| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
|
||
| 10mg |
|
||
| 25mg |
|
||
| 100mg |
|
||
| 250mg |
|
||
| 500mg | |||
| Other Sizes |
| Targets |
Mogrol targets multiple signaling pathways involved in metabolism, inflammation, and cancer. It functions by inhibiting the ERK1/2 and STAT3 pathways, reducing CREB activation, and activating AMPK signaling. This modulation of AMPK activation enhances lipid metabolism and suppresses adipogenesis, making it relevant for metabolic-disease research.
|
|---|---|
| ln Vitro |
Mogrol (0-250 μM) increases the number of cells in vitro and greatly inhibits K562 cell growth in a quantitative and temporal manner. In K562 cells, mogrol (0, 10, 100, and 250 μM) activates cell cycle components related to the G1 phase. While total ERK protein did not boost ERK phosphorylation, mogrol administration dramatically decreased it when compared to control cells. Growth is induced in the G0/G1 phase of the cycle dose-dependently by mogrol. In K562 cells, mogrol dramatically increases the expression of the growth inducer p21 protein [1]. Mogrol demonstrated a statistically significant suppression of TG accumulation at micromolar levels and considerably reduced the increase in cellular TG levels produced by exit stimulation. The inhibition was found above 10 μM. In 3T3-L1 cells, mogrol inhibits adipogenesis at doses that do not compromise cell viability. Mogrol is produced by at least two distinct fat-inhibiting processes, which are AMPK phosphorylation increase and CREB activation inhibition [2].
In vitro, Mogrol demonstrates significant biological activity. It suppresses lung cancer cell growth by activating AMPK-dependent autophagic death and inducing p53-dependent cell cycle arrest and apoptosis. In K562 leukemia cells, Mogrol (0-250 µM) significantly and dose- and time-dependently inhibits cell growth and increases the number of apoptotic cells. It also attenuates ulcerative colitis by promoting AMPK activation. |
| ln Vivo |
In vivo, Mogrol has shown efficacy in preclinical models. It attenuates ulcerative colitis in animal models by promoting AMPK activation. Its neuroprotective and anticancer activities have been observed. As the aglycone of mogrosides, it is believed to contribute to the overall health benefits, including anti-obesity, anti-diabetic, and anti-inflammatory effects, associated with monk fruit consumption.
|
| Enzyme Assay |
The in vitro kinase inhibition assay for Mogrol involves measuring its effect on ERK1/2 and STAT3 phosphorylation. Cells are treated with the compound, and the levels of phosphorylated and total ERK1/2 and STAT3 are measured by Western blotting. For AMPK activation, the phosphorylation of AMPK and its downstream target ACC is assessed. The IC50 for kinase inhibition can be determined from concentration-response curves.
|
| Cell Assay |
In vitro cell culture studies for Mogrol utilize various cancer cell lines, such as K562 leukemia cells and lung cancer cells. Cells are treated with varying concentrations of the compound. Cell viability is assessed using MTT or trypan blue exclusion. Apoptosis is detected by Annexin V/PI staining and flow cytometry. Cell cycle analysis is performed by propidium iodide staining. Autophagy is confirmed by detecting LC3-II conversion.
|
| Animal Protocol |
In vivo animal experiments for Mogrol have been performed in models of ulcerative colitis. In these studies, the compound is administered orally or intraperitoneally. Disease severity is assessed by measuring disease activity index, colon length, and histological scoring. Inflammatory cytokine levels are measured by ELISA. Its anticancer efficacy could be evaluated in xenograft models.
|
| ADME/Pharmacokinetics |
Mogrol is a lipophilic compound with a molecular weight of approximately 460 g/mol. It is soluble in organic solvents like DMSO and ethanol. As a metabolite, it is absorbed from the gut after consumption of mogrosides. It is typically stored as a powder at -20°C for long-term stability. Its stability is maintained under recommended storage conditions.
|
| Toxicity/Toxicokinetics |
Toxicological data for Mogrol indicate that it is generally safe at concentrations obtained through dietary consumption of monk fruit. However, as a research compound, it is not intended for therapeutic use. Its ability to activate AMPK and inhibit cell growth suggests it could have significant biological effects at higher doses. Comprehensive toxicity studies are limited.
|
| References |
|
| Additional Infomation |
Mogrol is a tetracyclic triterpenoid compound, a derivative of cucurbitacinol, whose side chain double bonds (positions 24-25) undergo formal oxidation, introducing hydroxyl groups at positions 24 and 25 (24R stereoisomer). It is a biometabolite of Mogrol and is found in the monk fruit tree (Siraitia grosvenorii). It possesses antitumor activity. Mogrol is a tetracyclic triterpenoid compound and also a hydroxyl-opening steroid. Its function is related to cucurbitacinol. Mogrol has been reported to be present in the monk fruit tree (Siraitia grosvenorii), and relevant data are available for reference.
Mogrol is a research compound with no clinical approval. It is a valuable tool for studying the pharmacology of mogrosides and the therapeutic potential of triterpenoids in metabolic and inflammatory diseases. Its role as an AMPK activator and inhibitor of ERK1/2 and STAT3 makes it a promising lead compound for drug discovery in cancer and metabolic disorders. |
| Molecular Formula |
C30H52O4
|
|---|---|
| Molecular Weight |
476.7315
|
| Exact Mass |
476.386
|
| CAS # |
88930-15-8
|
| PubChem CID |
14525327
|
| Appearance |
White to off-white solid powder
|
| Density |
1.1±0.1 g/cm3
|
| Boiling Point |
595.6±50.0 °C at 760 mmHg
|
| Flash Point |
242.9±24.7 °C
|
| Vapour Pressure |
0.0±3.8 mmHg at 25°C
|
| Index of Refraction |
1.553
|
| LogP |
5.49
|
| Hydrogen Bond Donor Count |
4
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
5
|
| Heavy Atom Count |
34
|
| Complexity |
817
|
| Defined Atom Stereocenter Count |
10
|
| SMILES |
C[C@H](CC[C@H](C(C)(C)O)O)[C@H]1CC[C@@]2([C@@]1(C[C@H]([C@@]3([C@H]2CC=C4[C@H]3CC[C@@H](C4(C)C)O)C)O)C)C
|
| InChi Key |
JLYBBRAAICDTIS-AYEHCKLZSA-N
|
| InChi Code |
InChI=1S/C30H52O4/c1-18(9-13-24(32)27(4,5)34)19-15-16-28(6)22-12-10-20-21(11-14-23(31)26(20,2)3)30(22,8)25(33)17-29(19,28)7/h10,18-19,21-25,31-34H,9,11-17H2,1-8H3/t18-,19-,21-,22+,23+,24-,25-,28+,29-,30+/m1/s1
|
| Chemical Name |
(3S,8S,9R,10R,11R,13R,14S,17R)-17-[(2R,5R)-5,6-dihydroxy-6-methylheptan-2-yl]-4,4,9,13,14-pentamethyl-2,3,7,8,10,11,12,15,16,17-decahydro-1H-cyclopenta[a]phenanthrene-3,11-diol
|
| 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 |
| 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) |
DMSO : ~50 mg/mL (~104.88 mM)
H2O : < 0.1 mg/mL |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.24 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 25.0 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: ≥ 2.5 mg/mL (5.24 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 25.0 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: ≥ 2.5 mg/mL (5.24 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 | 2.0976 mL | 10.4881 mL | 20.9762 mL | |
| 5 mM | 0.4195 mL | 2.0976 mL | 4.1952 mL | |
| 10 mM | 0.2098 mL | 1.0488 mL | 2.0976 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.