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Ganoderic acid DM (Ganoderic acid DM)

Cat No.:V34799 Purity: ≥98%
Ganoderic acid DM is a natural triterpene extracted from Ganoderma lucidum and can induce DNA damage, G1 cell cycle arrest and apoptosis in human breast cancer cells.
Ganoderic acid DM (Ganoderic acid DM)
Ganoderic acid DM (Ganoderic acid DM) Chemical Structure CAS No.: 173075-45-1
Product category: Apoptosis
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
1mg
5mg
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Product Description
Ganoderic acid DM is a natural triterpene extracted from Ganoderma lucidum and can induce DNA damage, G1 cell cycle arrest and apoptosis in human breast cancer cells. Ganoderic acid DM is also a specific inhibitor of osteoclastogenesis.
Ganoderic acid DM (Ganoderic acid DM) (CAS#: 173075-45-1) is a natural triterpenoid extracted from Ganoderma lucidum (reishi mushroom). It exhibits diverse biological activities including antiandrogenic, anti-osteoclastogenic, and anticancer properties. Ganoderic acid DM is used as a research tool to study androgen receptor signaling, osteoclast differentiation, and cancer cell proliferation. It is a pure natural product with well-characterized biological activities.
Biological Activity I Assay Protocols (From Reference)
Targets
Ganoderic acid DM targets multiple proteins including 5alpha-reductase (IC50 = 10.6 microM) and HMG-CoA reductase (IC50 = 9.5 microM). It binds to the ligand-binding domain of the androgen receptor. The compound suppresses the expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1), leading to inhibition of dendritic cell-specific transmembrane protein (DC-STAMP) expression and reduced osteoclast fusion.
ln Vitro
In MCF-7 human breast cancer cells, ganoderic acid DM (GADM) significantly suppresses colony formation and cell proliferation more potently than it does in MDA-MB-231 breast cancer cells[1]. Nuclear factor of activated T cells c1 (NFATc1) and c-Fos expression are specifically suppressed by ganoderic acid DM. The expression of TRAP mRNA and cathepsin K was significantly decreased by ganoderic acid DM[2]. Non-small cell lung cancer cells undergo autophagic apoptosis when ganoderic acid DM inhibits PI3K/Akt/mTOR activity[3].
In vitro, Ganoderic acid DM (GADM) effectively inhibits cell proliferation and colony formation in MCF-7 human breast cancer cells, with stronger activity than in MDA-MB-231 cells. GADM induces G1 cell cycle arrest in a concentration- and time-dependent manner and decreases protein levels of CDK2, CDK6, cyclin D1, p-Rb, and c-Myc in MCF-7 cells. The compound induces DNA fragmentation, PARP cleavage (apoptosis markers), and decreases mitochondrial membrane potential. DNA damage is confirmed by comet assay and gamma-H2AX upregulation. At 20 microM, GADM inhibits 5alpha-reductase by 55%.
ln Vivo
In vivo activity data for Ganoderic acid DM are limited. As a natural triterpenoid, it has potential anti-inflammatory and anticancer activities in animal models. The compound is primarily used in vitro for mechanistic studies. Its anti-osteoclastogenic activity suggests potential for bone-related disease research. In vivo studies would typically involve oral or intraperitoneal administration in rodent models to assess antitumor or anti-inflammatory efficacy, but specific published data are limited for this compound.
Enzyme Assay
In vitro enzyme inhibition assays for Ganoderic acid DM involve measuring its activity against 5alpha-reductase and HMG-CoA reductase. Enzyme activity is measured spectrophotometrically by following NADPH oxidation or product formation. IC50 values are calculated from dose-response curves. Androgen receptor binding is assessed using fluorescence polarization assays with labeled ligands. The carboxyl group of the side chain is essential for 5alpha-reductase inhibitory activity.
Cell Assay
Cell Viability Assay[1]
Cell Types: MCF-7 and MDA-MB-231 cells.
Tested Concentrations: 0-100 μM.
Incubation Duration: 48 h.
Experimental Results: diminished the cell viability in breast cancer cells.

Cell Viability Assay[2]
Cell Types: RAW-D cells.
Tested Concentrations: 0-100 μg/mL.
Incubation Duration: 0-100 μg/mL.
Experimental Results: Clearly suppressed osteoclastogenesis from the RAW 264 cell D-clone.
In vitro cell-based assays for Ganoderic acid DM use human breast cancer cell lines such as MCF-7 and MDA-MB-231. Cells are treated with GADM at various concentrations (typically 0-50 microM) for 24-72 hours. Cell proliferation is measured by MTT or colony formation assays. Cell cycle analysis is performed by flow cytometry after propidium iodide staining. Apoptosis is assessed by Annexin V/PI staining, PARP cleavage Western blot, and DNA fragmentation assays. Comet assay detects DNA damage.
Animal Protocol
In vivo animal studies for Ganoderic acid DM are limited. Standard protocols for evaluating natural products would involve administration via oral gavage or intraperitoneal injection in mouse models. For antitumor activity, xenograft models with MCF-7 cells could be used. For anti-osteoclastogenic effects, ovariectomized mouse models of osteoporosis might be employed. Blood and tissue samples would be collected for pharmacokinetic and biomarker analyses. Published in vivo data for this specific compound are scarce.
ADME/Pharmacokinetics
Pharmacokinetic properties of Ganoderic acid DM are not well-characterized. As a triterpenoid natural product, it is expected to have moderate oral bioavailability, extensive protein binding, and hepatic metabolism. The compound has a molecular weight of 468.67 g/mol and logP values typical of terpenoids. Detailed PK parameters such as half-life, Cmax, and AUC would require experimental determination. The compound is typically handled as a research chemical with standard laboratory precautions.
Toxicity/Toxicokinetics
Toxicity data for Ganoderic acid DM are limited. As a natural product from Ganoderma lucidum, it is generally considered to have low toxicity, but specific toxicological studies are lacking. The compound is for research use only and not for human consumption. In vitro cytotoxicity shows activity against cancer cells with some selectivity. Standard safety assessments including acute toxicity, genotoxicity, and repeated-dose studies would be needed for therapeutic development.
References

[1]. Ganoderic acid DM, a natural triterpenoid, induces DNA damage, G1 cell cycle arrest and apoptosis in human breast cancer cells. Fitoterapia. 2012 Mar;83(2):408-14.

[2]. Regulation of osteoclastogenesis by ganoderic acid DM isolated from Ganoderma lucidum. Eur J Pharmacol. 2009 Jan 5;602(1):1-7.

[3]. 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.

Additional Infomation
Ganoderic acid DM is a triterpenoid compound. (E,6R)-2-methyl-6-[(5R,10S,13R,14R,17R)-4,4,10,13,14-pentamethyl-3,7-dioxo-2,5,6,11,12,15,16,17-octahydro-1H-cyclopenta[a]phenanthrene-17-yl]hept-2-enoic acid has been reported in Ganoderma lucidum, and relevant data are available.
Ganoderic acid DM is a natural triterpenoid found in Ganoderma lucidum (reishi mushroom). It has diverse biological activities including 5alpha-reductase inhibition, HMG-CoA reductase inhibition, and androgen receptor binding. The compound induces DNA damage, G1 cell cycle arrest, and apoptosis in breast cancer cells. It also suppresses osteoclastogenesis through c-Fos and NFATc1 inhibition. The carboxyl group of the side chain is essential for its activity. It is used for research purposes only.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C30H44O4
Molecular Weight
468.67
Exact Mass
468.323
CAS #
173075-45-1
PubChem CID
11784642
Appearance
White to off-white solid powder
Density
1.1±0.1 g/cm3
Boiling Point
602.1±55.0 °C at 760 mmHg
Flash Point
332.0±28.0 °C
Vapour Pressure
0.0±3.7 mmHg at 25°C
Index of Refraction
1.547
LogP
6.9
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
4
Rotatable Bond Count
5
Heavy Atom Count
34
Complexity
984
Defined Atom Stereocenter Count
6
SMILES
C[C@H](CC/C=C(\C)/C(=O)O)[C@H]1CC[C@@]2([C@@]1(CCC3=C2C(=O)C[C@@H]4[C@@]3(CCC(=O)C4(C)C)C)C)C
InChi Key
ZTKZZRIVAYGFSF-PIPDTRPPSA-N
InChi Code
InChI=1S/C30H44O4/c1-18(9-8-10-19(2)26(33)34)20-11-16-30(7)25-21(12-15-29(20,30)6)28(5)14-13-24(32)27(3,4)23(28)17-22(25)31/h10,18,20,23H,8-9,11-17H2,1-7H3,(H,33,34)/b19-10+/t18-,20-,23+,28-,29-,30+/m1/s1
Chemical Name
(E,6R)-2-methyl-6-[(5R,10S,13R,14R,17R)-4,4,10,13,14-pentamethyl-3,7-dioxo-2,5,6,11,12,15,16,17-octahydro-1H-cyclopenta[a]phenanthren-17-yl]hept-2-enoic acid
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO : 50 mg/mL (106.68 mM)
Solubility (In Vivo)
Solubility in Formulation 1: 1.25 mg/mL (2.67 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 1.25 mg/mL (2.67 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 1.25 mg/mL (2.67 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.1337 mL 10.6685 mL 21.3370 mL
5 mM 0.4267 mL 2.1337 mL 4.2674 mL
10 mM 0.2134 mL 1.0668 mL 2.1337 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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What volume of a given 10 mM stock solution is required to make 25 ml of a 25 μM solution?
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Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
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In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

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