2. Autophagy MAPK/ERK Pathway Apoptosis Immunology/Inflammation Vitamin D Related/Nuclear Receptor Metabolic Enzyme/Protease Cell Cycle/DNA Damage
  3. Autophagy p38 MAPK TNF Receptor Interleukin Related PPAR
  4. Neomangiferin

Neomangiferin is an orally active natural flavonoid. Neomangiferin partially ameliorates non-alcoholic fatty liver disease (NAFLD) by regulating the expression of genes related to free fatty acid uptake and lipid oxidation. Neomangiferin exerts anti-colitis effects by inhibiting Th17/Treg cell differentiation. Neomangiferin exerts anti-aging and lifespan-extending effects by targeting upregulation of bas-1, which in turn activates the autophagy, IIS and MAPK pathways. Neomangiferin has the potential to prevent aseptic loosening of prostheses after total joint arthroplasty due to its significant anti-inflammatory and osteoclastogenesis-inhibiting effects.

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Neomangiferin

Neomangiferin Chemical Structure

CAS No. : 64809-67-2

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Based on 1 publication(s) in Google Scholar

Other Forms of Neomangiferin:

Neomangiferin Related Antibodies

Top Publications Citing Use of Products

1 Publications Citing Use of MCE Neomangiferin

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PPARα PPARβ/δ PPARγ PPAR PPARδ

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Neomangiferin is an orally active natural flavonoid. Neomangiferin partially ameliorates non-alcoholic fatty liver disease (NAFLD) by regulating the expression of genes related to free fatty acid uptake and lipid oxidation. Neomangiferin exerts anti-colitis effects by inhibiting Th17/Treg cell differentiation. Neomangiferin exerts anti-aging and lifespan-extending effects by targeting upregulation of bas-1, which in turn activates the autophagy, IIS and MAPK pathways. Neomangiferin has the potential to prevent aseptic loosening of prostheses after total joint arthroplasty due to its significant anti-inflammatory and osteoclastogenesis-inhibiting effects[1][2][3][4].

In Vitro

Neomangiferin (5, 10, 20 μM; 5 days) suppresses TGFβ/IL-6-induced Th17 cell differentiation in purified splenic CD4+ T cells from C57BL/6J mice, reducing IL-17 and RORγt expression[2].
Neomangiferin (5, 10, 20 μM; 5 days) promotes anti-CD3/anti-CD28-induced Treg cell differentiation in purified splenic T cells from C57BL/6J mice, increasing IL-10 expression[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Neomangiferin Related Antibodies
In Vivo

Neomangiferin (25-50 mg/kg; oral gavage; daily administration; for 13 consecutive weeks) significantly ameliorates high-fat diet-induced non-alcoholic fatty liver disease (NAFLD) in male SD rats via reducing body fat and hepatic lipid accumulation, normalizing serum and hepatic lipid as well as antioxidant parameters, improving glucose tolerance and metabolic rate, and regulating the expression of genes and proteins related to fatty acid uptake and oxidation in the liver[1].
Neomangiferin (10-20 mg/kg; p.o.; once daily; for 3 consecutive days) ameliorates TNBS-induced colitis in male C57BL/6J mice by inhibiting proinflammatory cytokine production and restoring the Th17/Treg balance; at the dose of 20 mg/kg, it inhibits myeloperoxidase activity by 73.9% and reduces IL-17 levels by 63.6%[2].
Neomangiferin (20 mg/kg; p.o.; daily; for 3 consecutive weeks) improves spontaneous chronic colitis in male C57BL/6 IL-10 knockout mice by reducing the production of proinflammatory cytokines, inhibiting myeloperoxidase activity by 52.6%, and restoring the Th17/Treg balance[2].
Neomangiferin (2.5-5 mg/kg, i.p., once every other day for 21 consecutive days) dose-dependently inhibits UHMWPE particle-induced inflammatory calvarial osteolysis in mice[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague-Dawley (SD) (male, 7-week-old, 200 g, high-fat diet-induced NAFLD)[1]
Dosage: 50 mg/kg·day-1 BW; 25 mg/kg·day-1 BW
Administration: oral gavage; daily; 13 weeks
Result: Significantly decreased body weight compared to HF control group after 3 weeks of treatment; by week 8, reduced body weight to normal control levels with high-dose treatment.
Significantly lowered relative weights of organs (liver, spleen, testicle, brain, heart) and adipose tissues (abdominal, perirenal, subcutaneous, epididymal fat) with high-dose treatment compared to HF control group.
Reduced serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT), aspartate aminotransferase (AST), AST/ALT ratio, glucose (GLU), and D-3-hydroxybutyric acid (D-3H) levels, and increased serum high-density lipoprotein cholesterol (HDL-C) levels and HDL-C/TC ratio after 13 weeks of treatment compared to HF control group.
Decreased hepatic TG, TC, and malondialdehyde (MDA) levels, and increased hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels compared to HF control group.
Increased fecal TG and TC levels compared to HF control group.
Reduced liver fat content from 43.6% (HF control) to a statistically significant lower level, decreased body fat content, and restored brown adipose tissue size with high-dose treatment compared to HF control group.
Significantly reduced hepatic fatty droplets, lipid accumulation, and renal lipid droplet accumulation compared to HF control group.
Lowered blood glucose levels at 30, 60, 90, and 120 minutes post-glucose gavage, and reduced glucose area under the curve (AUC) compared to HF control group.
Increased respiratory exchange rate (RER), oxygen consumption (VO2), and carbon dioxide production (VCO2) with high-dose treatment compared to HF control group, correcting diurnal metabolic rhythm defect.
Upregulated hepatic mRNA and protein expression of peroxisome proliferator-activated receptor α (PPARα) and carnitine palmitoyltransferase 1a (CPT1a), and downregulated hepatic mRNA and protein expression of fatty acid transport protein 2 (FATP2) and long-chain-fatty-acid-CoA ligase 1 (ACSL1) after 13 weeks of treatment compared to HF control group.
Animal Model: C57BL/6J (male, 6 weeks old, 20-23 g, TNBS-induced colitis)[2]
Dosage: 10 mg/kg; 20 mg/kg
Administration: p.o.; daily; 3 days
Result: Inhibited TNBS-induced colon shortening.
Reduced macroscopic colitis scores.
Suppressed myeloperoxidase activity by 73.9% (20 mg/kg dose).
Prevented TNBS-induced reduction in tight junction proteins ZO-1, occludin, and claudin-1.
Inhibited TNBS-induced ERK phosphorylation, NF-κB activation, and expression of inducible nitric oxide synthase and cyclooxygenase-2.
Reduced colon tissue levels of TNF-α by 45.5%, IL-1β by 78.1%, IL-17 by 63.6%, and IL-6 by 85.5%, while increasing IL-10 expression (20 mg/kg dose).
Inhibited TNBS-induced Th17 cell differentiation in colonic lamina propria and increased Treg cell differentiation.
Attenuated TNBS-mediated upregulation of IL-17, IFN-γ, RORγt, and T-bet mRNA, and restored TNBS-suppressed IL-10, IL-5, Foxp3, and GATA3 mRNA expression.
Animal Model: C57BL/6 IL-10 knockout (male, 13 weeks old at treatment initiation, 18-21 g, spontaneous chronic colitis)[2]
Dosage: 20 mg/kg
Administration: p.o.; daily; 3 weeks
Result: Reduced colonic myeloperoxidase activity by 52.6%.
Improved histopathological severity of colitis.
Increased expression of tight junction proteins ZO-1, occludin, and claudin-1.
Inhibited infiltration of antigen-presenting cells.
Suppressed ERK phosphorylation, NF-κB activation, and expression of inducible nitric oxide synthase and cyclooxygenase-2.
Reduced colon tissue levels of TNF-α by 17.3%, IL-1β by 54.5%, IFN-γ by 27.8%, and IL-17 by 52.8%.
Inhibited Th17 cell differentiation in colonic lamina propria and increased Treg cell differentiation.
Suppressed IL-17 and RORγt mRNA expression.
Animal Model: C57BL/6 (8-week-old male, specific pathogen free grade, UHMWPE particles implanted into calvarial subperiosteal space)[3]
Dosage: 2.5 mg/kg; 5 mg/kg
Administration: i.p.; every other day; 21 days
Result: Significantly increased bone mineral density (BMD) and bone volume/tissue volume ratio (BV/TV), and decreased the number of bone resorption pits and total skull porosity compared to the vehicle group, with 5 mg/kg group showing greater improvement than 2.5 mg/kg group.
Significantly reduced the number of TRAP-positive osteoclasts and the area of calvarial bone erosion compared to the vehicle group, with 5 mg/kg group showing greater reduction than 2.5 mg/kg group.
Significantly reduced serum levels of TNF-α, IL-1β, RANKL, OSCAR, and CTX-1, and increased serum OPG levels compared to the vehicle group, with 5 mg/kg group showing greater reductions in proinflammatory cytokines and osteoclast markers, and greater increase in OPG, than 2.5 mg/kg group.
Molecular Weight

584.48

Formula

C25H28O16
CAS No.
Appearance

Solid

Color

White to light yellow

SMILES

OC1=C(C2=O)C(OC3=CC(O)=C(O[C@@H]([C@@H]([C@@H](O)[C@@H]4O)O)O[C@@H]4CO)C=C23)=CC(O)=C1[C@@H]([C@@H]([C@@H](O)[C@@H]5O)O)O[C@@H]5CO
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (171.09 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.7109 mL 8.5546 mL 17.1092 mL
5 mM 0.3422 mL 1.7109 mL 3.4218 mL
View the 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 (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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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.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: ≥ 2.5 mg/mL (4.28 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.
  • Protocol 2

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: ≥ 2.5 mg/mL (4.28 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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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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).
Calculation results:
Working solution concentration: 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 (protect from light)

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
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.
Purity & Documentation

Purity: 99.80%

SDS (420 KB)

COA (252 KB) RP-HPLC (206 KB)

Handling Instructions (2659 KB)
References

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 (protect from light). 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 1.7109 mL 8.5546 mL 17.1092 mL 42.7731 mL
5 mM 0.3422 mL 1.7109 mL 3.4218 mL 8.5546 mL
10 mM 0.1711 mL 0.8555 mL 1.7109 mL 4.2773 mL
15 mM 0.1141 mL 0.5703 mL 1.1406 mL 2.8515 mL
20 mM 0.0855 mL 0.4277 mL 0.8555 mL 2.1387 mL
25 mM 0.0684 mL 0.3422 mL 0.6844 mL 1.7109 mL
30 mM 0.0570 mL 0.2852 mL 0.5703 mL 1.4258 mL
40 mM 0.0428 mL 0.2139 mL 0.4277 mL 1.0693 mL
50 mM 0.0342 mL 0.1711 mL 0.3422 mL 0.8555 mL
60 mM 0.0285 mL 0.1426 mL 0.2852 mL 0.7129 mL
80 mM 0.0214 mL 0.1069 mL 0.2139 mL 0.5347 mL
100 mM 0.0171 mL 0.0855 mL 0.1711 mL 0.4277 mL
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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Neomangiferin64809-67-2Autophagyp38 MAPKTNF ReceptorInterleukin RelatedPPARTumor Necrosis Factor ReceptorTNFRILPeroxisome proliferator-activated receptorsCPT1aPPARαACSL1nonalcoholic fatty liver diseaseFATP2rat liverTreg cellRORγtCaenorhabditis elegansTh17 cellInhibitorinhibitorinhibit

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