreased platelet aggregation to ameliorating Alzheimer disease. The study aim was to evaluate the antiadipogenic effect of ginkgolide C in 3T3-L1 adipocytes. Ginkgolide C was used to treat differentiated 3T3-L1 cells. Cell supernatant was collected to assay glycerol release, and cells were lysed to measure protein and gene expression related to adipogenesis and lipolysis by western blot and real-time PCR, respectively. Ginkgolide C significantly suppressed lipid accumulation in differentiated adipocytes. It also decreased adipogenesis-related transcription factor expression, including peroxisome proliferator-activated receptor and CCAAT/enhancer-binding protein. Furthermore, ginkgolide C enhanced adipose triglyceride lipase and hormone-sensitive lipase production for lipolysis and increased phosphorylation of AMP-activated protein kinase (AMPK), resulting in decreased activity of acetyl-CoA carboxylase for fatty acid synthesis. In coculture with an AMPK inhibitor (compound C), ginkgolide C also improved activation of sirtuin 1 and phosphorylation of AMPK in differentiated 3T3-L1 cells. The results suggest that ginkgolide C is an effective flavone for increasing lipolysis and inhibiting adipogenesis in adipocytes through the activated AMPK pathway.


Ginkgolide C Suppresses Adipogenesis in 3T3-L1 Adipocytes via the AMPK Signaling Pathway


Chian-Jiun Liou 1 , Xuan-Yu Lai 2 , Ya-Ling Chen 3 , Chia-Ling Wang 4 , Ciao-Han Wei 4 , Wen-Chung Huang 5

Publish date





Increasing evidence shows that inflammation plays a vital role in the occurrence and development of ischemia/reperfusion (I/R). Suppression of excessive inflammation can ameliorate impaired cardiac function, which shows therapeutic potential for clinical treatment of myocardial ischemia/reperfusion (MI/R) diseases. In this study, we investigated whether Ginkgolide C (GC), a potent anti-inflammatory flavone, extenuated MI/R injury through inhibition of inflammation. In vivo, rats with the occlusion of the left anterior descending (LAD) coronary artery were applied to mimic MI/R injury. In vitro, primary cultured neonatal ventricular myocytes exposed to hypoxia/reoxygenation (H/R) were applied to further discuss the anti-H/R injury property of GC. The results revealed that GC significantly improved the symptoms of MI/R injury, as evidenced by reducing infarct size, preventing myofibrillar degeneration and reversing the mitochondria dysfunction. Moreover, histological analysis and Myeloperoxidase (MPO) activity measurement showed that GC remarkably suppressed Polymorphonuclears (PMNs) infiltration and ameliorated the histopathological damage. Furthermore, GC pretreatment was shown to improve H/R-induced ventricular myocytes viability and enhance tolerance of inflammatory insult, as evidenced by suppressing expression of CD40, translocation of NF-κB p65 subunit, phosphorylation of IκB-α, as well as the activity of IKK-β. In addition, downstream inflammatory cytokines modulated by NF-κB signaling were effectively down-regulated both in vivo and in vitro, as determined by immunohistochemistry and ELISA. In conclusion, these results indicate that GC possesses a beneficial effect against MI/R injury via inflammation inhibition that may involve suppression of CD40-NF-κB signal pathway and downstream inflammatory cytokines expression, which may offer an alternative medication for MI/R diseases.


CD40; NF-κB; ginkgolide C; inflammation; myocardial ischemia/reperfusion injury.


Ginkgolide C Alleviates Myocardial Ischemia/Reperfusion-Induced Inflammatory Injury via Inhibition of CD40-NF-κB Pathway


Rui Zhang 1 , Dan Han 2 , Zhenyu Li 1 , Chengwu Shen 1 , Yahui Zhang 1 , Jun Li 1 , Genquan Yan 1 , Shasha Li 1 , Bo Hu 3 , Jiangbing Li 4 , Ping Liu 1

Publish date

2018 Feb 21

Description :

Ginkgolide C is a flavone isolated from Ginkgo biloba leaves, possessing multiple biological functions, such as decreasing platelet aggregation and ameliorating Alzheimer disease.