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Hyperoside

Alias: Hyperoside; 482-36-0; Hyperin; Hyperosid; Hyperozide; Quercetin-3-O-galactoside; Quercetin-3-galactoside; quercetin galactoside;
Cat No.:V34275 Purity: ≥98%
Hyperoside is natural product of the flavonoid class, found inCamptotheca acuminate, and has a variety of biological activities including antifungal,anti-oxidative, anti-inflammatory, anti-viral and anti-apoptotic activities.
Hyperoside
Hyperoside Chemical Structure CAS No.: 482-36-0
Product category: Natural Products
This product is for research use only, not for human use. We do not sell to patients.
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Product Description

Hyperoside is natural product of the flavonoid class, found in Camptotheca acuminate, and has a variety of biological activities including antifungal, anti-oxidative, anti-inflammatory, anti-viral and anti-apoptotic activities. It acts by inhibiting HMGB1 signaling pathway and activating Nur77 receptor.

Biological Activity I Assay Protocols (From Reference)
Targets
NF-κB; Natural occurring flavonoid; antioxidant
ln Vitro
MCF-7 and 4T1 cell proliferation is inhibited by hyperin (12.5–100 μM; 6–24 h) [2]. In breast cancer cells, hypericin (25-100 μM; 24 h) produces fluoroscopy [2].
Antifungal Activity against P. guepinii. [1]
P.guepinii showed a growth pattern similar to that of E. nigrum under control conditions (Figure 4). CPT-10 reduced mycelial growth by 43.5% on the 11th day when the fungus under the control treatment had covered the agar surface. Colonies exposed to CPT-10 treatment did not reach the Petri dish margins until day 20. Thus, it is estimated that the EC50 of CPT for P.guepinii is approximately 10 μg/mL. However, CPT totally inhibited growth only at ≥125 μg/mL. Both fungicides also successfully controlled P.guepinii. Trifolin and Hyperoside were similar in their abilities to inhibit P.guepinii. On day 11, colonies exposed to either trifolin-50 or hyperoside-50 were inhibited by 53.4% and 53.8%, respectively. The EC50 of both flavonoids for P.guepinii is estimated to be approximately 50 μg/mL. However, as concentrations increased to 100 μg/mL, the flavonoids were more effective in inhibition of P.guepinii than CPT; MICs of both trifolin and hyperoside for P.guepinii are most likely below 125 μg/mL, the level at which CPT successfully controlled the fungus.
Antifungal Activity against Drechslera sp. [1]
Drechslera sp. grew more slowly than A. alternata, E. nigrum, and P.guepinii under control conditions but was also more sensitive to CPT, flavonoids, and fungicides than the other fungi tested (Figure 5). CPT at all experimental levels showed greater inhibition rates than Bravo. This fungicide reduced mycelial growth by 54.4% on day 20, when control mycelium completely covered the agar surface. Thus, the EC50 of CPT for Drechslera is <10 μg/mL. However, CPT only completely inhibited fungal growth at ≥100 μg/mL. Trifolin-50 and hyperoside-50 (trifolin and Hyperoside at 50 μg/mL) were similar in their ability to inhibit Drechslera. On day 20, colonies exposed to either trifolin-50 or hyperoside-50 were inhibited by 76.1% and 74.3%, respectively. Thus, the EC50 values of both flavonoids against Drechslera are <50 μg/mL. Hyperoside-100 (hyperoside at 100 μg/mL) inhibited fungal growth successfully, with little growth by day 28, while trifolin-100 (trifolin at 100 μg/mL) totally controlled the fungus over the course of the entire experiment. CPT at ≥100 μg/mL, trifolin at ≥100 μg/mL, hyperoside at 150 μg/mL, and Maneb completely inhibited Drechslera.
Antifungal Activity against F. avenaceum. [1]
F.avenaceum exhibited the slowest growth rate of all experimental fungi under control conditions, but was somewhat less sensitive to CPT, flavonoids, and fungicides (Figure 6). Bravo showed effective inhibition of mycelial growth during the first several days of the experiment but was less effective in the later stages. On day 28, mycelium with Bravo treatment completely covered the agar surface similar to the control colonies. CPT-10 was much more effective than Bravo, with 70−80% inhibition of mycelial growth during the first several days of the experiment and approximately 40% inhibition in the later stages. CPT-30 inhibited the rate of mycelial growth by >60%. Thus, the EC50 of CPT for F.avenaceum is estimated to be between 10 and 30 μg/mL. Higher levels of CPT more effectively inhibited mycelial growth, but complete inhibition was not achieved until 125 μg/mL. Trifolin and Hyperoside exhibited similar inhibition patterns at 100 μg/mL, but trifolin was more effective than hyperoside at 50 μg/mL. Trifolin-50 and hyperoside-50 were less effective against F.avenaceum than Bravo and CPT-10 at the beginning of the experiment but more effective than Bravo and similar to CPT-10 during the later stages of the experiment. On day 28, trifolin and hyperoside inhibited fungal growth by 35.8% and 31.6%, respectively, at 50 μg/mL, and by 74.8% and 72.6%, respectively, at 100 μg/mL. Thus, it is estimated that EC50 values of both flavonoids against F.avenaceum are between 50 and 100 μg/mL. Hyperoside at 150 μg/mL completely inhibited fungal growth during the first four weeks, while trifolin at the same level totally controlled the fungus during the entire experiment. CPT at ≥125 μg/mL and Maneb also completely inhibited growth of F.avenaceum.
Hyperoside (quercetin 3-o-β-d-galactopyranoside) is one of the flavonoid glycosides with anti-inflammatory, antidepressant, and anti-cancer effects. But it remains unknown whether it had effects on breast cancer. Here, different concentrations of hyperoside were used to explore its therapeutic potential in both breast cancer cells and subcutaneous homotransplant mouse model. CCK-8 and wound healing assays showed that the viability and migration capability of Michigan Cancer Foundation-7 (MCF-7) and 4T1 cells were inhibited by hyperoside, while the apoptosis of cells were increased. Real-time quantitative PCR (qRT-PCR) and western blot analysis were used to detect mRNA and the protein level, respectively, which showed decreased levels of B cell lymphoma-2 (Bcl-2) and X-linked inhibitor of apoptosis (XIAP), and increased levels of Bax and cleaved caspase-3. After exploration of the potential mechanism, we found that reactive oxygen species (ROS) production was reduced by the administration of hyperoside, which subsequently inhibited the activation of NF-κB signaling pathway[2].
ln Vivo
The treatment of hypericin (intraperitoneal injection; 50 mg/kg; every two days for 18 days) reduces the growth of breast tumors in vivo [2].
Hyperoside Can Inhibit the Growth of Breast Tumor [2]
To evaluate the effect of Hyperoside on tumor growth in vivo, we used a subcutaneous homotransplant mouse model. As shown in Figure 5a–c, compared to the control group, the average tumor volume in the hyperoside-treated group was significantly reduced, which was also confirmed by H&E staining of tumor sections in each treatment group (Figure 5d). We further examined the expression of Bax and cleaved caspase-3. As shown in Figure 5e,f, Bcl-2 was decreased in the hyperoside-treated group, while Bax and cleaved caspase-3 were on the rise. All these results showed that apoptosis was induced in vivo when the tumors were injected with hyperoside, which resulted in the reduction of tumor volume.
Enzyme Assay
Antifungal Assays. [1]
A. alternata, E. nigrum, P. guepinii, Drechslera sp., and F. avenaceum were isolated from infected leaves and roots of C. acuminata grown in Nacogdoches, TX, in 2001 and 2002. The strains were cultured and maintained on potato dextrose agar (PDA) medium at 24 °C.
CPT, trifolin, and Hyperoside isolated from C. acuminata were tested for their ability to inhibit these fungi with two standard classical fungicides, Bravo (active ingredient chlorothalonil) and Maneb (active ingredient manganous ethylenebis[dithiocarbamate]). The concentrations of the fungicides were those recommended by the manufacturers (Bravo, 10000 μg/mL; Maneb, 3000 μg/mL). In addition to a negative control (0) and two fungicides as positive controls for each of the five isolated pathogens, seven concentrations of CPT were tested with each of the fungi and three levels of trifolin and Hyperoside were tested with P. guepinii, Drechslera sp., and F. avenaceum, respectively (Table 1). Trifolin and Hyperoside treatments were applied at concentrations of 50, 100, and 150 μg/mL, respectively. For all cultures, final concentrations were made in molten (50 °C) potato dextrose agar (Difco), and 10 mL aliquots were poured into Petri dishes (85 mm in diameter). Within 24 h after pouring, each of the plates was inoculated with one of the five fungi. One 5 × 5 mm mycelial plug was cut from the actively growing front of a 2 week old colony, then placed with the inoculum side down in the center of each treatment plate, and incubated at 24 °C. For all experiments, five replicate plates were inoculated for each treatment.
Mycelial growth on each plate was observed daily, recorded on a transparent film for the first two weeks, and then recorded on the 16th, 20th, 23rd, and 28th days. Colony radii were measured along four vertical radial directions. The mean of the four measurements was calculated as the growth rate on each plate. The mean and standard error were calculated from the five replicates of each treatment. For each of the fungi, values of EC50 and MIC of each compound were estimated.
Cell Assay
Cell Viability Assay[2]
Cell Types: MCF-7 and 4T1 cells
Tested Concentrations: 12.5, 25, 50, 75, or 100 µM
Incubation Duration: 6, 12, The production of ROS inhibits the activation of NF-κB signaling dye[2]. or 24-hour
Experimental Results: inhibition of cell growth in a time- and concentration-dependent manner.

Apoptosis analysis[2]
Cell Types: MCF-7 and 4T1 Cell
Tested Concentrations: 25, 50 and 100 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: Increased expression of Bax, cleaved caspase-3 and cleaved PARP in mRNA, diminished expression of Bcl-2 and protein levels.
Cell Viability Assay [2]
The extent of Hyperoside’s cytotoxicity on MCF-7 cells and 4T1 cells was examined by the Cell Counting Kit-8. There were five repeats for one group, and when density reached 5 × 103 cells/mL (37 °C, 12 h), they were added with hyperoside (50 μM) according to different time periods (6, 12, or 24 h) and the normal control group, and different concentrations of hyperoside (12.5, 25, 50, 75, or 100 μM) for 24 h. A total of 10 μL (5 mg/mL) CCK-8 was added for 2.5 h. Optical density (OD) was read on a microplate reader at an absorbance value of 450 nm. Each experiment was repeated three times. Data was expressed as mean ± SD.
Intracellular ROS Assay [2]
When reaching 1 × 10~6 cells/mL, cells were divided into 6-well plates for 12 h. The indicated concentrations of Hyperoside were added into cell plates for 24 h. After the treatment, as described before, cells were washed with pre-chilled phosphate buffer saline (PBS) and stained with cell-permeable 2′, 7′-dichlorofluorescein diacetate (DCFH-DA) at 37 °C for 30 min in the dark, and then washed by PBS to eliminate extracellular DCFH-DA to fluorescent dichlorofluorescein (DCF). Flow cytometry was then used to obtain the data.
Apoptosis Assay [2]
Annexin V-FITC (Fluorescein isothiocyanate) and propidium iodide (PI) double staining were used to perform the apoptosis trials. MCF-7 cells and 4T1 cells were used, they were first cultured in 6-well plates for 12 h. Then different concentrations of Hyperoside (25, 50, or 100 μM) were added for 24 h. They were centrifuged at a speed of 1200 r/min for 8 min, washed three times with cold PBS, and resuspended in binding buffer (400 μL). The cells were then incubated with Annexin V-FITC (5 μL) and PI (5 μL) for 20 min at 25 °C, shaded from light. Cell sorting analysis of collected cells, adherent cells, and flowing cells were performed by flow cytometry.
Wound-Healing Migration Assay [2]
As the previous study described [24], MCF-7 cells and 4T1 cells were placed onto 6-well plates. When cells grew to 80% confluence, the cell monolayer was scraped by sterile 200 μL plastic pipette tips, and then cells were washed twice. After washing, fresh medium containing various concentrations of Hyperoside was added at different time periods (6, 12, or 24 h). Serum-reduced Opti-MEM I medium were obtained from xxx. Images of wound closure were recorded by an inverted microscope.
Western Blot Analysis [2]
Cells were treated with previous concentrations of Hyperoside, NAC, and H2O2 peroxide for 24 h, then collected after being washed three times with PBS. A mix, which included radio immunoprecipitation assay (RIPA), phosphatase inhibitors, and PMSF, was used to extract the total protein. The total protein concentrations were determined by the Pierce BCA Protein Assay Kit. A 10% sodium dodecyl sulfate (SDS)-polyacrylamide gel was used for electrophoresis, then electric transfer was conducted with a polyvinylidene difluoride (PVDF) membrane for 2 h at 120 V. A 5% skim milk was used for membrane blocking for 3 h. Primary antibodies were incubated overnight with the indicated proteins (1:1000), stored at 4 °C; then, the membrane was washed three times with Tris-buffered saline tween (TBST) for 10 min. Secondary antibody (1:5000) was used for 2 h at 25 °C. Finally, the Vilber Lourmat Fusion FX7 Detection System was used for the acquirement of protein images. β-actin served as the internal standard.
Immunofluorescence Staining [2]
When reaching a density of 1 × 105 cells/mL, 4T1 cells were planted onto a 6-well plate with slides. Immunofluorescence staining was performed after Hyperoside was added as indicated for 24 h. Cells were fixed by 4% paraformaldehyde and then washed three times with PBS. Subsequently, the cells were blocked with goat serum for 30 min and incubated with primary antibodies overnight with a temperature of 4 °C, and then treated with the fluorescein (FITC)-conjugated AffiniPure Donkey Anti-rabbit IgG (H+L) in the dark for 2 h. The proteins were detected with 4,6-diamidino-2-phenylindole for nuclear counterstaining. A laser scanning confocal microscope was used for the acquirement of images.
Animal Protocol
Animal/Disease Models: balb/c (Bagg ALBino) mouse injected with 4T1 cells [2]
Doses: 50 mg/kg
Route of Administration: intraperitoneal (ip) injection; 50 mg/kg; once every two days for 18 days
Experimental Results: Compared with the control group, the average tumor Volume reduction. Bcl-2 is diminished and bax and caspase-3 cleavage is increased.
In Vivo Experiment [2]
Balb/c mice at 8–10 weeks old (25–30 g) were used. The mice were reared for a week after we carried out the experiment. Approximately 1.0 × 107 4T1 cells were harvested and suspended in 100μL PBS. Then we injected those cells into the fourth breast pad of the mice. Mice were randomized into three groups after rearing for 12 days, and the following administrations were executed: Hyperoside (50 mg/kg i.p. every two day for 18 days), NAC (100 mg/kg i.p. every two day for 18 days), or saline as the control group. Bodyweight and tumor volume were measured every two days. Tumor volume (V) = 0.5 × length × width2. Mice were then sacrificed after we finished the administration, and 4% paraformaldehyde was used for H&E.
References

[1]. Antifungal activity of camptothecin, trifolin, and hyperoside isolated from Camptotheca acuminata. J Agric Food Chem. 2005 Jan 12;53(1):32-7.

[2]. Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway. Int J Mol Sci. 2019 Dec 24;21(1):131.

Additional Infomation
Quercetin 3-O-beta-D-galactopyranoside is a quercetin O-glycoside that is quercetin with a beta-D-galactosyl residue attached at position 3. Isolated from Artemisia capillaris, it exhibits hepatoprotective activity. It has a role as a hepatoprotective agent and a plant metabolite. It is a tetrahydroxyflavone, a monosaccharide derivative, a beta-D-galactoside and a quercetin O-glycoside.
Isoquercitrin is under investigation in clinical trial NCT04622865 (Masitinib Combined With Isoquercetin and Best Supportive Care in Hospitalized Patients With Moderate and Severe COVID-19).
Hyperoside has been reported in Camellia sinensis, Geranium carolinianum, and other organisms with data available.
See also: Bilberry (part of); Menyanthes trifoliata leaf (part of); Crataegus monogyna flowering top (part of).
Leaf spots and root rots are major fungal diseases in Camptotheca acuminata that limit cultivation of the plant for camptothecin (CPT), a promising anticancer and antiviral alkaloid. Bioassays showed that pure CPT and flavonoids (trifolin and hyperoside) isolated from Camptotheca effectively control fungal pathogens in vitro, including Alternaria alternata, Epicoccum nigrum, Pestalotia guepinii, Drechslera sp., and Fusarium avenaceum, although antifungal activity of these compounds in the plant is limited. CPT inhibited mycelial growth by approximately 50% (EC50) at 10-30 microg/mL and fully inhibited growth at 75-125 microg/mL. The flavonoids were less effective than CPT at 50 microg/mL, particularly within 20 days after treatment, but more effective at 100 or 150 microg/mL. CPT, trifolin, and hyperoside may serve as leads for the development of fungicides.[1]
In summary, our experiments show that hyperoside can act as an anticancer drug by inhibiting NF-κB signaling and activating the Bax-caspase-3 axis through ROS-induced apoptosis. These data indicated that hyperoside has great potential as an anti-breast cancer drug and deserved further study in the future.[2]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C21H20O12
Molecular Weight
464.3763
Exact Mass
464.095
CAS #
482-36-0
PubChem CID
5281643
Appearance
Light yellow to yellow solid
Density
1.9±0.1 g/cm3
Boiling Point
872.6±65.0 °C at 760 mmHg
Melting Point
225-226ºC
Flash Point
307.5±27.8 °C
Vapour Pressure
0.0±0.3 mmHg at 25°C
Index of Refraction
1.803
LogP
1.75
Hydrogen Bond Donor Count
8
Hydrogen Bond Acceptor Count
12
Rotatable Bond Count
4
Heavy Atom Count
33
Complexity
758
Defined Atom Stereocenter Count
5
SMILES
O1[C@]([H])([C@@]([H])([C@]([H])([C@]([H])([C@@]1([H])C([H])([H])O[H])O[H])O[H])O[H])OC1C(C2=C(C([H])=C(C([H])=C2OC=1C1C([H])=C([H])C(=C(C=1[H])O[H])O[H])O[H])O[H])=O
InChi Key
OVSQVDMCBVZWGM-DTGCRPNFSA-N
InChi Code
InChI=1S/C21H20O12/c22-6-13-15(27)17(29)18(30)21(32-13)33-20-16(28)14-11(26)4-8(23)5-12(14)31-19(20)7-1-2-9(24)10(25)3-7/h1-5,13,15,17-18,21-27,29-30H,6H2/t13-,15+,17+,18-,21+/m1/s1
Chemical Name
2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3-[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one
Synonyms
Hyperoside; 482-36-0; Hyperin; Hyperosid; Hyperozide; Quercetin-3-O-galactoside; Quercetin-3-galactoside; quercetin galactoside;
HS Tariff Code
2934.99.9001
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)
Solubility Data
Solubility (In Vitro)
DMSO : ~125 mg/mL (~269.18 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.48 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 20.8 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: ≥ 2.08 mg/mL (4.48 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 20.8 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.

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Solubility in Formulation 3: 10 mg/mL (21.53 mM) in 50% PEG300 50% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.


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Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.1534 mL 10.7670 mL 21.5341 mL
5 mM 0.4307 mL 2.1534 mL 4.3068 mL
10 mM 0.2153 mL 1.0767 mL 2.1534 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.

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