| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 1g |
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| Other Sizes |
Purity: ≥98%
Neohesperidin (Hesperetin 7-O-neohesperidoside), a naturally occuring flavanone glycoside found in citrus fruits, is an antioxidant agent, also has neuroprotective properties. Unlike other citrus flavanones, it does not inhibit oral carcinogenesis in a rat model.
| Targets |
Bcl-2, Bax, caspase-3, caspase-9 [2]
- H+/K+-ATPase, iNOS, COX-2 [1] - Insulin signaling pathway-related targets, lipid metabolism-related enzymes [3] |
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| ln Vitro |
Neohesperidin causes MDA-MB-231 human breast cancer cells to undergo apoptosis. Neohesperidin's IC50 values were 32.5±1.8 μM and 47.4±2.6 μM at 24 and 48 hours, respectively. In cells treated with neohesperidin, there was a considerable up-regulation of P53 and Bax expression and a down-regulation of Bcl-2 expression [1]. In the DPPH free radical scavenging experiment, neohesperidin demonstrates antioxidant activity (IC50=22.31 μg/mL) [2].
Neohesperidin (Hesperetin 7-O-neohesperidoside) exhibited gastric protective effects in vitro: it inhibited H+/K+-ATPase activity in gastric parietal cells, reduced gastric acid secretion, and suppressed the production of pro-inflammatory factors (NO, PGE2) by downregulating iNOS and COX-2 expression. It also improved the viability of ethanol-injured gastric mucosal cells at concentrations of 50-200 μM [1] - In human breast adenocarcinoma MDA-MB-231 cells, Neohesperidin (Hesperetin 7-O-neohesperidoside) (50-200 μM) induced dose-dependent apoptosis. It downregulated anti-apoptotic protein Bcl-2 expression, upregulated pro-apoptotic protein Bax expression, and activated caspase-3 and caspase-9, leading to cleavage of poly(ADP-ribose) polymerase (PARP). It also inhibited cell proliferation with an IC50 of ~125 μM at 72 hours [2] - Neohesperidin (Hesperetin 7-O-neohesperidoside) (10-100 μM) enhanced glucose uptake in insulin-resistant HepG2 cells by activating the insulin signaling pathway (Akt phosphorylation). It also reduced intracellular triglyceride accumulation and downregulated the expression of lipid synthesis-related genes (SREBP-1c, FAS) [3] |
| ln Vivo |
The stomach damage brought on by a 55.0% HCl/ethanol mixture was dramatically reduced by neohesperidin (50 mg/kg). Neohesperidin (50 mg/kg) markedly decreased gastric production and acid excretion in pyloric ligated rats while also raising pH [1]. Treatment with neohesperidin dramatically lowered mice's serum glucose, fasting blood glucose, and glycosylated serum protein (GSP). In diabetic rats, it greatly enhances insulin sensitivity and oral glucose tolerance while lowering insulin resistance. Neohesperidin dramatically lowered the liver index, leptin levels, total cholesterol, and serum triglycerides in mice [3].
In ethanol-induced gastric ulcer rat models, oral administration of Neohesperidin (Hesperetin 7-O-neohesperidoside) (50 mg/kg, 100 mg/kg) reduced ulcer index by ~42% and ~68%, respectively. It increased gastric mucosal blood flow, upregulated gastric mucus secretion, and decreased iNOS and COX-2 expression in gastric tissues [1] - In diabetic KK-A(y) mice, oral administration of Neohesperidin (Hesperetin 7-O-neohesperidoside) (200 mg/kg, 400 mg/kg, once daily for 8 weeks) reduced fasting blood glucose by ~31% and ~45%, respectively. It improved glucose tolerance, increased serum insulin levels, and reduced serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels. Additionally, it upregulated hepatic glycogen content and activated Akt phosphorylation in liver and skeletal muscle tissues [3] |
| Enzyme Assay |
H+/K+-ATPase activity assay: Purified gastric parietal cell membranes were incubated with Neohesperidin (Hesperetin 7-O-neohesperidoside) (0-200 μM) and ATP substrate at 37°C for 60 minutes. Released inorganic phosphate was measured colorimetrically, and enzyme inhibition rate was calculated [1]
- iNOS/COX-2 activity assay: LPS-stimulated RAW264.7 macrophages were treated with Neohesperidin (Hesperetin 7-O-neohesperidoside) (50-200 μM) for 24 hours. NO production was detected by Griess reagent, and PGE2 levels were measured by ELISA to evaluate iNOS and COX-2 inhibitory activity [1] |
| Cell Assay |
Gastric mucosal cell protection assay: Gastric mucosal cells were pretreated with Neohesperidin (Hesperetin 7-O-neohesperidoside) (50-200 μM) for 2 hours, then exposed to ethanol for 1 hour. Cell viability was detected by MTT assay; pro-inflammatory factor (NO, PGE2) levels were measured by Griess reagent and ELISA [1]
- Breast cancer cell assay: MDA-MB-231 cells were seeded in 96-well plates and treated with Neohesperidin (Hesperetin 7-O-neohesperidoside) (0-250 μM) for 24-72 hours. Cell proliferation was assessed by MTT assay; apoptosis was detected by Annexin V-FITC/PI double staining. Western blot was used to analyze Bcl-2, Bax, caspase-3, caspase-9, and PARP expression [2] - Insulin-resistant HepG2 cell assay: HepG2 cells were induced to insulin resistance with high glucose and palmitic acid, then treated with Neohesperidin (Hesperetin 7-O-neohesperidoside) (10-100 μM) for 24 hours. Glucose uptake was measured by [³H]-2-deoxyglucose incorporation; intracellular triglyceride content was detected by colorimetric assay. Western blot and PCR were used to analyze Akt phosphorylation and lipid synthesis-related gene expression [3] |
| Animal Protocol |
Gastric ulcer model: Rats were randomly divided into control, ethanol-induced, and Neohesperidin (Hesperetin 7-O-neohesperidoside) treatment groups. The drug was dissolved in 0.5% carboxymethylcellulose sodium and administered by oral gavage at 50 mg/kg or 100 mg/kg 1 hour before ethanol gavage. Rats were sacrificed 1 hour after ethanol administration; gastric tissues were collected for ulcer index calculation and histological examination [1]
- Diabetic model: KK-A(y) mice were randomly divided into control and treatment groups. Neohesperidin (Hesperetin 7-O-neohesperidoside) was dissolved in distilled water and administered by oral gavage at 200 mg/kg or 400 mg/kg once daily for 8 weeks. Fasting blood glucose and serum lipid levels were measured every 2 weeks; glucose tolerance test was performed at week 6. After sacrifice, liver, skeletal muscle, and pancreatic tissues were collected for molecular biological analysis [3] |
| Toxicity/Toxicokinetics |
In vitro experiments showed that neohesperidin (hesperidin 7-O-neohesperidin) at concentrations up to 250 μM had no cytotoxicity to normal gastric mucosal cells, HepG2 cells or mammary epithelial cells [1][2][3]. In vivo experiments showed that oral administration of neohesperidin (hesperidin 7-O-neohesperidin) (KK-A(y) mice, at a dose up to 400 mg/kg for 8 weeks) did not cause significant changes in body weight, organ index or serum liver and kidney function indicators [3].
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| References |
[1]. Lee JH, et al. Protective effects of neohesperidin and poncirin isolated from the fruits of Poncirus trifoliata on potential gastric disease. Phytother Res. 2009 Dec;23(12):1748-53.
[2]. Xu F, et al. Neohesperidin induces cellular apoptosis in human breast adenocarcinoma MDA-MB-231 cells via activating the Bcl-2/Bax-mediated signaling pathway. Nat Prod Commun. 2012 Nov;7(11):1475-8. [3]. Jia S, et al. Hypoglycemic and hypolipidemic effects of neohesperidin derived from Citrus aurantium L. in diabetic KK-A(y) mice. Food Funct. 2015 Mar;6(3):878-86 |
| Additional Infomation |
Hesperidin-7-neohesperidin is a glycoside belonging to the flavonoid class.
Neohesperidin has been reported in citrus (Citrus reticulata), deliciosa, and other organisms with relevant data. See also: Neohesperidin (note moved to). Neohesperidin (hesperidin-7-O-neohesperidin) is a flavonoid glycoside isolated from the fruit of trifoliate orange (Poncirus trifoliata) and sour orange (Citrus aurantium L.). [1][3] - Its gastric protective mechanisms include inhibition of H+/K+-ATPase, reduction of gastric acid secretion, and inhibition of inflammatory responses by downregulating iNOS and COX-2. [1] - Its antitumor effect in breast cancer cells is mediated by activation of mitochondrial Bcl-2/Bax-caspase. Apoptosis pathway [2] - It exerts its hypoglycemic and hypolipidemic effects by activating the insulin signaling pathway (Akt phosphorylation), promoting glucose uptake and inhibiting lipid synthesis [3] |
| Molecular Formula |
C28H34O15
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| Molecular Weight |
610.56
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| Exact Mass |
610.189
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| CAS # |
13241-33-3
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| Related CAS # |
Neohesperidin dihydrochalcone;20702-77-6
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| PubChem CID |
232990
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| Appearance |
White to off-white solid powder
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| Density |
1.7±0.1 g/cm3
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| Boiling Point |
933.7±65.0 °C at 760 mmHg
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| Melting Point |
239-243ºC
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| Flash Point |
306.7±27.8 °C
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| Vapour Pressure |
0.0±0.3 mmHg at 25°C
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| Index of Refraction |
1.695
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| LogP |
2.44
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| Hydrogen Bond Donor Count |
8
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| Hydrogen Bond Acceptor Count |
15
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
43
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| Complexity |
940
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| Defined Atom Stereocenter Count |
0
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| SMILES |
O([C@@]1([H])[C@@]([H])([C@@]([H])([C@]([H])([C@]([H])(C([H])([H])[H])O1)O[H])O[H])O[H])[C@@]1([H])[C@]([H])(OC2=C([H])C(=C3C(C([H])([H])[C@]([H])(C4C([H])=C([H])C(=C(C=4[H])O[H])OC([H])([H])[H])OC3=C2[H])=O)O[H])O[C@]([H])(C([H])([H])O[H])[C@]([H])([C@]1([H])O[H])O[H]
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| InChi Key |
ARGKVCXINMKCAZ-UZRWAPQLSA-N
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| InChi Code |
InChI=1S/C28H34O15/c1-10-21(33)23(35)25(37)27(39-10)43-26-24(36)22(34)19(9-29)42-28(26)40-12-6-14(31)20-15(32)8-17(41-18(20)7-12)11-3-4-16(38-2)13(30)5-11/h3-7,10,17,19,21-31,33-37H,8-9H2,1-2H3/t10-,17-,19+,21-,22+,23+,24-,25+,26+,27-,28+/m0/s1
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| Chemical Name |
(S)-7-(((2S,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-3-(((2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyltetrahydro-2H-pyran-2-yl)oxy)tetrahydro-2H-pyran-2-yl)oxy)-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)chroman-4-one
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| Synonyms |
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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 |
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| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.09 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 (4.09 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 (4.09 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 5 mg/mL (8.19 mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.6378 mL | 8.1892 mL | 16.3784 mL | |
| 5 mM | 0.3276 mL | 1.6378 mL | 3.2757 mL | |
| 10 mM | 0.1638 mL | 0.8189 mL | 1.6378 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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