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Purity: =99.68%
Baohuoside I is a naturally occurring flavonoid extracted from Epimedium koreanum Nakai with anti-tumor activity. It acts as an inhibitor of CXCR4,can downregulate CXCR4 expression, and induce apoptosis.
| Targets |
CXCR4; Inflammation/Immunology
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|---|---|
| ln Vitro |
At 12–25 μM, baohuoside I, an inhibitor of CXCR4, suppresses the expression of CXCR4. In a dose-dependent manner, baohuoside I (0-25 μM) inhibits NF-κB activation and the invasion of cervical cancer cells provoked by CXCL12. Baohuoside I also prevents breast cancer cells from invasively growing[1]. At 24 hours, 11.5 hours, and 48 and 72 hours, respectively, baohuoside I reduces the viability of A549 cells with IC50s of 25.1 μM, 11.5 μM, and 9.6 μM. In A549 cells, baohuoside I (25 μM) stimulates the p38MAPK and JNK signaling cascades, increases ROS levels, and suppresses the caspase cascade[2]. The proliferation of esophageal squamous cell carcinoma Eca109 cells is considerably and dose-dependently inhibited by baohuoside I (3.125, 6.25, 12.5, 25.0, and 50.0 µg/mL), with an IC50 of 4.8 µg/mL at 48 hours[3].
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| ln Vivo |
In nude mice, baohuoside I (25 mg/kg) reduces the expression of survivin, cyclin D1, and β-catenin protein levels[3].
Baohuoside-I inhibits in vivo tumor growth in a xenograft tumor model of human esophageal cancer cells. We investigated the in vivo anticancer activity of Baohuoside I using a xenograft model of human esophageal squamous cell carcinoma cells. Briefly, exponentially growing firefly luciferase-tagged Eca109 cells were injected into the flanks of Babl/c nude mice. One week after cancer cell injection, Baohuoside-I was intralesionally administered (25 mg/kg body weight, once a day). Mice were subjected to Xenogen bioluminescence imaging on a weekly basis for an additional three weeks. As shown in Fig. 5, the Baohuoside-I treatment group exhibited a significantly decreased Xenogen imaging signal when compared with the control group. In fact, quantitative analysis revealed that Baohuoside-I-mediated inhibition of xenograft tumor growth was statistically significant (p<0.01) at three weeks after treatment, even though the tumors were not completely eliminated (Fig. 5A and B). Histologic analysis (H&E staining) indicated that the Baohuoside-I treatment group exhibited a decreased cellularity in the tumor mass.[3] |
| Enzyme Assay |
In this work, researchers investigate baohuoside I, a component of Epimedium koreanum, as a regulator of CXCR4 expression as well as function in cervical cancer and breast cancer cells. We observed that baohuoside I downregulated CXCR4 expression in a dose- and time-dependent manner in HeLa cells. Treatment with a pharmacological proteasome and lysosomal inhibitors did not have a substantial effect on baohuoside I’s ability to suppress CXCR4 expression. When we investigated the molecular mechanism of action, it was observed that the suppression of CXCR4 expression occurred at the level of mRNA. The decrease in the level of CXCR4 expression caused by baohuoside I was correlated with inhibition of the CXCL12-induced invasion of both cervical and breast cancer cells. Overall, our results show that baohuoside I exerts its antimetastatic effect through the downregulation of CXCR4 expression and, thus, has the potential to play a role in the suppression of cancer metastasis[1].
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| Cell Assay |
Western Blotting[1]
For detection of CXCR4, baohuoside I-treated whole cell extracts were lysed with RIPA buffer [150 mM NaCl, 10 mM Tris (pH 7.2), 0.1% sodium dodecyl sulfate (SDS), 1% Triton X-100, 1% deoxycholate, and 5 mM ethylenediaminetetraacetic acid (EDTA)] enriched with a complete protease inhibitor cocktail tablet and then incubated on ice for 30 min with regular vortexing before being centrifuged at 14000 rpm and 4 °C for 15 min. The protein concentration was determined by using the bicinchoninic acid (BCA) protein assay kit. The protein samples were boiled in SDS sample buffer for 5 min and were resolved on a 10% SDS–polyacrylamide gel. After electrophoresis, proteins were transferred onto a polyvinyl difluoride (PVDF) membrane, which was blocked with 5% nonfat dry milk in Tris-buffered saline with 0.1% Tween 20 (TBST) and incubated with the primary antibody at the appropriate final concentration followed by hybridization with a horseradish peroxidase-conjugated anti-rabbit or anti-mouse secondary antibody. For each step, the membrane was washed with TBST three times for 10 min and the transferred proteins were incubated with supersignal pico-chemiluminescent substrate or dura-luminol substrate for 2 min according to the manufacturer’s instructions and visualized with imagequant LAS 4000. Invasion Assay[1] The in vitro invasion assay was conducted using the Bio-Coat Matrigel invasion assay system according to the manufacturer’s instructions. Cancer cells (5 × 104 per milliliter) were suspended in medium and seeded into the Matrigel-precoated transwell chambers with polycarbonate membranes with a pore size of 8 μm. After preincubation with or without baohuoside I (25 μM), transwell chambers were then placed into 24-well plates, to which was added the basal medium only or basal medium containing 100 ng/mL CXCL12. After incubation (24 h for HeLa and MDA-MB-231), the upper surface of transwell chambers was wiped off with a cotton swab and invading cells were fixed and stained with a Diff-Quick stain. The invading cell numbers were counted in five randomly selected microscope fields (100×). |
| Animal Protocol |
Xenograft tumor model of human esophageal squamous cell carcinoma. [3]
The use and care of animals were carried out by following the guidelines approved by the Institutional Animal Care and Use Committee. Female Balb/c nude mice (4- to 6-weeks-old) were used. Subconfluent Eca109-Luc cells were harvested and resuspended in PBS to a final density of 2x107 cells/ml. Prior to injection, cells were resuspended in PBS and analyzed by 0.4% trypan blue exclusion assay (viable cells >90%). For subcutaneous injection, ~1x106 Eca109-Luc cells in 200 µl PBS were injected into the left flank of each mouse using 27G needles. At 1 week after tumor cell injection, Baohuoside-I (25 mg/kg per mouse) was injected intralesionally once a day, whereas the 10 mice intended for vehicle treatment were administered an equal volume of PBS. Xenogen bioluminescence imaging.[3] Small animal whole body optical imaging was carried out as described. Briefly, mice were anesthetized with isoflurane attached to a nosecone mask equipped with the Xenogen IVIS imaging system and subjected to imaging weekly after subcutaneous injection. For imaging, mice were injected (i.p.) with D-Luciferin sodium salt at 100 mg/kg body weight in 0.1 ml sterile PBS. Acquired pseudo-images were obtained by superimposing the emitted light over the grayscale photographs of the animal. Quantitative analysis was carried out with Xenogen's Living Image V2.50.1 software as described. Animals were sacrificed after 3 weeks, and tumor samples were retrieved for histological evaluation and Western blot analysis. |
| References |
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| Additional Infomation |
Icariside II is a glycosyloxyflavone that is 3,5,7-trihydroxy-4'-methoxy-8-prenylflavone in which the hydroxy group at position 3 has been converted into its alpha-L-rhamnopyranoside. It has a role as a plant metabolite, an anti-inflammatory agent, an antineoplastic agent and an apoptosis inducer. It is functionally related to an alpha-L-rhamnopyranose.
Baohuoside I has been reported in Epimedium pubescens, Epimedium acuminatum, and other organisms with data available. |
| Molecular Formula |
C27H30O10
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|---|---|
| Molecular Weight |
514.5211
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| Exact Mass |
514.183
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| CAS # |
113558-15-9
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| PubChem CID |
5488822
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| Appearance |
Light yellow to yellow solid powder
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| Density |
1.5±0.1 g/cm3
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| Boiling Point |
759.4±60.0 °C at 760 mmHg
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| Flash Point |
253.9±26.4 °C
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| Vapour Pressure |
0.0±2.7 mmHg at 25°C
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| Index of Refraction |
1.666
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| LogP |
4.65
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
37
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| Complexity |
874
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| Defined Atom Stereocenter Count |
5
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| SMILES |
O1[C@]([H])([C@@]([H])([C@@]([H])([C@]([H])([C@]1([H])C([H])([H])[H])O[H])O[H])O[H])OC1C(C2=C(C([H])=C(C(C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])=C2OC=1C1C([H])=C([H])C(=C([H])C=1[H])OC([H])([H])[H])O[H])O[H])=O
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| InChi Key |
NGMYNFJANBHLKA-LVKFHIPRSA-N
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| InChi Code |
InChI=1S/C27H30O10/c1-12(2)5-10-16-17(28)11-18(29)19-21(31)26(37-27-23(33)22(32)20(30)13(3)35-27)24(36-25(16)19)14-6-8-15(34-4)9-7-14/h5-9,11,13,20,22-23,27-30,32-33H,10H2,1-4H3/t13-,20-,22+,23+,27-/m0/s1
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| Chemical Name |
5,7-dihydroxy-2-(4-methoxyphenyl)-8-(3-methylbut-2-enyl)-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxychromen-4-one
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| Synonyms |
Baohuoside I; 113558-15-9; Icariside II; BAOHUOSIDEI; CHEBI:82619; 5,7-dihydroxy-2-(4-methoxyphenyl)-8-(3-methylbut-2-enyl)-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxychromen-4-one; CHEMBL560116; 4H-1-Benzopyran-4-one, 3-[(6-deoxy-alpha-L-mannopyranosyl)oxy]-5,7-dihydroxy-2-(4-methoxyphenyl)-8-(3-methyl-2-buten-1-yl)-;
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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 : ≥ 32 mg/mL (~62.19 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.04 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 (4.04 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. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (4.04 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: 20 mg/mL (38.87 mM) in 0.5% CMC/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 | 1.9436 mL | 9.7178 mL | 19.4356 mL | |
| 5 mM | 0.3887 mL | 1.9436 mL | 3.8871 mL | |
| 10 mM | 0.1944 mL | 0.9718 mL | 1.9436 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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