Ganoderic Acid DM
(Synonyms: 灵芝酸 DM) 目录号 : GC49303
A triterpenoid with diverse biological activities
Cas No.:173075-45-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Ganoderic acid DM is a triterpenoid that has been found in G. lucidum and has diverse biological activities. 1,2,3 It inhibits 5α-reductase and HMG-CoA reductase (IC50s = 10.6 and 9.5 µM, respectively) and binds to the ligand-binding domain of the androgen receptor in a fluorescence polarization assay.1,2 Ganoderic acid suppresses osteoclastogenesis of RAW 264.7 cells when used at a concentration of 12.5 µM and is cytotoxic to K562 leukemia and PC3 prostate cancer cells (IC50s = 18.8 and 81.6 µM, respectively). It reduces ear edema induced by phorbol 12-myristate 13-acetate in mice (ID50 = 0.08 mg/ear).3
1.Liu, J., Shiono, J., Shimizu, K., et al.Ganoderic acid DM: Anti-androgenic osteoclastogenesis inhibitorBioorg. Med. Chem. Lett.19(8)2154-2157(2009) 2.Wang, K., Bao, L., Xiong, W., et al.Lanostane triterpenes from the Tibetan medicinal mushroom Ganoderma leucocontextum and their inhibitory effects on HMG-CoA reductase and α?glucosidaseJ. Nat. Prod.78(8)1977-1989(2015) 3.Akihisa, T., Nakamura, Y., Tagata, M., et al.Anti-inflammatory and anti-tumor-promoting effects of triterpene acids and sterols from the fungus Ganoderma lucidumChem. Biodivers.4(2)224-231(2007)
| Cas No. | 173075-45-1 | SDF | |
| 别名 | 灵芝酸 DM | ||
| Canonical SMILES | C[C@]12C3=C(CC[C@@]1([C@]([C@@H](CC/C=C(C)/C(O)=O)C)([H])CC2)C)[C@@]4([C@@](C(C)(C(CC4)=O)C)([H])CC3=O)C | ||
| 分子式 | C30H44O4 | 分子量 | 468.7 |
| 溶解度 | DMSO : 50 mg/mL (106.68 mM; Need ultrasonic) | 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 | 2.1336 mL | 10.6678 mL | 21.3356 mL |
| 5 mM | 0.4267 mL | 2.1336 mL | 4.2671 mL |
| 10 mM | 0.2134 mL | 1.0668 mL | 2.1336 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。
Ganoderic acid A/DM-induced NDRG2 over-expression suppresses high-grade meningioma growth
Clin Transl Oncol 2020 Jul;22(7):1138-1145.PMID:31732915DOI:10.1007/s12094-019-02240-6.
Purpose: N-myc downstream-regulated gene 2 (NDRG2) is down-regulated in grade-III meningioma [anaplastic meningioma (AM)] and associated with clinically aggressive behavior. Current therapies in the treatment of high-grade meningioma are lacking with limited success. This study aims to validate the effect of NDRG2-targeted therapy using structurally related bioactive triterpene compounds derived from the edible mushroom Ganoderma lucidum (ganoderic acid A:GA-A/Ganoderic Acid DM:GA-DM) in human AM in relevant pre-clinical models. Methods: Tissue samples from the AM tumor regions of three human patients and control non-tumor samples were used to analyze the expression pattern of NDRG2. In vitro cell culture and in vivo cell-line-derived orthotopic xenograft animal models of AM were utilized to assess efficacy of treatment with GA-A/DM. Results: Downregulation of NDRG2 expression was observed in surgically resected high-grade meningiomas compared to normal brain. These results prompt us to use NDRG2-targeting agents GA-A/DM. In vitro results showed that 72-h treatments of 25 µM GA-A/DM induced AM cell death, upregulate NDRG2 protein expression, downregulate NDRG2 promoter methylation in meningioma cells as compared to azacitidine and decitabine, the most commonly used demethylating agents. Our results also demonstrated that GA-A/DM does not have any detrimental effect on normal human neurons and arachnoid cells. GA-A/DM promoted apoptotic factors (Bax) while suppressing MMP-9, p-P13K, p-AKT, p-mTOR, and Wnt-2 protein expression. RNAi-mediated knockdown of NDRG2 protein expression increased tumor proliferation, while forced expression of wt-NDRG2 decreased proliferation in an in vitro model. Magnetic resonance (MR) imaging and Hematoxylin (H&E) staining demonstrated gross reduction of tumor volume in GA-A/DM treated mice at 5 weeks when compared with saline-treated orthotopic AM xenografted controls. There was an overall decrease in tumor cell proliferation with increased survival in GA-A/DM-treated animals. Enzyme assays showed that GA-A/DM did not negatively impact hepatic function. Conclusion: GA-A/DM may be a promising natural therapeutic reagent in the treatment of AM by suppressing growth via NDRG2 modulation and altering of intracellular signal pathways. We have shown it could potentially be an effective treatment for AM with decreased cellular proliferation in vitro, decreased tumor volume and increased survival in vivo.
Ganoderic Acid DM induces autophagic apoptosis in non-small cell lung cancer cells by inhibiting the PI3K/Akt/mTOR activity
Chem Biol Interact 2020 Jan 25;316:108932.PMID:31874162DOI:10.1016/j.cbi.2019.108932.
The incidence and mortality of lung cancer are the highest among cancer-related deaths. However, the long-term use of currently available cytotoxic drugs can increase genetic alterations in cancer cells and cause drug-resistance, which significantly limits their usage. Since current systemic treatment options are limited, effective chemotherapeutic agents are urgently needed for non-small cell lung cancer (NSCLC) treatment. In this study, we demonstrated that Ganoderic Acid DM (GA-DM) could increase apoptosis in A549 and NCI-H460 NSCLC cells. GA-DM treatment decreased the protein expression levels of Bcl-2 and increased the expression levels of Bax, cleaved caspase-3 and cleaved PRAP. Furthermore, GA-DM could promote autophagic flux, and the cytotoxic effect against cancer cells of GA-DM was significantly inhibited by targeted suppression of autophagy, suggesting that autophagy contributed to GA-DM-induced cell death in NSCLC. Moreover, GA-DM clearly induced autophagy by inactivating the PI3K/Akt/mTOR pathway. When overexpression of Akt reactivated Akt/mTOR pathway in A549 or NCI-H460 cells, the increase of autophagy related marker LC3B-II and apoptosis related protein cleaved PARP and cleaved caspase 3 and the ration of apoptotic cells by GA-DM was reversed, suggesting that GA-DM promoted autophagy and apoptosis by inhibiting Akt/mTOR pathway-mediated autophagy induction. In conclusion, our study indicated that GA-DM can induce autophagic apoptosis in NSCLC by inhibiting Akt/mTOR activity. (209 words).
Anticancer Activity of Ganoderic Acid DM: Current Status and Future Perspective
J Clin Cell Immunol 2017;8(6):535.PMID:29399381DOI:10.4172/2155-9899.1000535.
Ganoderma lucidum is a mushroom that has a long history of medicinal use in the Far East countries as this mushroom is revered for its supposed miracle cures and life improving properties. Recently, this mushroom has come under scientific scrutiny to examine the possibility of finding biologically active compounds that may have an impact on human physiology. The main category of biologically active compounds produced in the G. lucidum, are the triterpenoids, which are known as Ganoderic Acids. In this review, we discuss one Ganoderic Acid in particular known as Ganoderic Acid-DM (GA-DM) that is extracted from the Ganoderma lucidum mushroom. We will discuss GA-DM as a potential therapeutic candidate for treating a number of diseases yet will focus on the potential to be used as an alternative or supplemental therapeutic agent in regards to various cancer types. The urge for this promising therapeutic agent is that GA-DM is capable of inducing cell death in cancer cells while exhibiting minimal toxicity to normal bystander cells. Furthermore, this review will look at GA-DM's ability to stimulate an immune response in the tumor environment to potentially provide long-term protection from the malignant tumors. We will also discuss the known routes of administration of GA-DM and pose the advantages and disadvantages of each route in a comparative manner. Finally, we will cover current status of the roles GA-DM may have as a therapeutic agent in respect to different cancer types as wells as discuss about its future perspective as a therapeutic candidate in other diseases as well.
Ganoderic Acid DM: anti-androgenic osteoclastogenesis inhibitor
Bioorg Med Chem Lett 2009 Apr 15;19(8):2154-7.PMID:19289282DOI:10.1016/j.bmcl.2009.02.119.
Prostate cancer is the most common cancer in men in Western countries, with a high incidence of bone metastasis. Ganoderic Acid DM, with 5alpha-reductase inhibitory and androgen receptor (AR) binding activity, isolated from the ethanol extracts of Ganoderma lucidum, can inhibit prostate cancer cell growth and block osteoclastogenesis.
Ganoderic Acid DM: An Alternative Agent for the Treatment of Advanced Prostate Cancer
Open Prost Cancer J 2010 Jan 1;3:78-85.PMID:24790681DOI:10.2174/1876822901003010078.
Prostate cancer is the most commonly diagnosed cancer in men and accounts for significant morbidity and mortality in the western world. While traditional therapies are effective at clearing early stage cancer, they often fail to treat late stage metastatic disease. Thus, an effective therapy that targets prostate tumor growth and metastasis is desired for alleviating the disease and improving patient outcomes. Natural extracts have been the focus of recent investigation, particularly those with reduced cellular toxicity to healthy tissue. In this review, we discuss one potential candidate, ganoderic acid, an extract from the Ganoderma lucidum mushroom that has been tested in multiple cancer models. Interestingly, Ganoderic Acid DM (GA-DM) has shown toxicity to both androgen-dependent and independent prostate cancer cells with reduced osteoclastogenesis in late stage metastatic disease. This review will discuss the current knowledge on this GA-DM extract and the potential benefit in treating advanced prostate cancer. We will also provide an overview on the targeted delivery of GA-DM through nanoparticles that would reduce bystander toxicity and improve the drug's effectiveness. An improved understanding of this drug and its uses will advance the field of natural chemotherapeutics, particularly in treating advanced prostate cancer.