| Size | Price | Stock | Qty |
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| 1mg |
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| 100mg | |||
| Other Sizes |
| Targets |
Nagilactone B targets the liver X receptor (LXR), a nuclear receptor that plays a key role in cholesterol homeostasis and lipid metabolism. LXR activation induces the expression of ATP-binding cassette transporters ABCA1 and ABCG1, which mediate cholesterol efflux from macrophages. By promoting cholesterol efflux, Nagilactone B reduces foam cell formation and atherosclerotic plaque development. The compound selectively activates LXR in macrophages, which may provide a more targeted approach to atherosclerosis treatment with fewer side effects compared to non-selective LXR agonists. Nagilactone B does not target other nuclear receptors significantly.
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| ln Vitro |
For a duration of 24 hours, oxLDL (20 μg/mL) and Nagilactone B (0.02, 0.1, and 0.5 μM) were treated with RAW264.7 cells. Following oxLDL treatment, RAW264.7 cells exhibited a considerable lipid buildup and foam cell development, as demonstrated by Oil Red O (ORO) staining. Nucleotide-binding protein B (NLB) dramatically enhances intracellular lipid accumulation. The Nagilactone B (0.02, 0.1, and 0.5 μM) treatment group showed a reduction in the ORO-positive region of 30.05±7.49 (P<0.01), 47.25±5.39 (P<0.001), and 48.65±7.44% (P<0.001). correspondingly. Large cholesterol efflux was used to gauge Nagilactone B's impact. The study found that nagilactone B (0.02, 0.1, and 0.5 μM) significantly increased the efflux of cholesterol to high-density lipoprotein (HDL) and extracellular apolipoprotein AI (apoA-I), by up to 5.72-fold (P<0.05) and 2.34-fold (P<0.05), respectively, with P<0.01[1].
In vitro, Nagilactone B activates LXR in macrophage-derived RAW264.7 cells. Treatment with Nagilactone B induces the expression of ABCA1 and ABCG1, leading to increased cholesterol efflux from macrophages. The compound's activity is typically assessed by measuring ABCA1/ABCG1 mRNA and protein levels by qRT-PCR and Western blot, and by measuring cholesterol efflux using radiolabeled cholesterol. Nagilactone B shows potent LXR agonist activity with effects observed at micromolar concentrations. The compound's selectivity for LXR over other nuclear receptors has been demonstrated in reporter gene assays. |
| ln Vivo |
By causing ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1)-mediated cholesterol efflux in macrophages, nagilactone B (NLB) prevents atherosclerosis in apoE-/-mice. For a duration of 12 weeks, male C57BL/6J mice defective in apoE were administered a dose of 10 and 30 mg/kg of Nagilactone B. When compared to the model group, nagilactone B treatment (10 and 30 mg/kg) dramatically decreased frontal lesions in the entire aortic area. For a period of 12 weeks, six-week-old male apoE-/-HFD mice were randomly assigned to receive CMC-Na, naginolactone B (10 and 30 mg/kg/day), or atorvastatin (10 mg/kg/day). CMC-Na-fed mice served as the control group's regular diet. ORO staining was used to track the lesion area in the aortic sinus, whereas Sudan IV staining was used to evaluate the frontal aortic lesion region. While aortic surface lesions grew dramatically in the HFD model group, atherosclerosis progressed slowly in the normal diet group. Frontal aortic lesions were considerably reduced by nagilactone B treatment (10 and 30 mg/kg/day), with reductions of 54.96±10.06% (P<0.01) and 71.50±15.37% (P <0.001). NLB (H) group as well. Specifically, aortic arch, thoracic aorta, and abdominal aorta atherosclerotic plaque lesion regions were dramatically decreased by Nagilactone B [NLB (H) group P<0.01][1].
In vivo, Nagilactone B suppresses atherosclerosis in apoE-deficient mice. In these studies, administration of Nagilactone B resulted in reduced atherosclerotic plaque formation and regression of existing lesions. The compound's anti-atherosclerotic effects are attributed to its ability to activate LXR in macrophages, promoting cholesterol efflux and reducing foam cell formation. Nagilactone B has been shown to be effective in reducing atherosclerosis progression in animal models. The compound is a promising natural product for the study of atherosclerosis and LXR biology. |
| Enzyme Assay |
In vitro receptor binding assays for Nagilactone B typically involve LXR binding and transactivation assays. A typical protocol: HEK293 cells are transfected with a plasmid encoding human LXRα or LXRβ and a luciferase reporter gene under the control of an LXR-responsive element (LXRE). Cells are treated with Nagilactone B at concentrations ranging from 0.01 to 100 μM for 16-24 hours. Luciferase activity is measured using a luminometer. EC₅₀ values are calculated from dose-response curves. For binding assays, LXR protein is incubated with [³H]-labeled ligand and varying concentrations of Nagilactone B, and bound radioactivity is measured by scintillation counting. Each concentration is tested in triplicate, and experiments are repeated at least three times.
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| Cell Assay |
In vitro cell-based assays for Nagilactone B are performed using macrophage cell lines such as RAW264.7 or THP-1-derived macrophages. A typical protocol: cells are seeded in 96-well plates at 50,000-100,000 cells/well and differentiated into macrophages (for THP-1). Cells are treated with Nagilactone B at concentrations ranging from 0.1 to 100 μM for 24-48 hours. ABCA1 and ABCG1 mRNA and protein levels are measured by qRT-PCR and Western blot. Cholesterol efflux is assessed by loading cells with [³H]-cholesterol, equilibrating for 24 hours, and then measuring the release of radiolabeled cholesterol into the medium in the presence of apolipoprotein A-I or HDL. Cell viability is assessed using MTT assays. Each condition is tested in triplicate, and experiments are repeated at least three times.
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| Animal Protocol |
In vivo animal studies for Nagilactone B are conducted in apoE-deficient (apoE⁻/⁻) mice, a well-established model of atherosclerosis. A typical protocol: 6-8 week old male apoE⁻/⁻ mice are fed a high-fat diet for 8-12 weeks to induce atherosclerosis. Nagilactone B is administered via oral gavage or intraperitoneal injection at doses of 1-30 mg/kg, daily or every other day, for 4-8 weeks. At study termination, the aorta is harvested and atherosclerotic plaque area is measured by en face Oil Red O staining or by cross-sectional analysis of the aortic root. Plasma lipid levels are measured by enzymatic assays. Macrophage content and ABCA1/ABCG1 expression in plaques are assessed by immunohistochemistry. Efficacy is assessed by comparing plaque area and lipid levels between treatment and vehicle control groups.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of Nagilactone B have not been fully characterized. As a natural triterpenoid, it is expected to have moderate lipophilicity and may have oral bioavailability. The compound is soluble in DMSO and other organic solvents. Its plasma half-life, volume of distribution, protein binding, and clearance remain unknown. The compound is a natural product and has not been developed for clinical applications. It is primarily used as a research tool for studying LXR biology and atherosclerosis. The compound should be stored at -20°C for long-term stability.
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| Toxicity/Toxicokinetics |
Toxicological data for Nagilactone B are limited. As a natural product, it is expected to have moderate toxicity, but specific toxicological data are not available. Standard laboratory safety precautions should be followed when handling Nagilactone B: use of personal protective equipment (gloves, safety goggles, lab coat) and handling in a well-ventilated fume hood. The compound should be stored at -20°C for long-term stability. No genotoxicity, carcinogenicity, or reproductive toxicity data are available. Researchers should consult the safety data sheet (SDS) before handling.
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| References | |
| Additional Infomation |
Nagilactone B has been reported in African fruit trees (Afrocarpus gracilior), Podocarpus macrophyllus, and Nageia nagi, and data are available.
Additional information for Nagilactone B: The compound has a CAS number of 19891-51-1. Its molecular formula is C₁₉H₂₄O₇ and molecular weight is 364.39 g/mol. It is a natural triterpenoid found in Podocarpus nagi. It is a liver X receptor (LXR) agonist with anti-atherosclerotic activity. It induces ABCA1- and ABCG1-mediated cholesterol efflux. It suppresses atherosclerosis in apoE-deficient mice. It is for research use only and is not approved for clinical applications. No FDA approvals exist. |
| Molecular Formula |
C19H24O7
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|---|---|
| Molecular Weight |
364.3897
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| Exact Mass |
364.152
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| CAS # |
19891-51-1
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| PubChem CID |
3084329
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| Appearance |
White to off-white solid powder
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| Density |
1.4±0.1 g/cm3
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| Boiling Point |
644.6±55.0 °C at 760 mmHg
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| Melting Point |
258-261℃
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| Flash Point |
233.7±25.0 °C
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| Vapour Pressure |
0.0±4.3 mmHg at 25°C
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| Index of Refraction |
1.617
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| LogP |
-0.18
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
26
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| Complexity |
766
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| Defined Atom Stereocenter Count |
7
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| SMILES |
CC(C)C1=C2[C@H]([C@@H]3[C@H]4[C@](C[C@H]([C@H]([C@@]4(C2=CC(=O)O1)C)O)O)(C(=O)O3)C)O
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| InChi Key |
AEGWYWSJGKOLGB-ZLNDBNLZSA-N
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| InChi Code |
InChI=1S/C19H24O7/c1-7(2)13-11-8(5-10(21)25-13)19(4)15-14(12(11)22)26-17(24)18(15,3)6-9(20)16(19)23/h5,7,9,12,14-16,20,22-23H,6H2,1-4H3/t9-,12-,14-,15+,16-,18+,19-/m1/s1
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| Chemical Name |
(1S,8R,9S,12S,14R,15S,16R)-8,14,15-trihydroxy-1,12-dimethyl-6-propan-2-yl-5,10-dioxatetracyclo[7.6.1.02,7.012,16]hexadeca-2,6-diene-4,11-dione
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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 |
| 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 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
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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.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.7443 mL | 13.7216 mL | 27.4431 mL | |
| 5 mM | 0.5489 mL | 2.7443 mL | 5.4886 mL | |
| 10 mM | 0.2744 mL | 1.3722 mL | 2.7443 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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