Lunularin
Based on 1 Customer Validation
Lunularin is an inhibitor of 11β-hydroxysteroid dehydrogenase 1, with an IC50 of 45.44 μM and a Ki of 35.8 μM against human 11β-HSD1, and an IC50 of 17.39 μM and a Ki of 10.31 μM against rat 11β-HSD1. Lunularin upregulates the transcription levels of Sirt1 and Hmox1 genes in the liver. Lunularin reduces food intake and body weight gain, and decreases blood glucose levels in mice fed a high-fat diet. Lunularin inhibits LPS-induced TLR4-mediated NF-κB pathway activation and nitric oxide production. Lunularin inhibits the proliferation and colony formation of renal cancer and colon cancer cells, and exhibits cancer cell-specific cytotoxicity. Lunularin binds to the steroid-binding site of human 11β-HSD1 and the steroid/NADPH-binding region of rat 11β-HSD1, but does not inhibit 11β-HSD2 or mouse 11β-HSD1. Lunularin can be used in research related to diet-induced obesity, renal cancer, colorectal cancer, inflammatory diseases and metabolic syndrome.
For research use only. We do not sell to patients.
- Purity : 99.87%
- CAS No.: 37116-80-6
- Formula: C14H14O2
- Molecular Weight:214.26
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Storage:
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
All Endogenous Metabolite Isoforms
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | IC50 |
150 μM
Compound: Lunularin
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Cytotoxic activity against human A549 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay
Cytotoxic activity against human A549 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay
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[PMID: 30848895] |
| J774 | IC50 |
>512 μM
Compound: HO21
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Cytotoxicity against mouse J774 cells assessed as cell viability after 48 hrs by resazurin assay
Cytotoxicity against mouse J774 cells assessed as cell viability after 48 hrs by resazurin assay
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[PMID: 25884114] |
| MRC5 | IC50 |
200 μM
Compound: Lunularin
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Cytotoxic activity against human MRC5 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay
Cytotoxic activity against human MRC5 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay
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[PMID: 30848895] |
In Vitro
Lunularin (0.5×-1.5×; 26.8-80.4 nmol/g) dose-dependently inhibits the proliferation of 786-O human renal adenocarcinoma cells, with greater activity than dihydroresveratrol alone at concentrations relevant to kidney tissue levels[2].
Lunularin (0.5×-1.5×; 26.8-80.4 nmol/g) dose-dependently inhibits the proliferation of A498 human renal carcinoma cells, with greater activity than dihydroresveratrol alone at concentrations relevant to kidney tissue levels[2].
Lunularin (1×; 53.6 nmol/g) significantly inhibits the clonogenic growth of 786-O human renal adenocarcinoma cells at concentrations relevant to kidney tissue levels, with enhanced activity when combined with dihydroresveratrol[2].
Lunularin (1×100; 53.6 nmol/g) significantly inhibits the clonogenic growth of A498 human renal carcinoma cells at concentrations relevant to kidney tissue levels, with enhanced activity when combined with dihydroresveratrol[2].
Lunularin (0.5×-1.5×; 30.25-90.75 nmol/g) inhibits the proliferation of HCT-116 human colorectal carcinoma cells, with enhanced activity when combined with dihydroresveratrol at concentrations relevant to colonic tissue levels[2].
Lunularin (1×; 60.5 nmol/g; 12 days) significantly inhibits the clonogenic growth of HT-29 human colon adenocarcinoma cells at concentrations relevant to colonic tissue levels, with enhanced activity when combined with dihydroresveratrol[2].
Lunularin (0.5×-1.5×; 30.25-90.75 nmol/g) dose-dependently inhibits LPS-induced NO production in RAW264.7 mouse macrophages, with enhanced activity when combined with dihydroresveratrol at concentrations relevant to colonic tissue levels[2].
Lunularin (0.5×-1.5×; 30.25-90.75 nmol/g) dose-dependently inhibits LPS-induced SEAP production in HEK-Blue mTLR-4 cells (targeting the TLR-4-mediated NF-κB pathway), with greater activity than resveratrol alone at concentrations relevant to colonic tissue levels[2].
Lunularin (20-100 μM; 30 min to standard assay conditions) competitively inhibits human liver microsomal 11β-HSD1 with an IC50 of 45.44 μM and a Ki of 35.8 μM by binding to the enzyme's steroid-binding site[4].
Lunularin (12.5-100 μM; 30 min to standard assay conditions) acts as a mixed inhibitor of rat liver microsomal 11β-HSD1 with an IC50 of 17.39 μM and a Ki of 10.31 μM by binding to the enzyme's combined NADPH and steroid-binding region[4].
Lunularin does not inhibit mouse liver microsomal 11β-HSD1 activity[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Lunularin is a gut microbiota-derived metabolite of resveratrol, is highly abundant in mouse tissues, biological fluids, and gastrointestinal tract compared to resveratrol itself, and is eliminated when gut microbiota is depleted via antibiotics[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6JRj (13-month-old, diet-induced obesity model)[1]
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Dosage:24 mg/kg
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Administration:intraperitoneal injection; 3 times per week; 8 weeks
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Result:Slightly reduced feed intake to 2.81 ± 0.1 g per day.
Showed a highly significant reduction in body weight gain over the study period.
Had slightly lower blood glucose levels after 8 weeks of treatment.
Had significantly elevated hepatic Sirt1 mRNA levels
Had significantly elevated hepatic Hmox1 mRNA level.
Reached mean liver tissue concentrations of 28.8 pmol/g liver.
Did not alter plasma levels of cholesterol, insulin, leptin, or adiponectin; did not alter hepatic phosphorylated AMPK levels, major urinary protein levels, or hepatic mRNA levels of Pck1, Pgc1α, Foxo3, or Tnfα.
Chemical Information
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CAS No. 37116-80-6
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Appearance Solid
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Molecular Weight 214.26
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Formula C14H14O2
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Color White to off-white
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SMILES
OC1=CC=C(CCC2=CC=CC(O)=C2)C=C1
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Structure Classification
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (466.72 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (11.67 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (11.67 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Soft Agar Colony Formation Assay
Soft agar colony formation assay measures anchorage-independent growth, in which transformed or tumorigenic cells proliferate as colonies in a semisolid agar matrix while many non-transformed adherent cells fail to proliferate without attachment; classic studies showed that growth in semisolid medium correlates with tumorigenicity in nude mice, and later protocol papers describe the method as a stringent in vitro assay for malignant transformation. The readout is the number, size, morphology, or signal intensity of colonies formed within agar after incubation; published formats include manual colony counting after staining, 96-well or 384-well quantitative formats, DNA-binding dye detection, MTT/tetrazolium-based detection, digital image analysis, and PCR-based marker detection from soft agar cultures.
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Colony Formation (Clonogenic) Assay
The clonogenic (colony formation) assay measures the ability of a single cell to retain reproductive viability and form a macroscopic colony, typically defined as a cluster derived from one progenitor cell after a defined growth period. This assay is widely used to evaluate cell survival after exposure to ionizing radiation or cytotoxic treatments and is considered a standard method in radiation biology for generating dose-response relationships of reproductive cell death. Colony formation reflects long-term proliferative capacity rather than short-term metabolic activity, and survival is quantified by comparing treated versus untreated conditions based on colony number and derived survival fractions.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
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Data Sheet (277 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1]. Pallauf K, et al. Resveratrol, lunularin and dihydroresveratrol do not act as caloric restriction mimetics when administered intraperitoneally in mice. Sci Rep. 2019;9(1):4445. Published 2019 Mar 14. [Content Brief]
[2]. Li F, et al. Gut Microbiota-Derived Resveratrol Metabolites, Dihydroresveratrol and Lunularin, Significantly Contribute to the Biological Activities of Resveratrol. Front Nutr. 2022;9:912591. Published 2022 May 11. [Content Brief]
[4]. Hu C, et al. Resveratrol analogues and metabolites selectively inhibit human and rat 11β-hydroxysteroid dehydrogenase 1 as the therapeutic drugs: structure-activity relationship and molecular dynamics analysis. SAR QSAR Environ Res. 2024;35(7):641-663. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 4.6672 mL | 23.3361 mL | 46.6723 mL | 116.6807 mL |
| 5 mM | 0.9334 mL | 4.6672 mL | 9.3345 mL | 23.3361 mL | |
| 10 mM | 0.4667 mL | 2.3336 mL | 4.6672 mL | 11.6681 mL | |
| 15 mM | 0.3111 mL | 1.5557 mL | 3.1115 mL | 7.7787 mL | |
| 20 mM | 0.2334 mL | 1.1668 mL | 2.3336 mL | 5.8340 mL | |
| 25 mM | 0.1867 mL | 0.9334 mL | 1.8669 mL | 4.6672 mL | |
| 30 mM | 0.1556 mL | 0.7779 mL | 1.5557 mL | 3.8894 mL | |
| 40 mM | 0.1167 mL | 0.5834 mL | 1.1668 mL | 2.9170 mL | |
| 50 mM | 0.0933 mL | 0.4667 mL | 0.9334 mL | 2.3336 mL | |
| 60 mM | 0.0778 mL | 0.3889 mL | 0.7779 mL | 1.9447 mL | |
| 80 mM | 0.0583 mL | 0.2917 mL | 0.5834 mL | 1.4585 mL | |
| 100 mM | 0.0467 mL | 0.2334 mL | 0.4667 mL | 1.1668 mL |
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