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Ganoderic acid A


  • Brand : BIOFRON

  • Catalogue Number : BD-P0729

  • Specification : 99.0%(HPLC&TLC)

  • CAS number : 81907-62-2

  • PUBCHEM ID : 471002

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight


White crystalline powder

Botanical Source

Ganoderma Lucidum(Leyss. ex Fr.) Karst.

Structure Type



Standards;Natural Pytochemical;API




ganoderic acid A/(7β,15α,20E)-7,15-Dihydroxy-3,11,23-trioxolanosta-8,20(22)-dien-26-oic acid/Ganoderic acid/Lanosta-8,20(22)-dien-26-oic acid, 7,15-dihydroxy-3,11,23-trioxo-, (7β,15α,20E)-


(2R,6R)-6-[(5R,7S,10S,13R,14R,15S,17R)-7,15-dihydroxy-4,4,10,13,14-pentamethyl-3,11-dioxo-2,5,6,7,12,15,16,17-octahydro-1H-cyclopenta[a]phenanthren-17-yl]-2-methyl-4-oxoheptanoic acid


Ganoderic acid can Inhibitt of the JAK-STAT3 signaling pathway, also inhibit proliferation, viability, ROS.In vitro: A lower doses of Ganoderic acid enhance HLA class II-mediated antigen presentation and CD4+ T cell recognition of lymphoma. [1] ganoderic acid A promots cisplatin-induced cell death by enhancing the sensitivity of HepG2 cells to cisplatin mainly via the signal transducer and activator of transcription 3 suppression. [2] Ganoderic acid A inhibits proliferation, viability, ROS, DPPH, and analyzed the expression of SOD1, SOD2, and SOD3 by Real time PCR in a PC-3 cell in a dose-dependent manner.[3] GA-A effectively inhibites the proliferation of human osteosarcoma HOS and MG-63 cells in a dose-dependent manner, and induced obvious cell apoptosis in both cells.[4]In vivo: Ganoderic acid -treatment significantly prolonged survival of EL4 challenged mice and decreased tumor metastasis to the liver.[1]


1.2±0.1 g/cm3


Methanol; Acetontrile; Water; DMSO

Flash Point

391.3±29.4 °C

Boiling Point

700.3±60.0 °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#:81907-62-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Wnt signaling pathways are the group of signaling transduction controlling the embryonic development, cell proliferation, cell migration, cell fate specification, and body axis pattern. Nuclear accumulation of β-catenin in Wnt signaling is a widely recognized marker of poor cancer prognosis which regulates fat and glucose metabolism. Ganoderic acid is a triterpene isolated from fungus Ganoderma lucidum renowned for its pharmacological effects. The present study revealed the mechanistic study of β-catenin with 50 isoforms of ganoderic acid by molecular docking using Maestro 9.6 (Schrodinger Inc) in Wnt signaling pathway. Molecular docking reveals the binding interaction of β-catenin and ganoderic acid A with GScore (-9.44), kcal/mol, lipophilic EvdW (-2.86), electro (-0.72), Glide emodel (-50.401), MM-GBSA (-87.441), H bond (-1.91) with Lys 180 and Asn 220 residues involved in hydrogen bonding. Qikprop analyzed the absorption, distribution, metabolism, excretion, and toxicity and confirmed that most of the isoforms satisfies Lipinski rule but needs little modifications in their structure. The ganoderic acid A is the best-docked isoforms which inhibits the proliferation, viability, and intracellular ROS of pancreatic cancer RIN-5F cells in a dose-dependent manner.


Diabetes II; Ganoderic acid; Molecular docking; Wnt signaling; β-catenin


Ganoderic Acid A Targeting β-Catenin in Wnt Signaling Pathway: In Silico and In Vitro Study.


Gill BS1, Kumar S1, Navgeet2.

Publish date

2018 Jun




Ganoderic acid A (GAA) isolated from Ganoderma lucidum, shows various benefit activities, such as anti-tumor activity, anti-HIV activity and hepatoprotective activity. However, the potential effects of GAA on hypoxia-induced injury of cardiomyocytes are still unclear. In this study, we aimed to reveal the effects of GAA on hypoxic-induced H9c2 cell injury, as well as potential underlying molecular mechanisms.

Rat H9c2 cardiomyocytes were cultured in hypoxia condition with different doses of GAA. Cell viability and apoptosis were detected by CCK-8 assay and flow cytometry, respectively. qRT-PCR was performed to assess the expression levels of microRNA-182-5p (miR-182-5p) and phosphatase and tensin homologue (PTEN). Cell transfection was conducted to change the expression levels of miR-182-5p and PTEN in H9c2 cells. Finally, protein levels of key factors involved in cell proliferation, cell apoptosis and PTEN/PI3K/AKT pathway were evaluated using western blotting.

Hypoxia treatment significantly induced H9c2 cell viability loss and apoptosis. GAA incubation remarkably protected H9c2 cells from hypoxia-induced viability loss, proliferation inhibition and apoptosis. In addition, GAA obviously enhanced the expression level of miR-182-5p in H9c2 cells. Suppression of miR-182-5p notably alleviated the protective effects of GAA on hypoxia-treated H9c2 cells. Furthermore, miR-182-5p negatively regulated the mRNA and protein levels of PTEN in H9c2 cells. GAA attenuated hypoxia-induced inactivation of PI3K/AKT pathway in H9c2 cells by up-regulating miR-182-5p and then down-regulating PTEN.

GAA protected rat H9c2 cardiomyocytes from hypoxia-induced injury might via up-regulating miR-182-5p, down-regulating PTEN and then activating PI3K/AKT signaling pathway.

© 2018 The Author(s). Published by S. Karger AG, Basel.


Ganoderic acid A; H9c2 cardiomyocytes; Hypoxia; PI3K/AKT signaling pathway; PTEN; microRNA-182-5p


Ganoderic Acid A Protects Rat H9c2 Cardiomyocytes from Hypoxia-Induced Injury via Up-Regulating miR-182-5p.


Zhang X1, Xiao C2, Liu H3.

Publish date





To study the protective effects of ganoderic acid A (GAA) on bleomycin (BLM)-induced pulmonary fibrosis.

ICR mice were intratracheally instilled with BLM to induce pulmonary fibrosis on day 0. Then the mice were orally given GAA (25, 50 mg/kg) or dexamethasone (2 mg/kg). After treatment for 21 days, the mice were sacrificed. Wet dry weight (W/D) ratio of lung was used to detect pulmonary edema. Myeloperoxidase (MPO), interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), and superoxide dismutase (SOD) were detected by enzyme-linked immunosorbent assay. Hematoxylin and eosin staining was used to evaluate the pathological changes. The levels of transforming growth factor β (TGF-β), phosphorylated-smad3 (p-smad3), p-IκB, and p-nuclear factor-kappa B (NF-κB) in lung tissue were detected by western blot.

GAA treatment significantly improved MPO activity, W/D ratio, and lung histopathology. The protective effect of GAA may be related to downregulation of TNF-α, IL-1β, IL-6, MDA and upregulation of SOD. In addition, GAA significantly decreased the levels of TGF-β, p-smad3, p-IκB, and p-NF-κB, compared with those in BLM group.

GAA has protective effect on BLM-induced lung injury, and TGF-β/Smad-3/NF-κB signaling pathway may play an important role in the pathogenesis of BLM-induced lung injury.

© 2020 S. Karger AG, Basel.


Ganoderic acid A; Inflammation; Lung fibrosis; Nuclear factor kappa B; Smad-3; Transforming growth factor -β


Ganoderic Acid A Inhibits Bleomycin-Induced Lung Fibrosis in Mice.


Wen G1,2, Li T2, He H2, Zhou X1,3, Zhu J4,5.

Publish date

2020 Jan 15