| Size | Price | Stock | Qty |
|---|---|---|---|
| 1mg |
|
||
| Other Sizes |
| Targets |
Rubropunctatin has multiple molecular targets due to its complex structure and biological activities. Its anti-inflammatory and immunosuppressive effects are likely mediated through the modulation of key inflammatory signaling pathways, such as the NF-kappaB pathway, leading to a reduction in the production of pro-inflammatory cytokines like TNF-alpha and IL-6. Its antioxidant activity results from its ability to scavenge free radicals and reduce oxidative stress, which is beneficial for protecting against oxidative protein damage. It also exhibits anti-tumor activity, potentially through the induction of apoptosis in cancer cells. The exact molecular targets for its anti-cancer effects are still under investigation but may involve the modulation of cell cycle regulators and pro-apoptotic proteins. It is also being studied for its role in immunoregulation in the context of COVID-19.
|
|---|---|
| ln Vitro |
Rubropunctatin (1.5-30 μM; 24 h) selectively kills human gastric cancer BGC-823 cells while posing no appreciable risk to normal GES-1 epithelial cells[1]. BGC-823 cells undergo apoptosis in response to rubropunctatin (5-30 μM; 6-24 h) in a dose- and time-dependent manner[1]. Ferric reducing activity, suppression of super oxide radical production, and DDPH radical scavenging activity are all demonstrated by rubropunctatin (0.75-8.0 µg/ml)[2].
In vitro, rubropunctatin has been shown to exhibit various biological activities. It has a protective and antioxidative effect against oxidative protein damage induced by metal-catalyzed reactions. This suggests the compound can directly or indirectly reduce protein carbonylation and other markers of oxidative damage. It has demonstrated anti-inflammatory effects in cell-based assays, likely by suppressing the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in LPS-stimulated macrophages. Rubropunctatin also exhibits immunosuppressive activity. For its anti-tumor activity, the compound has been shown to inhibit the proliferation of various cancer cell lines. It possesses a higher anti-atherosclerosis effect and fewer side effects related to increasing creatinine phosphokinase activity compared to other compounds. The compound's potential anti-COVID-19 immunoregulatory activity is being explored, likely involving the modulation of the host immune response to the virus. The exact IC₅0 values for these activities are not specified in the public domain. |
| ln Vivo |
In mice, rubropunctatin (8–32 mg/kg; intravenously five times) exhibits antitumor properties[1]. Rubropunctamine has an ID50 of 0.11 mg/ear and reduces the inflammation that 12-O-tetradecanoylphorbol-13-acetate (TPA) induces in mice[3].
In vivo studies of rubropunctatin are less common in the literature, but its known anti-atherosclerotic effects suggest it can affect lipid metabolism. It has been shown to have a protective effect against atherosclerosis, with a lower incidence of side effects such as increased creatinine phosphokinase activity, which is an indicator of muscle damage. This suggests that rubropunctatin might have a favorable safety profile compared to other compounds. Its anti-inflammatory and immunosuppressive properties suggest it could be effective in animal models of autoimmune diseases. For its anti-tumor activity, it would likely be tested in mouse xenograft models of various cancers. Its potential role in COVID-19 immunoregulation is under active research, possibly in animal models that recapitulate the hyperinflammatory state seen in severe COVID-19, such as the ACE2-transgenic mouse model infected with SARS-CoV-2. In such a model, rubropunctatin might be tested for its ability to reduce the "cytokine storm" and improve survival. |
| Enzyme Assay |
A typical non-cellular assay to measure the antioxidant activity of Rubropunctatin is a protein oxidation assay using a metal-catalyzed oxidation (MCO) system. A model protein, such as bovine serum albumin (BSA) (2 mg/mL), is incubated with an MCO system consisting of 25 uM CuSO4 and 5 mM ascorbic acid in 50 mM phosphate buffer (pH 7.4) at 37degC for 4 hours. Rubropunctatin is added at various concentrations (0-50 uM) to the reaction mixture. The extent of protein oxidation is assessed by measuring the levels of protein carbonyls. A 2,4-dinitrophenylhydrazine (DNPH) colorimetric assay is used: after incubation, the protein is precipitated with 20% trichloroacetic acid (TCA), washed with ethanol/ethyl acetate, and dissolved in guanidine hydrochloride solution. The absorbance is measured at 360 nm. A decrease in carbonyl formation indicates protection against oxidative damage. An anti-inflammatory assay can be performed by measuring the inhibition of nitric oxide (NO) production in a cell-free system using a NO donor like sodium nitroprusside (SNP). SNP (10 uM) is incubated with rubropunctatin (0-100 uM) in PBS at 37degC for 1 hour. The amount of NO generated is measured by the Griess reaction, which involves measuring the absorbance at 540 nm.
|
| Cell Assay |
Cell Viability Assay[1]
Cell Types: BGC-823 and GES-1cells Tested Concentrations: 1.5, 3, 6, 12, 15, 18, 30 μM Incubation Duration: 24 hrs (hours) Experimental Results: diminished the viability of BGC-823 cells with an IC50 of 12.57 μM for 24 h. Did not show obvious cytotoxic effects on the normal cells. Cell Cycle Analysis[1] Cell Types: BGC-823 cells Tested Concentrations: 0, 5, 10, 30 μM Incubation Duration: 0, 6, 12, 24 hrs (hours) Experimental Results: Increased the percentage of cells in sub-G1 phase in a dose- and time-dependent manner. A standard in vitro cell-based assay for rubropunctatin uses a murine macrophage cell line, such as RAW 264.7, to assess its anti-inflammatory activity. RAW 264.7 cells are cultured in DMEM medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin at 37degC in a 5% CO2 incubator. For the assay, cells are seeded in 96-well plates at 1 × 10⁵ cells/well. After overnight incubation, the medium is replaced with fresh medium containing rubropunctatin at various concentrations (0.1-25 uM). The cells are pre-incubated with the compound for 1 hour, then stimulated with 1 ug/mL of lipopolysaccharide (LPS) for 24 hours. After the incubation, the culture supernatants are collected. The concentration of nitric oxide (NO) is measured using the Griess reagent, which quantifies nitrite as a stable end product of NO. The absorbance is read at 540 nm. Cell viability is assessed using the MTT assay to ensure that the anti-inflammatory effects are not due to cytotoxicity. The IC₅0 for NO inhibition is calculated. The levels of other cytokines (TNF-alpha, IL-6) in the supernatant can also be measured by ELISA to further characterize the anti-inflammatory profile. |
| Animal Protocol |
Animal/Disease Models: Male nude mice (5 weeks) are inoculated with BGC-823 cells[1]
Doses: 8, 32 mg/kg Route of Administration: Iv five times (day 1st, 4th, 7th, 10th, and 13th) Experimental Results: Diminished the tumor volume by 11.1% (8 mg/kg) and 24.2% (32 mg/kg). decreased the tumor weight by 23.5% (8 mg/kg) and 37.7% (32 mg/kg). No significant difference was observed on the body weight. An in vivo animal study for rubropunctatin could be performed to evaluate its anti-atherosclerotic effects. The study uses male ApoE knockout mice (ApoE-/-, 6-8 weeks old), which are a well-established model for atherosclerosis. Mice are fed a high-fat diet (HFD, containing 21% fat and 0.15% cholesterol) for 12 weeks to induce atherosclerosis. The mice are then randomized into groups (n=10). Rubropunctatin is suspended in 0.5% carboxymethyl cellulose (CMC) and administered orally (PO) by gavage at doses of 10, 25, and 50 mg/kg once daily for an additional 8 weeks. The control group receives the vehicle alone (0.5% CMC). At the end of the treatment period, mice are euthanized, and blood is collected for serum biochemical analysis, including measurement of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and creatinine phosphokinase (CPK) activity. The aorta is dissected, opened longitudinally, and stained with Oil Red O to visualize atherosclerotic plaques. The percentage of the aortic surface area covered by plaque is quantified. The heart is also sectioned and stained with H&E to assess plaque formation in the aortic root. All animal procedures must be approved by the Institutional Animal Care and Use Committee (IACUC). |
| ADME/Pharmacokinetics |
The pharmacokinetic (PK) properties of rubropunctatin are not well-defined in the public domain. As a natural pigment with a molecular weight of 354.40 g/mol (C21H22O₅), it is a relatively small molecule. The compound is soluble in chloroform, dichloromethane, ethyl acetate, DMSO, and acetone, indicating a lipophilic character. This suggests it would have moderate to good membrane permeability. Its oral bioavailability is unknown, but as a lipophilic compound, it could be absorbed. It is likely metabolized in the liver by cytochrome P450 enzymes. No specific PK parameters, such as half-life, Cmax, or volume of distribution, are publicly available. The compound's stability in physiological conditions is not known. For research use, it is typically stored desiccated at -20degC to maintain stability. Human PK data is not available.
|
| Toxicity/Toxicokinetics |
No comprehensive toxicological data is available for rubropunctatin. In the study on its anti-atherosclerotic effects, it was noted that rubropunctatin had fewer side effects involving increasing creatinine phosphokinase (CPK) activity, which is an indicator of muscle damage (e.g., rhabdomyolysis). This suggests it may have a better safety profile compared to some other compounds. However, formal toxicological studies to determine the acute oral LD₅0 or NOAEL (No Observed Adverse Effect Level) have not been reported. As with all research chemicals, it should be handled with caution using appropriate personal protective equipment (PPE). It is for research use only and is not intended for human consumption.
|
| References |
|
| Additional Infomation |
Red dot mycoside is a type of cyclohexenone compound. It has been reported that Monascus purpureus and Monascus purpureus contain red dot mycoside, and relevant data are available for reference.
Rubropunctatin is not an approved drug and has no clinical development history. It is a naturally occurring compound from red yeast rice that serves as a research tool for studying inflammation, cancer, and immunoregulation. Its mechanism of action is multi-faceted, involving anti-inflammatory, immunosuppressive, antioxidative, and anti-tumor pathways. It is of particular interest for its potential role in COVID-19 immunoregulation, where it may help to modulate the hyperactive immune response seen in severe cases. It is used in natural product chemistry and pharmacological research as a reference standard and a lead compound for drug discovery. No clinical trials have been registered for rubropunctatin. For research use only; not for diagnostic or therapeutic applications in humans. |
| Molecular Formula |
C21H22O5
|
|---|---|
| Molecular Weight |
354.40
|
| Exact Mass |
354.147
|
| CAS # |
514-67-0
|
| PubChem CID |
6452445
|
| Appearance |
Yellow to orange solid powder
|
| Density |
1.23g/cm3
|
| Boiling Point |
638.8ºC at 760 mmHg
|
| Flash Point |
280ºC
|
| Index of Refraction |
1.58
|
| LogP |
3.631
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
5
|
| Rotatable Bond Count |
6
|
| Heavy Atom Count |
26
|
| Complexity |
835
|
| Defined Atom Stereocenter Count |
1
|
| SMILES |
CCCCCC(=O)C1=C2C=C3C=C(OC=C3C(=O)[C@@]2(OC1=O)C)/C=C/C
|
| InChi Key |
SULYDLFVUNXAMP-WKOQKXSESA-N
|
| InChi Code |
InChI=1S/C21H22O5/c1-4-6-7-9-17(22)18-16-11-13-10-14(8-5-2)25-12-15(13)19(23)21(16,3)26-20(18)24/h5,8,10-12H,4,6-7,9H2,1-3H3/b8-5+/t21-/m1/s1
|
| Chemical Name |
(9aR)-3-hexanoyl-9a-methyl-6-[(E)-prop-1-enyl]furo[3,2-g]isochromene-2,9-dione
|
| 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 (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
|
|---|---|
| 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 | 2.8217 mL | 14.1084 mL | 28.2167 mL | |
| 5 mM | 0.5643 mL | 2.8217 mL | 5.6433 mL | |
| 10 mM | 0.2822 mL | 1.4108 mL | 2.8217 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.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
