Ganodermanontriol
(Synonyms: 灵芝马酮) 目录号 : GC49229
A triterpene with diverse biological activities
Cas No.:106518-63-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Ganodermanontriol is a triterpene that has been found in G. lucidum and has diverse biological activities.1,2,3,4 It inhibits the activity of HIV-1 protease (IC50 = 70 µM), as well as reduces the activity of 5α-reductase by 32% when used at a concentration of 667 µM.1,2 Ganodermanontriol (25 and 50 µM) inhibits proliferation, colony formation, invasion, and migration of MDA-MB-231 human breast cancer cells.3 It reduces hepatocyte necrosis and increases in hepatic TNF-α and IL-6 levels in a mouse model of LPS/D-galactosamine-induced acute liver injury when administered at a dose of 5 mg/kg.4
1.Min, B.-S., Nakamura, N., Miyashiro, H., et al.Triterpenes from the spores of Ganoderma lucidum and their inhibitory activity against HIV-1 proteaseChem. Pharm. Bull.46(10)1607-1612(1998) 2.Liu, J., Kurashiki, K., Shimizu, K., et al.Structure-activity relationship for inhibition of 5α-reductase by triterpenoids isolated from Ganoderma lucidumBioorg. Med. Chem.14(24)8654-8660(2006) 3.Jiang, J., Jedinak, A., and Silva, D.Ganodermanontriol (GDNT) exerts its effect on growth and invasiveness of breast cancer cells through the down-regulation of CDC20 and uPABiochem. Biophys. Res. Commun.415(2)325-329(2011) 4.Hu, Z., Du, R., Xiu, L., et al.Protective effect of triterpenes of Ganoderma lucidum on lipopolysaccharide-induced inflammatory responses and acute liver injuryCytokine127154917(2020)
| Cas No. | 106518-63-2 | SDF | |
| 别名 | 灵芝马酮 | ||
| Canonical SMILES | C[C@@]12C3=CC[C@](C)([C@]([C@@H](CC[C@H](O)[C@@](O)(C)CO)C)([H])CC4)[C@]4(C)C3=CC[C@@]1([H])C(C)(C(CC2)=O)C | ||
| 分子式 | C30H48O4 | 分子量 | 472.7 |
| 溶解度 | Chloroform: soluble | 储存条件 | -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.1155 mL | 10.5775 mL | 21.1551 mL |
| 5 mM | 0.4231 mL | 2.1155 mL | 4.231 mL |
| 10 mM | 0.2116 mL | 1.0578 mL | 2.1155 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Ganodermanontriol inhibits expression of special AT rich sequence binding protein 1 gene in human hepatocellular carcinoma
J Cancer Res Ther 2018 Dec;14(Supplement):S964-S968.PMID:30539830DOI:10.4103/0973-1482.203597.
Context: The metastasis of liver cancer is a major cause of clinical treatment failure, restrain, and control the cancer metastasis is the major strategy of the treatment and prevention of the disease. Special AT-rich sequence-binding protein 1 (SATB1) gene was overexpressed in many malignant tumors and considered as a potential target of anticancer drug. This study investigated the mechanism how Ganodermanontriol effect the expression of SATB1 and thus inhibits the growth and metastasis in hepatocellular carcinoma (HCC). Aims: This study explored mainly on the mechanism how Ganodermanontriol affects the expression of SATB1 and inhibits proliferation of tumor on human hepatoma cell line HepG2. Settings and design: The cancer cells were treated with Ganodermanontriol. The status of the cells was detected by different methods. The mechanism was checked by various methods. Materials and methods: In HepG2 cancer cells treated with various concentrations of Ganodermanontriol, the cell proliferation of was detected by MTT assay, cell apoptosis was analyzed by flow cytometry; the mRNA of SATB1, Bcl-2, Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR) and the protein level of SATB1, Bcl-2, Bax, and caspase 3 were analyzed by Western blot. Statistical analysis used: Data are presented as the mean ± standard deviation. The data were analyzed using SPSS 18.0 software (SPSS, Inc., Chicago, IL, USA) and GraphPad Prism software (GraphPad Software, Inc., La Jolla, CA, USA). A one-way analysis of variance test was used to compare the differences among groups. Results: This study showed that Ganodermanontriol could significantly reduce the expression level of SATB1. Conclusion: Therefore, downregulate the cascade effect caused by the expression level of Bcl-2 in HCC HepG2 cells.
Semisynthesis and biological evaluation of Ganodermanontriol and its stereoisomeric triols
J Nat Prod 2011 Nov 28;74(11):2332-7.PMID:22044278DOI:10.1021/np200205n.
The first synthesis of Ganodermanontriol, a bioactive lanostane triterpene from the medicinal mushroom Ganoderma lucidum, has been achieved in 15.3% yield over nine steps, along with its three stereoisomeric triols and ganoderol A. The key steps leading to this family of isomers involve the reconstruction of the trisubstituted alkene by stereoselective and chemoselective phosphonate reactions and the formation of the unusual Δ7,9(11)-diene core by the mild acidic opening of a lanosterone-derived epoxide. Ganodermanontriol showed promising activity on the inhibition and proliferation of breast cancer cells. The effect of Ganodermanontriol and its isomers on cell proliferation was assayed; IC50 values of 5.8 and 9.7 μM on breast cancer cell lines MCF-7 and MDA-MB-231, respectively, were found for Ganodermanontriol.
Ganodermanontriol (GDNT) exerts its effect on growth and invasiveness of breast cancer cells through the down-regulation of CDC20 and uPA
Biochem Biophys Res Commun 2011 Nov 18;415(2):325-9.PMID:22033405DOI:10.1016/j.bbrc.2011.10.055.
Ganoderma lucidum is a medicinal mushroom that has been recognized by Traditional Chinese Medicine (TCM). Although some of the direct anticancer activities are attributed to the presence of triterpenes-ganoderic and lucidenic acids-the activity of other compounds remains elusive. Here we show that Ganodermanontriol (GDNT), a Ganoderma alcohol, specifically suppressed proliferation (anchorage-dependent growth) and colony formation (anchorage-independent growth) of highly invasive human breast cancer cells MDA-MB-231. GDNT suppressed expression of the cell cycle regulatory protein CDC20, which is over-expressed in precancerous and breast cancer cells compared to normal mammary epithelial cells. Moreover, we found that CDC20 is over-expressed in tumors when compared to the tissue surrounding the tumor in specimens from breast cancer patients. GDNT also inhibited invasive behavior (cell adhesion, cell migration, and cell invasion) through the suppression of secretion of urokinase-plasminogen activator (uPA) and inhibited expression of uPA receptor. In conclusion, mushroom GDNT is a natural agent that has potential as a therapy for invasive breast cancers.
Ganodermanontriol, a lanostanoid triterpene from Ganoderma lucidum, suppresses growth of colon cancer cells through ß-catenin signaling
Int J Oncol 2011 Mar;38(3):761-7.PMID:21225227DOI:10.3892/ijo.2011.898.
Colorectal cancer is one of the most common cancers in men and women in the world. Previous molecular studies have revealed that deregulation of the ß-catenin signaling pathway plays a crucial role in the progression of colorectal cancer. Therefore, modulation of the ß-catenin pathway offers a strategy to control colorectal cancer progression. The medicinal mushroom Ganoderma lucidum (GL) is a rich source of triterpenes with anticancer properties. Here, we show that Ganodermanontriol (GNDT), a purified triterpene from GL, inhibited proliferation of HCT-116 and HT-29 colon cancer cells without a significant effect on cell viability. Moreover, GNDT inhibited transcriptional activity of ß-catenin and protein expression of its target gene cyclin D1 in a dose-dependent manner. A marked inhibition effect was also seen on Cdk-4 and PCNA expression, whereas expression of Cdk-2, p21 and cyclin E was not affected by the GNDT treatment. In addition, GNDT caused a dose-dependent increase in protein expression of E-cadherin and ß-catenin in HT-29 cells. Finally, GNDT suppressed tumor growth in a xenograft model of human colon adenocarcinoma cells HT-29 implanted in nude mice without any side-effects and inhibited expression of cyclin D1 in tumors. In conclusion, our data suggest that Ganodermanontriol might be a potential chemotherapeutic agent for the treatment of cancer.
In vitro and in vivo hepatoprotective effect of Ganodermanontriol against t-BHP-induced oxidative stress
J Ethnopharmacol 2013 Dec 12;150(3):875-85.PMID:24140584DOI:10.1016/j.jep.2013.09.039.
Ethnopharmacological relevance: Ganoderma lucidum (Fr.) Karst. (Ganodermataceae) is a mushroom which is used as a traditional remedy in the treatment of human diseases such as hepatitis, liver disorders, hypercholesterolemia, arthritis, bronchitis and tumorigenic diseases. This study targets the evaluation of hepatoprotective activity of Ganodermanontriol, a sterol isolated from Ganoderma lucidum, and the investigation of its mechanism of action in Hepa1c1c7 and murine liver cells upon tert-butyl hydroperoxide (t-BHP)-induced inflammation. t-BHP was utilized to stimulate an anti-inflammatory reaction in the hepatic cell lines and murine hepatic tissue examined. Western blot and reverse transcription-quantitative polymerase chain reaction (RT-PCR) were used to estimate the expression of Ganodermanontriol (GDT)-induced proteins, including heme oxidase-1 (HO-1) and mitogen-activated protein kinases (MAPKs) as well as the corresponding mRNA. Luciferase assays were conducted to evaluate the interaction between NF-E2-related factor-2 (Nrf-2), the antioxidant response element (ARE), and the promoter region of the HO-1 gene and subsequent gene expression. Biochemical markers for hepatotoxicity were monitored to assess whether GDT protected the cells from the t-BHP-mediated oxidative stimuli. Results: GDT induced HO-1 expression via the activation of Nrf-2 nuclear translocation and the subsequent transcription of the HO-1 gene in vitro and in vivo, which seemed to be regulated by phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and p38 signaling pathways. GDT exhibited in vitro and in vivo hepatoprotective activity as determined by the lowered levels of hepatic enzymes and malondialdehydes and the elevated glutathione levels. Conclusions: This study validates the ethnopharmacological application of Ganoderma lucidum as a treatment for hepatic disorders. GDT induced in vitro and in vivo anti-inflammatory activity in t-BHP-damaged hepatic cells through the expression of HO-1, and in which PI3K/Akt and p38 kinases are involved. Our study motivates further research in the exploration of potent hepatoprotective agents from Ganoderma lucidum.