| Field | Specification |
|---|---|
| CAS no. | |
| Applications | |
| Source | Plant — Conocephalum conicum (L.) Dumort.; Endogenous metabolite — Human Gut Microbiota Metabolites |
| Molecular weight | |
| Molecular formula | C14H14O2 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Lunularin inhibits 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), with an IC50 of 45.44 μM and a Ki of 35.8 μM against the human enzyme, and an IC50 of 17.39 μM and a Ki of 10.31 μM against the rat enzyme. It upregulates hepatic Sirt1 and Hmox1 transcription, reduces food intake and body weight gain, and lowers blood glucose in mice fed a high-fat diet, while also inhibiting LPS-induced TLR4-mediated NF-κB activation and nitric oxide production. It inhibits proliferation and colony formation of renal and colon cancer cells with cancer cell-specific cytotoxicity, and binds the steroid-binding site of human 11β-HSD1 and the steroid/NADPH-binding region of rat 11β-HSD1, without inhibiting 11β-HSD2 or mouse 11β-HSD1; it can be used in research on diet-induced obesity, renal and colorectal cancer, inflammatory disease and metabolic syndrome[1][2][3][4]. It is supplied as a white to off-white solid (C14H14O2, MW 214.26) at 99.87% purity and occurs naturally in the plant Conocephalum conicum (L.) Dumort. and as a human gut microbiota metabolite.
Physical & Chemical Properties
| CAS Number | 37116-80-6 |
|---|---|
| Molecular Formula | C14H14O2 |
| Molecular Weight | 214.26 g/mol |
| Purity | 99.87% |
| Appearance | Solid |
| Color | White to off-white |
| Structure Classification | Phenols Polyphenols |
| SMILES | OC1=CC=C(CCC2=CC=CC(O)=C2)C=C1 |
| Signaling Pathway | Metabolic Enzyme/Protease |
| Initial Source | Plant — Conocephalum conicum (L.) Dumort.; Endogenous metabolite — Human Gut Microbiota Metabolites |
| Solubility | In Vitro: DMSO: 100 mg/mL (466.72 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | 4°C, stored under nitrogen. In solvent: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
[3]. Suire C, et al. Chirality of terpenoids isolated from the liverwort Conocephalum Conicum[J]. Phytochemistry, 1982, 21(2): 349-352.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 100 mg/mL (466.72 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); stored under nitrogen; avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (11.67 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.5 mg/mL (11.67 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (11.67 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
In 786-O human renal adenocarcinoma cells, proliferation is dose-dependently inhibited by Lunularin (0.5×-1.5×; 26.8-80.4 nmol/g), which outperforms dihydroresveratrol alone when concentrations match kidney tissue levels[2]. Lunularin (0.5×-1.5×; 26.8-80.4 nmol/g) reduces A498 human renal carcinoma cell proliferation in a dose-dependent fashion, and its activity exceeds that of dihydroresveratrol alone at concentrations matching kidney tissue levels[2]. Clonogenic growth of 786-O human renal adenocarcinoma cells is significantly inhibited by Lunularin (1×; 53.6 nmol/g) at concentrations relevant to kidney tissue levels, and the effect is enhanced when dihydroresveratrol is added[2]. Lunularin (1×100; 53.6 nmol/g) significantly suppresses clonogenic growth of A498 human renal carcinoma cells at kidney-tissue-relevant concentrations, and combining it with dihydroresveratrol strengthens this activity[2]. Proliferation of HCT-116 human colorectal carcinoma cells is inhibited by Lunularin (0.5×-1.5×; 30.25-90.75 nmol/g), and co-treatment with dihydroresveratrol boosts this activity at concentrations relevant to colonic tissue levels[2]. In HT-29 human colon adenocarcinoma cells, clonogenic growth is significantly blocked by Lunularin (1×; 60.5 nmol/g; 12 days) at colonic-tissue-relevant concentrations, with enhanced activity upon combination with dihydroresveratrol[2]. LPS-induced NO production in RAW264.7 mouse macrophages is dose-dependently inhibited by Lunularin (0.5×-1.5×; 30.25-90.75 nmol/g), and activity is enhanced by dihydroresveratrol co-treatment at concentrations relevant to colonic tissue levels[2]. In HEK-Blue mTLR-4 cells, LPS-induced SEAP production is dose-dependently inhibited by Lunularin (0.5×-1.5×; 30.25-90.75 nmol/g), which acts on the TLR-4-mediated NF-κB pathway and outperforms resveratrol alone at colonic-tissue-relevant concentrations[2]. By binding to the steroid-binding site of the enzyme, Lunularin (20-100 μM; 30 min to standard assay conditions) competitively inhibits 11β-HSD1 in human liver microsomes (IC50 = 45.44 μM; Ki = 35.8 μM)[4]. Lunularin (12.5-100 μM; 30 min to standard assay conditions) produces mixed inhibition of rat liver microsomal 11β-HSD1 (IC50 = 17.39 μM; Ki = 10.31 μM), binding at the region where NADPH and steroid bind together[4]. Mouse liver microsomal 11β-HSD1 activity is not inhibited by Lunularin[4].
In Vivo
In 13-month-old C57BL/6JRj mice on a high fat, high sugar diet, Lunularin (24 mg/kg; intraperitoneal injection; 3 times per week; 8 weeks) slightly lowers feed intake and body weight gain, reduces blood glucose levels, and raises hepatic Sirt1 and Hmox1 mRNA expression, yet does not reproduce the full metabolic effects of caloric restriction[1]. As a gut microbiota-derived metabolite of resveratrol, Lunularin is highly abundant in mouse tissues, biological fluids, and the gastrointestinal tract relative to resveratrol itself, and is eliminated when gut microbiota is depleted with antibiotics[2].
| Animal Model | C57BL/6JRj (13-month-old, diet-induced obesity model)[1] |
|---|---|
| Dosage | 24 mg/kg |
| Administration | intraperitoneal injection; 3 times per week; 8 weeks |
| 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. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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