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| Targets |
Cerevisterol targets multiple cellular pathways. It is a known inhibitor of DNA polymerase alpha, a key enzyme involved in DNA replication. By inhibiting this enzyme, cerevisterol can interfere with cell proliferation, which may contribute to its cytotoxic and anticancer effects. Additionally, cerevisterol acts as a potent inhibitor of NF-κB activation. The nuclear factor kappa-B (NF-κB) is a protein complex that controls transcription of DNA, cytokine production, and cell survival. Its activation is a central event in inflammatory responses. Cerevisterol's mechanism involves blocking the nuclear translocation of NF-κB by preventing the phosphorylation of IκBα, the inhibitory protein that retains NF-κB in the cytoplasm. This leads to the suppression of NF-κB's transcriptional activation, thereby reducing the expression of pro-inflammatory genes. Furthermore, cerevisterol can stimulate NGF-mediated neurite outgrowth on PC12 cells, suggesting it may interact with neurotrophic signaling pathways, possibly through the MAPK, NF-κB, AP-1, and Nrf2-mediated HO-1 signaling cascade. This multi-targeted action profile underscores its potential as a therapeutic agent for various diseases.
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| ln Vitro |
In vitro, cerevisterol has demonstrated significant biological activities. It inhibits the activity of DNA polymerase alpha, an effect that can be measured in cell-free enzyme assays. It also stimulates NGF-mediated neurite outgrowth on PC12 cells, a commonly used model for studying neuronal differentiation. The compound exhibits cytotoxicity against several mammalian cell lines, indicating its potential as an anticancer agent. For instance, it is active against the bacteria S. typhi. While specific IC50 values for its various activities are not universally reported in the available literature, its effects are well-documented in several studies. For example, its ability to inhibit NF-κB activation and its anti-inflammatory properties have been demonstrated in cellular models. The compound's diverse in vitro activities make it a valuable tool for studying various biological processes and for evaluating its potential as a lead compound for drug development.
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| ln Vivo |
In vivo activity data for cerevisterol are limited in the available literature. Most studies have focused on its in vitro biological activities. While its anti-inflammatory and anticancer properties have been suggested, detailed in vivo efficacy studies in animal models are not extensively documented. The compound has been isolated from various sources and studied for its pharmacological properties, but systematic in vivo investigations, including pharmacokinetics and toxicology, are lacking. This gap in knowledge highlights the need for further research to translate its promising in vitro activities into in vivo benefits and to assess its safety and efficacy as a potential therapeutic agent.
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| Enzyme Assay |
Non-cell-based assays for cerevisterol typically involve measuring its effect on specific enzyme activities in a cell-free system. For instance, to assess its inhibition of DNA polymerase alpha, the enzyme is incubated with cerevisterol at various concentrations (e.g., 0-100 µM) in a reaction mixture containing the template DNA and radiolabeled nucleotides. After incubation, the incorporation of radiolabeled nucleotides into DNA is measured, and the inhibition of polymerase activity is calculated relative to control samples without the compound. Similarly, to study its effect on NF-κB, cell-free assays could involve measuring the binding of NF-κB to its DNA consensus sequence in the presence of the compound, or assessing the phosphorylation status of IκBα in cell lysates. These assays are crucial for confirming the direct biochemical targets of cerevisterol and for understanding its mechanism of action at the molecular level, independent of cellular complexities.
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| Cell Assay |
For in vitro cellular experiments, PC12 cells are a commonly used model. These cells are cultured in medium containing NGF and treated with cerevisterol at various concentrations. After 48 to 72 hours of treatment, neurite outgrowth is quantified by microscopy. Cells with neurites longer than the cell body diameter are counted as differentiated, and the percentage of neurite-bearing cells is compared between treated and control groups. This assay is used to evaluate the compound's neurotrophic activity. For studying its anti-inflammatory effects, immune cells such as macrophages could be treated with cerevisterol and stimulated with LPS. The production of inflammatory mediators such as NO, TNF-α, and IL-6 would then be measured. Inhibition of these mediators would indicate anti-inflammatory activity. These cell-based assays are essential for assessing the functional consequences of cerevisterol's activity in a living cellular context.
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| Animal Protocol |
In vivo animal studies for cerevisterol have not been extensively reported in the available literature. The primary focus of research has been on its in vitro biological activities. While its potential for treating inflammatory diseases has been suggested, detailed in vivo studies in animal models, such as those for inflammation or cancer, are not widely documented. Further research is necessary to evaluate its efficacy, pharmacokinetics, and safety in living organisms.
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| ADME/Pharmacokinetics |
Cerevisterol has a molecular weight of 430.66 and is soluble in chloroform, dichloromethane, ethyl acetate, DMSO, and acetone. Its melting point is reported to be 255-256°C. No detailed pharmacokinetic data, such as absorption, distribution, metabolism, and excretion (ADME), are available in the public literature. As a natural product and research compound, its pharmacokinetic properties have not been a primary focus of investigation.
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| Toxicity/Toxicokinetics |
Toxicological data for cerevisterol are not available in the public literature. As a research chemical, its safety profile has not been systematically evaluated. Researchers should handle it with standard laboratory precautions.
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| References | |
| Additional Infomation |
Cerevisterol is an ergosterol compound with the structure (22E)-ergosterol-7,22-diene, substituted with hydroxyl groups at positions 3, 5, and 6 (3β,5α,6β stereoisomers). It has been isolated from Trichoderma fungi. Cerevisterol is a metabolite of Aspergillus. It is a 3β-hydroxysterol, 5α-hydroxysterol, 6β-hydroxysterol, and ergosterol compound. Cerevisterol has been reported in Agaricus brasiliensis, Psilocybe globosum, and other organisms with relevant data.
Cerevisterol is a naturally occurring compound with potential applications in antimicrobial, anti-inflammatory, and anticancer research. It has been isolated from the fruit body of Ganoderma lucidum and other fungi. Its mechanism of action involves the inhibition of DNA polymerase alpha and the suppression of NF-κB activation. It is a cytotoxic steroid and is used as a reference standard and for pharmacological research. The compound is typically stored at 2-8°C, protected from air and light. It is for research use only and is not intended for human therapeutic applications. |
| Molecular Formula |
C28H46O3
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|---|---|
| Molecular Weight |
430.66
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| Exact Mass |
430.344
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| CAS # |
516-37-0
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| PubChem CID |
10181133
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| Appearance |
White to off-white solid powder
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| Density |
1.1±0.1 g/cm3
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| Boiling Point |
535.0±50.0 °C at 760 mmHg
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| Flash Point |
221.2±24.7 °C
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| Vapour Pressure |
0.0±3.2 mmHg at 25°C
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| Index of Refraction |
1.557
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| LogP |
7.38
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
31
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| Complexity |
741
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| Defined Atom Stereocenter Count |
10
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| SMILES |
C[C@H](/C=C/[C@H](C)C(C)C)[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3C2=C[C@H]([C@@]4([C@@]3(CC[C@@H](C4)O)C)O)O)C
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| InChi Key |
ARXHRTZAVQOQEU-BRVLHLJYSA-N
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| InChi Code |
InChI=1S/C28H46O3/c1-17(2)18(3)7-8-19(4)22-9-10-23-21-15-25(30)28(31)16-20(29)11-14-27(28,6)24(21)12-13-26(22,23)5/h7-8,15,17-20,22-25,29-31H,9-14,16H2,1-6H3/b8-7+/t18-,19+,20-,22+,23-,24-,25+,26+,27+,28-/m0/s1
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| Chemical Name |
(3S,5R,6R,9S,10R,13R,14R,17R)-17-[(E,2R,5R)-5,6-dimethylhept-3-en-2-yl]-10,13-dimethyl-1,2,3,4,6,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthrene-3,5,6-triol
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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 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.) |
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| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.3220 mL | 11.6101 mL | 23.2202 mL | |
| 5 mM | 0.4644 mL | 2.3220 mL | 4.6440 mL | |
| 10 mM | 0.2322 mL | 1.1610 mL | 2.3220 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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