| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| 100mg |
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| Targets |
Ganoderic Acid A targets multiple signaling pathways involved in cancer cell survival and proliferation. It inhibits nuclear transcription factor-kappaB (NF-κB) and activator protein-1 (AP-1), two key transcription factors that regulate genes involved in inflammation, cell proliferation, and survival. The compound also inhibits the JAK-STAT3 signaling pathway, which is frequently hyperactivated in cancers and promotes cell proliferation and survival. Ganoderic Acid A can upregulate pro-apoptotic protein Bax while downregulating anti-apoptotic proteins Bcl-2 and survivin. The compound also inhibits 5-alpha reductase.
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| ln Vitro |
Reduced ganoderic acid A dosages improve HLA class II-mediated diagnostic presentation delay and CD4+ T cell identification in response [1]. Cell death brought on by platinum is intensified by ganoderic acid A. Signal transducer and activator 3 is primarily responsible for the inhibition of HepG2 cells' response to cisplatin [2]. Real-time PCR was used to assess the SOD1, SOD2, and SOD3 levels in PC-3 cells. Ganoderic acid A also decreases the growth, viability, ROS, and DPPH of PC-3 cells. Human osteosarcoma HOS and MG-63 are both efficiently inhibited by ganoderic acid A in a dose-dependent manner. cell division and cause a considerable amount of cellular inflammation in each cell [4].
Ganoderic Acid A induces remarkable cytotoxicity in various leukemia and lymphoma cell lines and primary tumors, with minor toxicity to nonmalignant B-cells. It can upregulate pro-apoptotic protein Bax while downregulating anti-apoptotic proteins Bcl-2 and survivin. The compound induces proliferation inhibition, apoptosis, and suppression of invasion in human osteosarcoma HOS and MG-63 cells. It down-regulates the expression level of phosphorylated STAT3 and increases the phosphorylation level of p38 and NF-κB1 expression. Ganoderic Acid A promotes cisplatin-induced cell death by enhancing the sensitivity of HepG2 cells to cisplatin through STAT3 suppression. |
| ln Vivo |
Treatment with ganoderic acid A considerably increased the survival time of mice challenged with EL4 and decreased liver metastasis of tumors [4].
Ganoderic Acid A exhibits antitumor activity in vivo through inhibition of NF-κB and AP-1. The compound demonstrates analgesic, antioxidant, hepatoprotective, and anti-tumor activities in animal models. It may play dual roles in inducing apoptosis and enhancing HLA class II antigen presentation. The compound could be used as a novel adjunctive therapy for the treatment of hematological malignancies. Its hepatoprotective effects have been demonstrated in models of liver injury. |
| Enzyme Assay |
In vitro enzyme/receptor binding assays for ganoderic Acid A involve measuring its effects on NF-κB and AP-1 transcriptional activity using reporter gene assays. JAK-STAT3 signaling inhibition is assessed by measuring STAT3 phosphorylation levels in cell lysates using Western blotting or ELISA. The compound's binding to and inhibition of 5-alpha reductase can be measured using purified enzyme preparations. These cell-free and cell-based assays provide mechanistic insights into the compound's antitumor and anti-inflammatory activities.
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| Cell Assay |
In vitro cell-based assays for ganoderic Acid A involve treating cancer cell lines such as leukemia, lymphoma, and osteosarcoma cells with varying concentrations of the compound. Cell viability is measured using MTT, CCK-8, or similar assays. Apoptosis is quantified by flow cytometry using Annexin V/PI staining or by measuring caspase activity. Protein expression levels of Bax, Bcl-2, survivin, STAT3, and NF-κB are analyzed by Western blotting. Cell invasion is assessed using Transwell or Matrigel invasion assays. Combination studies with cisplatin are performed to evaluate synergistic effects.
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| Animal Protocol |
In vivo animal experiments for ganoderic Acid A have been conducted in tumor xenograft models in immunodeficient mice. Cancer cells (e.g., HepG2 liver cancer cells, leukemia cells) are implanted subcutaneously, and mice are treated with ganoderic Acid A orally or via injection. Tumor growth inhibition is monitored. Hepatoprotective effects are assessed in models of liver injury. Analgesic activity is evaluated using pain models. Efficacy endpoints include tumor volume reduction, survival prolongation, histopathological analysis, and biomarker assessment (e.g., STAT3 phosphorylation, NF-κB activity).
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| ADME/Pharmacokinetics |
Ganoderic Acid A has a molecular weight of 516.7 and a molecular formula of C30H44O7. It is a lanostane triterpene with a complex polycyclic structure. The compound is isolated from Ganoderma lucidum, a medicinal mushroom with a long history of use in traditional medicine. Its solubility properties are characteristic of triterpenoid compounds. Specific pharmacokinetic data such as absorption, distribution, metabolism, and elimination have not been extensively reported. The compound is typically stored at -20°C for long-term preservation.
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| Toxicity/Toxicokinetics |
Specific toxicity data for ganoderic Acid A is not extensively reported. The compound exhibits minor toxicity to nonmalignant B-cells while inducing remarkable cytotoxicity in various leukemia and lymphoma cell lines, suggesting some degree of selectivity. As a natural compound from Ganoderma lucidum, which has a long history of use in traditional medicine, it is generally considered to have a favorable safety profile. Comprehensive toxicological studies would be required for therapeutic development. Standard safety precautions should be taken when handling the compound in research settings.
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| References |
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| Additional Infomation |
Ganoderic acid A is a triterpenoid compound. It has been reported that ganoderic acid A exists in Ganoderma lucidum, Ganoderma sinense, and Poria cocos, and relevant data are available. See also: Ganoderma lucidum (partial).
Ganoderic Acid A is a lanostane triterpene from Ganoderma lucidum with antitumor activity mediated through NF-κB and AP-1 inhibition. It inhibits the JAK-STAT3 signaling pathway and suppresses cell proliferation and ROS. The compound induces apoptosis in cancer cells by upregulating Bax and downregulating Bcl-2 and survivin. Ganoderic Acid A promotes cisplatin sensitivity in cancer cells. It has analgesic, antioxidant, hepatoprotective, and anti-tumor activities. The compound could be used as adjunctive therapy for hematological malignancies. |
| Molecular Formula |
C30H44O7
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| Molecular Weight |
516.6662
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| Exact Mass |
516.308
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| CAS # |
81907-62-2
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| PubChem CID |
471002
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| Appearance |
White to off-white solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
700.3±60.0 °C at 760 mmHg
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| Flash Point |
391.3±29.4 °C
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| Vapour Pressure |
0.0±5.0 mmHg at 25°C
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| Index of Refraction |
1.575
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| LogP |
2.15
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
37
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| Complexity |
1070
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| Defined Atom Stereocenter Count |
9
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| SMILES |
C[C@H](CC(=O)C[C@@H](C)C(=O)O)[C@H]1C[C@@H]([C@@]2([C@@]1(CC(=O)C3=C2[C@H](C[C@@H]4[C@@]3(CCC(=O)C4(C)C)C)O)C)C)O
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| InChi Key |
DYOKDAQBNHPJFD-JNTBEZBXSA-N
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| InChi Code |
InChI=1S/C30H44O7/c1-15(10-17(31)11-16(2)26(36)37)18-12-23(35)30(7)25-19(32)13-21-27(3,4)22(34)8-9-28(21,5)24(25)20(33)14-29(18,30)6/h15-16,18-19,21,23,32,35H,8-14H2,1-7H3,(H,36,37)/t15-,16-,18-,19+,21+,23+,28+,29-,30+/m1/s1
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| Chemical Name |
(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
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~62.5 mg/mL (~120.97 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.03 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% 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 20.8 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: ≥ 2.08 mg/mL (4.03 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 20.8 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. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (4.03 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.9355 mL | 9.6774 mL | 19.3547 mL | |
| 5 mM | 0.3871 mL | 1.9355 mL | 3.8709 mL | |
| 10 mM | 0.1935 mL | 0.9677 mL | 1.9355 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.
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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