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Neohesperidin dihydrochalcone (Neohesperidin DC; NHDC), an artificial sweetener and a synthetic glycoside chalcone, is added to various foods and beverages as a low caloric artificial sweetener.
| Targets |
- Neohesperidin dihydrochalcone acts as an allosteric effector targeting porcine pancreatic alpha-amylase (PPA), functioning as a non-essential activator with maximal activation (up to threefold) at 4.8 mM [2]
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| ln Vitro |
Reactive oxygen species (ROS) and stable free radicals are both effectively scavenged by neohesperidin dihydrochalcone in a concentration-dependent manner. Particularly, the most potent H2O2 and HOCl inhibitor is neohesperidin dihydrochalcone. Neohesperidin dihydrochalcone has a 93.5% HOCl scavenging activity and a 73.5% H2O2 scavenging activity. Neohesperidin dihydrochalcone has IC50 values of 205.1 and 25.5 μM and exhibits broad inhibitory effects, particularly on non-radical ROS H2O2 and HOCl [1]. It was discovered that neohesperidin dihydrochalcone, with an IC50 of 389 μM, activates porcine pancreatic α-amylase (PPA) [2].
- Neohesperidin dihydrochalcone exhibited concentration-dependent radical scavenging activity against various reactive oxygen species (ROS) and stable radicals, including .ABTS+, .O2-, .OH, H2O2, and HOCl. It showed the most potent activity against HOCl (93.5% scavenging rate) and H2O2 (73.5% scavenging rate), outperforming ascorbic acid and BHT. Additionally, it inhibited HOCl-induced plasmid DNA strand breakage, serum albumin degradation, and cell death in HIT-T15 and HUVEC cells, while mannitol, BHT, and ascorbic acid failed to provide effective protection [1] - Neohesperidin dihydrochalcone activated porcine pancreatic alpha-amylase (PPA) instead of inhibiting it (in contrast to other flavonoids). Molecular docking simulation suggested it interacts with a hydrophilic site at the N-terminal of PPA, far from the enzyme's active site. The maximal activation of PPA reached up to threefold at a concentration of 4.8 mM, with alpha < 1 < beta parameters indicating a high activation profile [2] |
| ln Vivo |
When neohesperidin dihydrochalcone was administered, the activity of two helpful indicators of liver impairment, AST and ALT, significantly decreased. The relative amounts of NF-κB, IL-6, IL-1β, and TNF-α proteins in the livers of mice treated with PQ can be inhibited by neohesperidin dihydrochalcone [3]. Neohesperidin dihydrochalcone's embryotoxicity and teratogenicity were investigated in Wistar Crl:(WI)WU BR rats. Neohesperidin dihydrochalcone did not cause any negative effects in rats when used at diet levels as high as 5% (about 3.3 g/kg body weight per day) [4].
- In mice with paraquat (PQ)-induced acute liver injury (75 mg/kg body weight, i.p. single dose), Neohesperidin dihydrochalcone exerted protective effects by reversing abnormal parameters. It reduced serum activities of aspartate transaminase (AST) and alanine transaminase (ALT) (key liver damage biomarkers), restored antioxidant capacity by increasing activities of glutathione peroxidase (GP-X), glutathione-S-transferase (GST), and catalase (CAT), as well as levels of glutathione (GSH) and total antioxidant capacity (T-AOC). It also decreased levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS), ameliorated liver tissue histopathological changes, downregulated expressions of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), inhibited nuclear factor-kappa B (NF-κB) expression and mitochondrial-driven apoptotic signaling, and reduced PQ-induced apoptosis (confirmed by TUNEL assay) [3] |
| Enzyme Assay |
- Alpha-amylase activation assay: Porcine pancreatic alpha-amylase (PPA) was prepared into a reaction system with appropriate substrates. Different concentrations of Neohesperidin dihydrochalcone were added to the system, and the enzyme activity was detected to evaluate the activation effect. Molecular docking simulation was further performed to predict the binding site of Neohesperidin dihydrochalcone with PPA, analyzing the interaction mode between the compound and the enzyme [2]
- Radical scavenging activity assay: Reaction systems for different reactive oxygen species (ROS) and stable radicals (.ABTS+, .O2-, .OH, H2O2, HOCl) were established. Various concentrations of Neohesperidin dihydrochalcone, ascorbic acid, and BHT were added to the respective systems. The scavenging rate of each radical/ROS by the compounds was measured to compare their antioxidant capacities [1] |
| Cell Assay |
- Cell viability assay: HIT-T15 and HUVEC cells were cultured and exposed to HOCl to induce cell death. Neohesperidin dihydrochalcone, mannitol, BHT, and ascorbic acid were added to the cell cultures separately. After incubation, the survival rate of the cells was detected to assess the protective effect of Neohesperidin dihydrochalcone against HOCl-induced cell death [1]
- DNA strand breakage assay: Plasmid DNA was incubated with HOCl to induce strand cleavage. Neohesperidin dihydrochalcone was added to the reaction system, and agarose gel electrophoresis was performed to detect the integrity of the plasmid DNA, evaluating the inhibitory effect of the compound on HOCl-induced DNA strand breakage [1] - Protein degradation assay: Serum albumin was incubated with HOCl to induce degradation. Neohesperidin dihydrochalcone was added to the mixture, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) was used to analyze the degradation degree of serum albumin, determining the inhibitory effect of the compound on HOCl-induced protein degradation [1] |
| Animal Protocol |
- Paraquat-induced liver injury model in mice: Male mice were randomly divided into groups. The model group was given a single intraperitoneal injection of paraquat (75 mg/kg body weight) to induce acute liver injury. The treatment groups were administered Neohesperidin dihydrochalcone (specific dosage not specified in the literature) through an appropriate route (not specified in the literature) before or after PQ injection. The control group received normal saline or vehicle. After a certain period of intervention, blood samples were collected to detect serum AST and ALT activities; liver tissues were harvested to measure antioxidant-related indicators (GP-X, GST, CAT, GSH, T-AOC, ROS, TBARS), perform histopathological examination, immunochemical staining for COX-2 and iNOS, and TUNEL assay to evaluate apoptosis [3]
- Embryotoxicity and teratogenicity study in rats: Twenty-eight mated female Wistar Crl:(WI)WU BR rats per group were fed diets containing Neohesperidin dihydrochalcone at concentrations of 0, 1.25%, 2.5%, or 5% from day 0 to 21 of gestation. The intake of Neohesperidin dihydrochalcone in the low-, mid-, and high-dose groups was 0.8-0.9, 1.6-1.7, and 3.1-3.4 g/kg bw/day, respectively. At Cesarean section, the number of pregnant rats, body weights and weight gains of dams, fecundity and gestation index, number of corpora lutea, implantation sites, live/dead fetuses, resorptions, pre- and post-implantation losses, sex ratio, weights of gravid/empty uterus, ovaries, and placenta were recorded. Fetuses were examined for external, visceral, and skeletal changes [4] |
| Toxicity/Toxicokinetics |
During pregnancy, Wistar rats were given neohesperidin dihydrochalcone at a dietary concentration of up to 5% (approximately 3.3 g/kg body weight/day), and no adverse reactions were observed. All animals survived, and there were no significant differences in maternal weight and weight gain compared to the control group. No embryotoxicity, fetal toxicity, or teratogenicity was found, reproductive parameters were normal, and no abnormalities were found in the external, visceral, and skeletal examinations of the fetus. The only observed change was cecal enlargement, which is a physiological adaptive response to high doses of indigestible substances and has no toxicological significance [4]. In mice with paraquat-induced liver injury, neohesperidin dihydrochalcone did not show obvious toxic side effects and had a protective effect on the liver, manifested as recovery of liver function and antioxidant capacity, and did not cause other pathological changes [3].
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| References |
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| Additional Infomation |
Neohesperidin dihydrochalcone is a grayish-white crystal or powder that is insoluble in water. (NTP, 1992) Neohesperidin dihydrochalcone belongs to the dihydrochalcone class of compounds. Its structure is 3,2',4',6'-tetrahydroxy-4-methoxydihydrochalcone linked to the neohesperidin residue at the 4' position via a glycosidic bond. It is found in sweet oranges. Neohesperidin dihydrochalcone can be used as an environmental pollutant, exogenous substance, plant metabolite and sweetener. It is a neohesperidin, a disaccharide derivative, belonging to the dihydrochalcone class of compounds. It has been reported that neohesperidin dihydrochalcone is found in citrus (Citrus reticulata), broad bean (Vicia faba) and deliciosa, and there is relevant data. - Neohesperidin dihydrochalcone is a non-nutritive artificial sweetener obtained by hydrogenation of neohesperidin [1].
- It is a potent antioxidant and a novel hypochlorous acid (HOCl) scavenger with potential therapeutic effects on reactive oxygen species (ROS)-related inflammatory diseases [1]. - Unlike most flavonoids and their precursor trans-chalcone (a mammalian α-amylase inhibitor), neohesperidin dihydrochalcone can act as an allosteric activator of porcine pancreatic α-amylase [2]. - It has antioxidant and anti-inflammatory properties and exerts anti-apoptotic effects on paraquat-induced acute liver injury in mice through multiple mechanisms, including regulating antioxidant enzyme activity, inhibiting the expression of inflammatory factors, and inhibiting apoptosis signaling pathways [3]. |
| Molecular Formula |
C₂₈H₃₆O₁₅
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|---|---|
| Molecular Weight |
612.58
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| Exact Mass |
612.205
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| CAS # |
20702-77-6
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| Related CAS # |
Neohesperidin;13241-33-3
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| PubChem CID |
30231
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| Appearance |
White to off-white solid powder
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| Density |
1.6±0.1 g/cm3
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| Boiling Point |
927.1±65.0 °C at 760 mmHg
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| Melting Point |
156-158 °C(lit.)
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| Flash Point |
302.6±27.8 °C
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| Vapour Pressure |
0.0±0.3 mmHg at 25°C
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| Index of Refraction |
1.684
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| LogP |
3.09
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| Hydrogen Bond Donor Count |
9
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| Hydrogen Bond Acceptor Count |
15
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| Rotatable Bond Count |
10
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| Heavy Atom Count |
43
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| Complexity |
882
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| Defined Atom Stereocenter Count |
10
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| SMILES |
C[C@H]1[C@@H]([C@H]([C@H]([C@@H](O1)O[C@@H]2[C@H]([C@@H]([C@H](O[C@H]2OC3=CC(=C(C(=C3)O)C(=O)CCC4=CC(=C(C=C4)OC)O)O)CO)O)O)O)O)O
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| InChi Key |
ITVGXXMINPYUHD-CUVHLRMHSA-N
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| InChi Code |
InChI=1S/C28H36O15/c1-11-21(34)23(36)25(38)27(40-11)43-26-24(37)22(35)19(10-29)42-28(26)41-13-8-16(32)20(17(33)9-13)14(30)5-3-12-4-6-18(39-2)15(31)7-12/h4,6-9,11,19,21-29,31-38H,3,5,10H2,1-2H3/t11-,19+,21-,22+,23+,24-,25+,26+,27-,28+/m0/s1
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| Chemical Name |
1-[4-[(2S,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxyoxan-2-yl]oxy-2,6-dihydroxyphenyl]-3-(3-hydroxy-4-methoxyphenyl)propan-1-one
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| Synonyms |
Neohesperidin DC NHDC
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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) |
DMSO : ~100 mg/mL (~163.24 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.08 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 (4.08 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 (4.08 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.6324 mL | 8.1622 mL | 16.3244 mL | |
| 5 mM | 0.3265 mL | 1.6324 mL | 3.2649 mL | |
| 10 mM | 0.1632 mL | 0.8162 mL | 1.6324 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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