| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 100mg | |||
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| Targets |
Lucidenic acid B targets multiple cellular pathways involved in cancer cell survival and invasion. It induces apoptosis in cancer cells through the activation of caspase-9 and caspase-3, and the cleavage of PARP (poly (ADP-ribose) polymerase). The activation of these caspases is a hallmark of the intrinsic (mitochondrial) apoptotic pathway. Furthermore, Lucidenic acid B inhibits PMA-induced invasion of human hepatocellular carcinoma cells by inactivating the MAPK/ERK signaling pathway and decreasing the binding activities of NF-κB and AP-1. This dual mechanism—inducing apoptosis and inhibiting invasion—makes it a potent anticancer agent.
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| ln Vitro |
In vitro, Lucidenic acid B has been shown to induce apoptosis in various cancer cell lines. It causes the activation of caspase-9 and caspase-3, and the cleavage of PARP. Importantly, it does not affect the cell cycle profile or increase the number of necrotic cells, suggesting a specific induction of apoptosis rather than non-specific cell death. The compound also exhibits antioxidant properties and anti-invasive effects. It inhibits PMA-induced invasion of human hepatoma cells by inactivating the MAPK/ERK signal transduction pathway and reducing the binding activities of NF-κB and AP-1.
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| ln Vivo |
In vivo, the anticancer activities of Lucidenic acid B observed in vitro suggest it has significant therapeutic potential. Studies have shown that it can induce apoptosis in leukemia cells and inhibit liver cancer cell invasion in animal models. Its ability to trigger apoptosis and block invasion pathways makes it a promising candidate for cancer therapy. However, detailed in vivo efficacy data are limited in the public literature. Further studies are needed to fully characterize its pharmacokinetics, toxicity, and efficacy in vivo.
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| Enzyme Assay |
For in vitro apoptosis assays, Lucidenic acid B is evaluated using cancer cell lines, such as leukemia or hepatoma cells. Cells are treated with varying concentrations of the compound, and apoptosis is measured using flow cytometry with Annexin V and propidium iodide (PI) staining. The activation of caspases is assessed by measuring caspase-3 and caspase-9 activity using fluorogenic substrates. PARP cleavage is detected by Western blotting. For invasion assays, transwell chambers coated with Matrigel are used.
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| Cell Assay |
For in vitro cell-based assays, the effects of Lucidenic acid B on cell signaling pathways are studied using Western blotting. Cells are treated with the compound, and cell lysates are probed with antibodies against phosphorylated and total ERK, NF-κB, and AP-1. This allows researchers to confirm the inactivation of the MAPK/ERK pathway and the reduction of transcription factor binding activities. Cell viability is measured using MTT or CCK-8 assays to assess the compound's cytotoxic effects.
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| Animal Protocol |
For in vivo animal studies, Lucidenic acid B is typically administered orally or intraperitoneally in rodent models of cancer. To evaluate its anticancer efficacy, xenograft or orthotopic models of leukemia or liver cancer can be used. Tumor-bearing mice are treated with the compound, and tumor growth and the incidence of metastasis are monitored. At the end of the study, tumors are collected for histology and molecular analysis to assess apoptosis and signaling pathway modulation.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of Lucidenic acid B: The compound has a molecular formula of C27H38O7, a molecular weight of 474.59, and a melting point of 179-181°C. It has a LogP of 3.105. It is typically stored as a powder at -20°C, protected from light. As a triterpenoid, it is expected to have poor oral bioavailability. Detailed pharmacokinetic parameters are not publicly available.
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| Toxicity/Toxicokinetics |
Specific toxicity data for Lucidenic acid B are limited. As a natural compound from Ganoderma lucidum, it is generally considered to have a favorable safety profile based on its traditional use. However, comprehensive toxicological studies have not been published. The compound is used for research purposes only and is not intended for human use. Standard laboratory safety precautions should be observed.
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| References | |
| Additional Infomation |
Ganoderic acid B is a triterpenoid compound. It has been reported that ganoderic acid B is present in Ganoderma lucidum, and relevant data are available for reference.
Lucidenic acid B is a research compound with no clinical trial or regulatory approval status. It is a natural triterpenoid isolated from Ganoderma lucidum and is used as a research tool to study apoptosis and cancer cell invasion. It is commercially available from chemical suppliers for research purposes only. The compound is a key bioactive component of Ganoderma lucidum and is of significant interest in cancer research. |
| Molecular Formula |
C27H38O7
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|---|---|
| Molecular Weight |
474.5864
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| Exact Mass |
474.262
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| CAS # |
95311-95-8
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| PubChem CID |
102410351
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| Appearance |
White to off-white solid powder
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| Melting Point |
179-181 °C
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| LogP |
3.105
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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 |
4
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| Heavy Atom Count |
34
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| Complexity |
1010
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| Defined Atom Stereocenter Count |
8
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| SMILES |
C[C@H](CCC(=O)O)[C@H]1CC(=O)[C@@]2([C@@]1([C@@H](C(=O)C3=C2[C@H](C[C@@H]4[C@@]3(CCC(=O)C4(C)C)C)O)O)C)C
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| InChi Key |
GYRDSOABOBCYST-HFAARYGVSA-N
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| InChi Code |
InChI=1S/C27H38O7/c1-13(7-8-19(31)32)14-11-18(30)27(6)20-15(28)12-16-24(2,3)17(29)9-10-25(16,4)21(20)22(33)23(34)26(14,27)5/h13-16,23,28,34H,7-12H2,1-6H3,(H,31,32)/t13-,14-,15+,16+,23-,25+,26+,27+/m1/s1
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| Chemical Name |
(4R)-4-[(5R,7S,10S,12S,13R,14R,17R)-7,12-dihydroxy-4,4,10,13,14-pentamethyl-3,11,15-trioxo-1,2,5,6,7,12,16,17-octahydrocyclopenta[a]phenanthren-17-yl]pentanoic 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: 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)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.1071 mL | 10.5354 mL | 21.0708 mL | |
| 5 mM | 0.4214 mL | 2.1071 mL | 4.2142 mL | |
| 10 mM | 0.2107 mL | 1.0535 mL | 2.1071 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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