Ganoderic acid DM

Ganoderic acid DM
Product Name Ganoderic acid DM
CAS No.: 173075-45-1
Catalog No.: CFN99815
Molecular Formula: C30H44O4
Molecular Weight: 468.7 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Targets: PARP | CDK | Androgen Receptor | 5-alpha Reductase | NF-kB | TNF-α
Source: The fruit body of Ganoderma lucida
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $592/5mg
Ganoderic acid DM is an antiandrogenic osteoclastogenesis inhibitor, it especially suppresses the expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1), this suppression leads to the inhibition of dendritic cell-specific transmembrane protein (DC-STAMP) expression and reduces osteoclast fusion. Ganoderic acid DM has shown toxicity to both androgen-dependent and independent prostate cancer cells with reduced osteoclastogenesis in late stage metastatic disease, it may an alternative agent for the treatment of advanced prostate cancer.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
  • Semyung UniversityJan. 2017;
  • Evid Based Complement Alternat Med. 2016 Jun 13.
  • Food Chem.2018 Jun 30;
  • Tissue and Organ Culture (PCTOC)2016 Jun 28;
  • Am J Chin Med.2015 Jul 30:1-22.
  • Fitoterapia. 2018 Jan;
  • Sci Rep. 2016 Apr 27
  • International Journal of Pharmacognosy.2015 7(1).
  • Korean J. of Horticultural Sci. & Tech. No.2, 2017.2
  • Int J Mol Sci. 2018 Jan 23;
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    Fitoterapia. 2012 Mar;83(2):408-14.
    Ganoderic acid DM, a natural triterpenoid, induces DNA damage, G1 cell cycle arrest and apoptosis in human breast cancer cells.[Pubmed: 22178684]
    Ganoderic acid DM (GADM) is a triterpenoid isolated from Ganoderma lucidum, a well-known edible medicinal mushroom.
    METHODS AND RESULTS:
    In the present study, we found that GADM effectively inhibited cell proliferation and colony formation in MCF-7 human breast cancer cells, which was much stronger than that of MDA-MB-231 breast cancer cells. GADM both concentration- and time-dependently mediated G1 cell cycle arrest and significantly decreased the protein level of CDK2, CDK6, cycle D1, p-Rb and c-Myc in MCF-7 cells. Moreover, GADM obviously induced DNA fragmentation and cleavage of PARP which are the characteristics of apoptosis and decreased the mitochondrial membrane potential in MCF-7 cells. Besides, we also showed that GADM elicited DNA damage as measured by comet assay which is a sensitive method for DNA damage detection. γ-H2AX, a marker of DNA damage, was also slightly up-regulated after treated with GADM for 6h, suggesting that the G1 cell cycle arrest and apoptosis induced by GADM may be partially resulted from GADM-induced DNA damage.
    CONCLUSIONS:
    These results have advanced our current understandings of the anti-cancer mechanisms of GADM.
    Open Prost Cancer J. 2010 Jan 1;3:78-85.
    Ganoderic Acid DM: An Alternative Agent for the Treatment of Advanced Prostate Cancer.[Pubmed: 24790681]
    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.
    CONCLUSIONS:
    This review will discuss the current knowledge on this Ganoderic acid DM extract and the potential benefit in treating advanced prostate cancer. We will also provide an overview on the targeted delivery of Ganoderic acid 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.
    Bioorg Med Chem Lett. 2009 Apr 15;19(8):2154-7.
    Ganoderic acid DM: anti-androgenic osteoclastogenesis inhibitor.[Pubmed: 19289282]
    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.
    Eur J Pharmacol. 2009 Jan 5;602(1):1-7.
    Regulation of osteoclastogenesis by ganoderic acid DM isolated from Ganoderma lucidum.[Pubmed: 19026632 ]

    METHODS AND RESULTS:
    The preventative effects of the ethanol extracts of Ganoderma lucidum against the ovariectomized (Ovx)-induced deterioration of bone density in 11-week-old female Sprague Dawley (SD) rats were investigated. The results showed that the G. lucidum-treated Ovx rats showed improved bone density compared with the Ovx rats. We studied the effects of G. lucidum on osteoclastic differentiation using bone marrow cells and RAW 264 cell D-clone (RAW-D). Differentiation, in response to receptor activator of NF-kappaB ligand (RANKL) and a tumor necrosis factor alpha (TNF-alpha), was inhibited by the ethanol extracts of G. lucidum and Ganoderic acid DM which was isolated as one of the active compounds by bioassay-guided fractionation. Ganoderic acid DM especially suppresses the expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1).
    CONCLUSIONS:
    This suppression leads to the inhibition of dendritic cell-specific transmembrane protein (DC-STAMP) expression and reduces osteoclast fusion.
    Sci Rep. 2012;2:905.
    Target proteins of ganoderic acid DM provides clues to various pharmacological mechanisms.[Pubmed: 23205267]
    Ganoderma fungus (Ganodermataceae) is a multifunctional medicinal mushroom and has been traditionally used for the treatment of various types of disease. Ganoderic acid DM (1) is a representative triterpenoid isolated from G. lingzhi and exhibits various biological activities. However, a universal starting point that triggers multiple signaling pathways and results in multifunctionality of 1 is unknown.
    METHODS AND RESULTS:
    Here we demonstrate the important clues regarding the mechanisms underlying multi-medicinal action of 1. We examined structure-activity relationships between 1 and its analogs and found that the carbonyl group at C-3 was essential for cytotoxicity. Subsequently, we used 1-conjugated magnetic beads as a probe and identified tubulin as a specific 1-binding protein. Furthermore, 1 showed a similar Kd to that of vinblastine and also affected assembly of tubulin polymers.
    CONCLUSIONS:
    This study revealed multiple biological activities of 1 and may contribute to the design and development of new tubulin-inhibiting agents.
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