| Size | Price | Stock | Qty |
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| 5mg |
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| Targets |
Epimedin B targets multiple biological pathways and molecular entities, contributing to its diverse pharmacological profile. The compound exhibits estrogen-like activity by binding to estrogen receptors (ERα and ERβ), although its affinity is lower than that of endogenous estrogens. This estrogenic activity is particularly relevant to its anti-osteoporotic effects, as Epimedin B promotes osteoblast differentiation and inhibits osteoclast-mediated bone resorption through estrogen receptor-mediated signaling pathways. The compound also modulates the immune system by enhancing T cell proliferation and cytokine production, likely through interactions with T cell receptors and costimulatory molecules. Epimedin B exhibits anti-inflammatory effects by inhibiting the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and suppressing the activation of NF-κB and MAPK signaling pathways in macrophages and other immune cells. The antioxidant activity of Epimedin B is mediated through direct free radical scavenging and upregulation of endogenous antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Furthermore, Epimedin B has been shown to inhibit tumor cell proliferation by inducing G0/G1 cell cycle arrest and promoting apoptosis through the mitochondrial pathway. The prenyl groups on the flavonoid scaffold enhance the compound's lipophilicity and membrane affinity, facilitating its interaction with cellular membranes and intracellular targets. The glycosidic moieties may influence the compound's solubility, stability, and selectivity for certain cell types, contributing to its overall pharmacological profile.
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| ln Vitro |
In vitro studies have extensively characterized the biological activities of Epimedin B across multiple cell-based systems. In osteoblast-like cells (e.g., MC3T3-E1 and primary calvarial osteoblasts), Epimedin B stimulates cell proliferation and osteogenic differentiation, as evidenced by increased ALP activity, collagen synthesis, and mineralization. These effects are mediated through the activation of the BMP/Smad and Wnt/β-catenin signaling pathways, leading to increased expression of osteogenic transcription factors such as Runx2 and Osterix. In osteoclast precursor cells (RAW 264.7 macrophages and bone marrow-derived macrophages), Epimedin B inhibits RANKL-induced osteoclast differentiation and bone resorption by suppressing NF-κB and MAPK signaling and reducing the expression of osteoclast-specific genes including TRAP, Cathepsin K, and MMP-9. In immune cells, Epimedin B enhances lymphocyte proliferation and promotes the production of Th1-type cytokines (IL-2, IFN-γ), indicating a potent immunostimulatory effect. The compound also exhibits anti-inflammatory activity by reducing the production of TNF-α, IL-1β, and IL-6 in LPS-stimulated macrophages. Epimedin B shows antioxidant activity in cell-free DPPH radical scavenging assays, and in cellular models of oxidative stress, it protects against H₂O₂-induced cell death by reducing intracellular ROS levels and maintaining mitochondrial membrane potential. The compound demonstrates direct cytotoxic activity against various cancer cell lines, including breast cancer (MCF-7), prostate cancer (PC-3), and leukemia (HL-60) cells, with IC₅₀ values typically in the range of 10-50 µM. Mechanistically, Epimedin B induces apoptosis through the intrinsic mitochondrial pathway, characterized by Bax upregulation, Bcl-2 downregulation, cytochrome c release, and caspase-3/9 activation. The anti-aging effects of Epimedin B are attributed to its ability to reduce oxidative damage and enhance cellular stress resistance.
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| ln Vivo |
In vivo studies have demonstrated the therapeutic potential of Epimedin B in several disease models, particularly in the areas of bone health, immunomodulation, and anti-inflammatory therapy. In ovariectomized (OVX) rats or mice, a well-established model of postmenopausal osteoporosis, oral administration of Epimedin B at doses of 10-50 mg/kg/day for 8-12 weeks significantly prevented bone loss and improved bone microarchitecture, as assessed by bone mineral density (BMD) measurements and micro-CT analysis. Serum levels of bone formation markers (osteocalcin, P1NP) were increased, while bone resorption markers (CTX-1, TRAP-5b) were decreased, confirming the bone-protective effects of the compound. Histomorphometric analysis revealed increased trabecular bone volume, trabecular number, and trabecular thickness, as well as decreased trabecular separation, indicating improved bone quality. In immunomodulatory studies, Epimedin B administration in mice enhanced antibody responses to antigen challenge, increased the proportion of CD4⁺ and CD8⁺ T cells, and elevated serum immunoglobulin levels. In models of inflammation, such as carrageenan-induced paw edema and LPS-induced acute lung injury, Epimedin B reduced edema, inflammatory cell infiltration, and pro-inflammatory cytokine production, demonstrating its anti-inflammatory efficacy. In tumor xenograft models, Epimedin B (20-50 mg/kg, oral or i.p.) significantly inhibited tumor growth, with tumor growth inhibition rates of 30-50% compared to controls. The antitumor effect was associated with increased apoptosis and reduced angiogenesis in tumor tissues. In a model of D-galactose-induced aging, Epimedin B improved cognitive function, reduced oxidative stress markers, and increased antioxidant enzyme activities in the brain, supporting its anti-aging potential. These in vivo findings support the traditional uses of Epimedium species for bone health, immune enhancement, and longevity, and suggest that Epimedin B may be a promising candidate for the development of pharmaceuticals targeting osteoporosis, inflammatory diseases, and cancer.
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| Enzyme Assay |
For in vitro enzyme/receptor binding assays, Epimedin B is typically evaluated for its binding affinity to estrogen receptors (ERα and ERβ) using competitive radioligand binding assays. Recombinant human ERα or ERβ proteins are incubated with varying concentrations of Epimedin B (0.1 nM-10 µM) and a fixed concentration of ³H-estradiol (0.5-1 nM) in binding buffer (50 mM Tris-HCl, pH 7.4, 1 mM EDTA, 10% glycerol, 0.1% BSA) for 2-4 hours at 4°C. Non-specific binding is determined in the presence of 100- to 1000-fold excess of unlabeled estradiol. Bound and free ligand are separated by charcoal-dextran precipitation or filtration, and radioactivity is measured by liquid scintillation counting. The binding affinity (Ki) is calculated from competition curves using non-linear regression analysis. For antioxidant assays, the DPPH radical scavenging activity of Epimedin B is measured by incubating the compound (1-100 µg/mL) with DPPH solution (0.1 mM in ethanol) for 30 minutes at room temperature, and the decrease in absorbance at 517 nm is recorded. The IC₅₀ value for DPPH scavenging is determined from dose-response curves, with ascorbic acid or Trolox used as positive controls. For enzyme inhibition assays, Epimedin B is tested against targets such as COX-1, COX-2, and LOX using commercially available kits. The compound is incubated with the enzyme and substrate in a suitable buffer, and enzyme activity is measured by monitoring the formation of a chromogenic or fluorogenic product. IC₅₀ values are determined from dose-response curves, with appropriate positive controls included in each assay. All experiments are performed in triplicate, and results are expressed as mean ± standard deviation.
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| Cell Assay |
For in vitro cell-based assays, Epimedin B is evaluated using a panel of cell lines relevant to its pharmacological activities. For osteogenic differentiation studies, MC3T3-E1 pre-osteoblast cells or primary calvarial osteoblasts are seeded in 24-well plates at 1-2 × 10⁴ cells per well and cultured in differentiation medium (α-MEM with 10% FBS, 50 µg/mL ascorbic acid, 10 mM β-glycerophosphate). Cells are treated with Epimedin B at concentrations of 0.1-10 µM for 7-21 days, with media changes every 2-3 days. ALP activity is measured at day 7 using a colorimetric assay kit, and mineralization is assessed at day 14-21 by Alizarin Red S staining. For osteoclastogenesis assays, RAW 264.7 macrophages are seeded in 96-well plates at 5 × 10³ cells per well and treated with RANKL (50 ng/mL) and M-CSF (25 ng/mL) with or without Epimedin B (0.1-10 µM) for 5-7 days. Osteoclast formation is assessed by TRAP staining, and TRAP-positive multinucleated cells are counted. For immunomodulatory studies, murine splenocytes are cultured with Epimedin B (1-50 µg/mL) for 48-72 hours, and cell proliferation is measured by MTT or CellTiter-Glo assay. Cytokine production in culture supernatants is quantified by ELISA. For anti-inflammatory studies, RAW 264.7 macrophages are stimulated with LPS (1 µg/mL) in the presence or absence of Epimedin B (1-50 µM) for 24 hours, and TNF-α, IL-1β, and IL-6 levels in the supernatant are measured by ELISA. For cytotoxicity assays, cancer cells are seeded in 96-well plates at 5 × 10³ cells per well, treated with Epimedin B (0.1-100 µM) for 48-72 hours, and cell viability is determined using the MTT assay. Apoptosis is confirmed by flow cytometry using Annexin V-FITC/PI staining and by Western blot analysis of apoptosis-related proteins. For antioxidant studies, cells are pretreated with Epimedin B for 24 hours and then exposed to H₂O₂ (200-500 µM) for 4-6 hours, and cell viability and intracellular ROS levels are measured using fluorescent probes.
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| Animal Protocol |
For in vivo animal experiments, Epimedin B is typically administered to female ICR or Sprague-Dawley rats (6-8 weeks old) that have undergone bilateral ovariectomy (OVX) to induce osteoporosis. Surgery is performed 4 weeks prior to treatment to allow for bone loss development. Epimedin B is suspended in 0.5% carboxymethyl cellulose (CMC) or saline and administered orally by gavage at doses of 10, 25, or 50 mg/kg/day for 8-12 weeks. Sham-operated animals and OVX controls receive vehicle alone. At the end of the treatment period, animals are euthanized, and blood samples are collected for serum analysis of bone turnover markers (osteocalcin, P1NP, CTX-1, TRAP-5b). Femurs and tibiae are harvested for micro-CT analysis of bone microarchitecture (bone volume fraction, trabecular number, trabecular thickness, trabecular separation) and for histomorphometric analysis after embedding and sectioning. For immunomodulatory studies, mice are treated with Epimedin B for 7-14 days and immunized with ovalbumin (OVA) or sheep red blood cells (SRBC) to assess humoral and cellular immune responses. Spleens and thymuses are harvested for lymphocyte subset analysis by flow cytometry, and serum antibody titers are measured by ELISA. For anti-inflammatory studies, carrageenan-induced paw edema models are used: mice are treated with Epimedin B (10-50 mg/kg, oral) 1 hour prior to subplantar injection of carrageenan (1% in saline, 50 µL), and paw volume is measured using a plethysmometer at 1, 2, 4, and 6 hours post-injection. For tumor xenograft models, mice are subcutaneously inoculated with 1 × 10⁶ tumor cells (e.g., S180 sarcoma or H22 hepatoma) and randomized into treatment groups (n=8-10 per group). Epimedin B is administered orally or intraperitoneally at doses of 20-50 mg/kg/day for 10-21 days, and tumor growth is monitored every 3 days. At the end of the study, tumors are excised, weighed, and processed for histopathological and immunohistochemical analysis. All animal procedures are conducted in accordance with institutional guidelines for the care and use of laboratory animals.
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| ADME/Pharmacokinetics |
Pharmacokinetic studies of Epimedin B have been conducted in rodent models to characterize its absorption, distribution, metabolism, and excretion (ADME) properties. Following oral administration of Epimedin B at doses of 10-50 mg/kg in rats, the compound is absorbed with a Tmax of approximately 1-2 hours, indicating relatively rapid absorption. The Cmax ranges from 0.2 to 2 µg/mL, depending on the dose. The oral bioavailability of Epimedin B is estimated to be 5-12%, reflecting poor membrane permeability and extensive first-pass metabolism associated with the glycosylated structure. Upon absorption, Epimedin B undergoes extensive deglycosylation to release the aglycone, which is further metabolized via oxidation, reduction, and conjugation reactions (glucuronidation and sulfation). The major metabolites detected in plasma and urine include desugarized, dehydrogenated, and hydroxylated products. The compound is widely distributed to various tissues, with higher concentrations observed in the liver, kidney, and bone, consistent with its therapeutic targets. The elimination half-life of Epimedin B in plasma is approximately 2-3 hours, and the compound is primarily excreted in the urine and feces as metabolites. The compound is stable for up to 24 months when stored as a powder at 2-8°C in a tightly sealed container, protected from light and moisture. For in vivo administration, Epimedin B can be formulated in 0.5% CMC, saline, or other suitable vehicles, with sonication or heating to enhance solubility. Further detailed pharmacokinetic studies, including determination of tissue distribution profiles and identification of metabolites, are needed to fully characterize the ADME properties of Epimedin B.
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| Toxicity/Toxicokinetics |
Toxicological data for Epimedin B indicate a favorable safety profile at pharmacologically relevant doses. In acute toxicity studies in mice, the oral LD₅₀ of Epimedin B has been estimated to be greater than 2000 mg/kg, indicating low acute toxicity. In subacute toxicity studies, mice administered Epimedin B at doses of 10-100 mg/kg/day for 28 days showed no significant changes in body weight, organ weights, hematological parameters, or serum biochemical parameters, compared to vehicle controls. Histopathological examination of major organs (liver, kidneys, heart, lungs, spleen, thymus) revealed no treatment-related abnormalities. No significant genotoxicity was observed in the Ames test or in the mouse micronucleus assay. At very high doses (≥200 mg/kg), mild gastrointestinal disturbances, including soft stools and reduced appetite, have been reported. As a flavonoid glycoside with estrogenic activity, Epimedin B may have the potential to cause hormone-related effects at high doses, although this has not been observed in standard toxicity studies. The compound is classified as a research-grade reagent and is not intended for human therapeutic use. Standard laboratory safety practices should be followed when handling Epimedin B.
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| References |
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| Additional Infomation |
Epimedin B is a glycoside belonging to the flavonoid class of compounds. It has been reported that Epimedin B exists in Epimedium brevicornu, Epimedium truncatum, and other organisms with relevant data.
Epimedin B is a research-use only compound and has not been approved for clinical applications by any regulatory authority. It is also known as 朝藿定B or 淫羊霍定B in Chinese and is one of the major bioactive flavonoid glycosides isolated from plants of the Epimedium genus. Epimedium species have been used in traditional Chinese medicine for over 2,000 years for the treatment of kidney-yang deficiency, impotence, osteoporosis, and arthralgia. The compound is a prenylated flavonol glycoside with a molecular formula of C₃₈H₄₈O₁₉ and a molecular weight of 808.78 g/mol. It is typically isolated from the aerial parts of Epimedium plants using chromatography techniques and is characterized by HPLC, NMR, and mass spectrometry to confirm its identity and purity. The compound is available from various research chemical suppliers with purities typically ≥98% (HPLC). Epimedin B is soluble in DMSO, methanol, and ethanol, with limited solubility in water. Storage recommendations include keeping the compound in a sealed container, protected from light and moisture, at 2-8°C for short-term storage or -20°C for long-term storage. The compound is of significant interest for research in bone biology, immunology, inflammation, and oncology, and ongoing studies continue to explore its mechanisms of action and therapeutic potential. However, further preclinical and clinical studies are needed to establish its efficacy and safety for any specific indication before it can be considered for drug development. |
| Molecular Formula |
C₃₈H₄₈O₁₉
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|---|---|
| Molecular Weight |
808.78
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| Exact Mass |
808.278
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| CAS # |
110623-73-9
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| PubChem CID |
5748393
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| Appearance |
Light yellow to yellow solid powder
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| Density |
1.6±0.1 g/cm3
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| Boiling Point |
1066.1±65.0 °C at 760 mmHg
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| Flash Point |
325.6±27.8 °C
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| Vapour Pressure |
0.0±0.3 mmHg at 25°C
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| Index of Refraction |
1.685
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| LogP |
2.87
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| Hydrogen Bond Donor Count |
10
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| Hydrogen Bond Acceptor Count |
19
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| Rotatable Bond Count |
11
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| Heavy Atom Count |
57
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| Complexity |
1420
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| Defined Atom Stereocenter Count |
14
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| SMILES |
C[C@H]1[C@@H]([C@H]([C@H]([C@@H](O1)OC2=C(OC3=C(C2=O)C(=CC(=C3CC=C(C)C)O[C@H]4[C@@H]([C@H]([C@@H]([C@H](O4)CO)O)O)O)O)C5=CC=C(C=C5)OC)O[C@H]6[C@@H]([C@H]([C@@H](CO6)O)O)O)O)O
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| InChi Key |
OCZZCFAOOWZSRX-LRHLXKJSSA-N
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| InChi Code |
InChI=1S/C38H48O19/c1-14(2)5-10-18-21(53-37-31(49)28(46)26(44)22(12-39)54-37)11-19(40)23-27(45)34(32(55-33(18)23)16-6-8-17(50-4)9-7-16)56-38-35(29(47)24(42)15(3)52-38)57-36-30(48)25(43)20(41)13-51-36/h5-9,11,15,20,22,24-26,28-31,35-44,46-49H,10,12-13H2,1-4H3/t15-,20+,22+,24-,25-,26+,28-,29+,30+,31+,35+,36-,37+,38-/m0/s1
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| Chemical Name |
3-[(2S,3R,4R,5R,6S)-4,5-dihydroxy-6-methyl-3-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxyoxan-2-yl]oxy-5-hydroxy-2-(4-methoxyphenyl)-8-(3-methylbut-2-enyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one
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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 Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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 (~123.64 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 0.83 mg/mL (1.03 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 8.3 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of 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: ≥ 0.83 mg/mL (1.03 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 8.3 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.2364 mL | 6.1822 mL | 12.3643 mL | |
| 5 mM | 0.2473 mL | 1.2364 mL | 2.4729 mL | |
| 10 mM | 0.1236 mL | 0.6182 mL | 1.2364 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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