| Size | Price | Stock | Qty |
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| 10mg |
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| 25mg |
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| Other Sizes |
| Targets |
Epmedin C targets multiple biological pathways and molecular entities, reflecting its diverse pharmacological profile. The compound exhibits estrogen-like activity by binding to estrogen receptors (ERα and ERβ), although its affinity for these receptors is lower than that of endogenous estrogens. This estrogenic activity is particularly relevant in the context of bone metabolism, where Epmedin C promotes osteoblast differentiation and inhibits osteoclast activity through estrogen receptor-mediated signaling. In addition to its hormonal effects, Epmedin C modulates the immune system by activating T cells and enhancing the production of immunoglobulins, likely through interactions with cell surface receptors and intracellular signaling pathways. The compound has been shown to inhibit the proliferation of various cancer cell lines by inducing cell cycle arrest and apoptosis, mechanisms that may involve the modulation of the PI3K/AKT, MAPK/ERK, and NF-κB signaling pathways. Furthermore, Epmedin C exhibits antioxidant activity by scavenging reactive oxygen species (ROS) and upregulating endogenous antioxidant enzymes, contributing to its cytoprotective effects. The prenyl groups on the flavonoid scaffold are believed to enhance membrane affinity and interactions with lipid bilayers, facilitating the compound's access to intracellular targets. The glycosidic moieties may play a role in determining the compound's selectivity for certain cell types and its overall pharmacokinetic profile.
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| ln Vitro |
In vitro studies have extensively characterized the biological activities of Epmedin C across multiple cell-based systems. In osteoblast-like cells (e.g., MC3T3-E1 and primary calvarial osteoblasts), Epmedin C stimulates cell proliferation, alkaline phosphatase (ALP) activity, and mineralization, indicating enhanced osteogenic differentiation. These effects are mediated through the estrogen receptor and the BMP/Smad signaling pathway, as evidenced by increased expression of osteogenic markers such as Runx2, Osterix, and osteocalcin. In osteoclast precursor cells (RAW 264.7 macrophages), Epmedin C inhibits RANKL-induced osteoclastogenesis and bone resorption by suppressing the NF-κB and MAPK pathways and reducing the expression of osteoclast-specific genes like TRAP, Cathepsin K, and MMP-9. In immune cells, Epmedin C enhances the proliferation of lymphocytes and promotes the production of IL-2, IFN-γ, and other Th1-type cytokines, indicating a potent immunostimulatory effect. The compound also exhibits direct cytotoxic activity against several cancer cell lines, including human breast cancer (MCF-7), prostate cancer (PC-3), and liver cancer (HepG2) cells, with IC₅₀ values typically ranging from 10 to 50 µM. Mechanistically, Epmedin C induces apoptosis through the intrinsic mitochondrial pathway, characterized by the loss of mitochondrial membrane potential, cytochrome c release, and activation of caspase-3 and caspase-9. The compound also shows moderate antioxidant activity in DPPH and ABTS radical scavenging assays, although the glycosylation of the flavonoid core may reduce its direct radical-scavenging capacity compared to the aglycone form.
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| ln Vivo |
In vivo studies have demonstrated the therapeutic potential of Epmedin C in several disease models, particularly in the areas of bone health, immunomodulation, and cancer prevention. In ovariectomized (OVX) mice, a well-established model of postmenopausal osteoporosis, oral administration of Epmedin C at doses of 10-50 mg/kg/day for 8-12 weeks significantly prevented bone loss, as evidenced by increased bone mineral density (BMD), improved trabecular microarchitecture (assessed by micro-CT), and reduced serum levels of bone resorption markers such as CTX-1 and TRAP-5b. Histomorphometric analysis revealed increased osteoblast surface and decreased osteoclast surface in the trabecular bone, confirming the compound's bone-protective effects. In immunomodulatory studies, Epmedin C administration in mice enhanced the antibody response to ovalbumin (OVA) immunization, increased the proportion of CD4⁺ and CD8⁺ T cells in the spleen, and elevated serum levels of immunoglobulins (IgG, IgM, IgA). In tumor xenograft models, Epmedin C (20-50 mg/kg, i.p. or oral) significantly inhibited the growth of implanted tumors (e.g., S180 sarcoma and H22 hepatoma) in mice, with tumor growth inhibition rates of 30-50% compared to vehicle controls. The antitumor effect was associated with increased infiltration of immune cells into the tumor microenvironment and reduced expression of angiogenesis markers such as VEGF and CD31. In a murine model of cyclophosphamide-induced immunosuppression, Epmedin C restored immune function by increasing white blood cell counts, spleen and thymus weights, and NK cell activity. These in vivo findings support the traditional use of Epimedium species for bone health and immune support and suggest that Epmedin C may be a promising candidate for the development of nutraceuticals or pharmaceuticals targeting osteoporosis and immune-related disorders.
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| Enzyme Assay |
For in vitro enzyme/receptor binding assays, Epmedin C is typically evaluated for its affinity to estrogen receptors (ERα and ERβ) using competitive binding assays. Briefly, recombinant human ERα or ERβ proteins are incubated with varying concentrations of Epmedin C (0.1 nM-10 µM) and a fixed concentration of radiolabeled estradiol (³H-E₂, 0.5-1 nM) in binding buffer (50 mM Tris-HCl, pH 7.4, containing 1 mM EDTA, 10% glycerol, and 0.1% BSA) for 2-4 hours at 4°C. Non-specific binding is determined in the presence of a 100- to 1000-fold excess of unlabeled estradiol. Bound and free ligand are separated by charcoal-dextran precipitation or filtration through glass fiber filters, and radioactivity is measured using a liquid scintillation counter. The binding affinity (Ki) is calculated from competition curves using non-linear regression analysis. For enzyme inhibition assays, Epmedin C is tested against targets such as protein tyrosine phosphatases, cyclooxygenases (COX-1 and COX-2), and lipoxygenases (LOX) using commercially available assay 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 using a microplate reader. IC₅₀ values are determined from dose-response curves, with appropriate positive controls (e.g., estradiol for ER binding, indomethacin for COX inhibition) 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, Epmedin C 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- or 48-well plates at a density of 1-2 × 10⁴ cells per well and cultured in α-MEM supplemented with 10% FBS, 50 µg/mL ascorbic acid, and 10 mM β-glycerophosphate to induce differentiation. Cells are treated with Epmedin C 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 ALP assay kit. Mineralization is assessed at day 14-21 by Alizarin Red S staining, and the stained nodules are quantified by destaining with cetylpyridinium chloride and measuring absorbance at 562 nm. 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) in the presence or absence of Epmedin C (0.1-10 µM) for 5-7 days. Osteoclast formation is assessed by TRAP staining, and the number of TRAP-positive multinucleated cells (≥3 nuclei) is counted. For immunomodulatory studies, murine splenocytes are cultured with Epmedin C (1-50 µg/mL) for 48-72 hours, and cell proliferation is measured using the MTT or CellTiter-Glo assay. Cytokine levels in culture supernatants are quantified by ELISA. For cytotoxicity assays, cancer cells are seeded in 96-well plates at 5 × 10³ cells per well, treated with Epmedin C (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 (Bax, Bcl-2, cleaved caspase-3).
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| Animal Protocol |
For in vivo animal experiments, Epmedin C is typically administered to female ICR or C57BL/6 mice (6-8 weeks old, 18-22 g) that have undergone bilateral ovariectomy (OVX) to induce osteoporosis, or to immunocompetent mice for immunomodulatory studies. For the OVX model, surgery is performed 4 weeks prior to treatment to allow for the development of bone loss. Epmedin C 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 mice and OVX control mice receive vehicle alone. At the end of the treatment period, mice are euthanized, and blood samples are collected for serum analysis of bone turnover markers (osteocalcin, P1NP, CTX-1, TRAP-5b) and calcium/phosphate levels. Femurs and tibiae are harvested and fixed in 10% formalin for micro-CT analysis, or processed for histomorphometry after embedding in methyl methacrylate and sectioning. For tumor xenograft models, mice are subcutaneously inoculated with 1 × 10⁶ tumor cells (e.g., S180 or H22) and randomized into treatment groups (n=8-10 per group). Epmedin C 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 by caliper measurement. At the end of the study, tumors are excised, weighed, and processed for histopathological and immunohistochemical analysis. For immunomodulatory studies, mice are treated with Epmedin C for 7-14 days, and then immunized with OVA or sheep red blood cells (SRBC) to assess the 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. 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 Epmedin C have been conducted in rodent models to characterize its absorption, distribution, metabolism, and excretion (ADME) properties. Following oral administration of Epmedin C at doses of 10-50 mg/kg in rats, the compound is absorbed with a time to reach maximum plasma concentration (Tmax) of approximately 1-3 hours, indicating moderate to rapid absorption. The maximum plasma concentration (Cmax) ranges from 0.5 to 5 µg/mL, depending on the dose administered. The oral bioavailability of Epmedin C is relatively low, estimated at 5-15%, due to extensive first-pass metabolism in the liver and intestine, as well as poor membrane permeability associated with the glycosylated structure. Upon absorption, Epmedin C is extensively metabolized via deglycosylation, yielding the aglycone (which may be further metabolized to icaritin and other derivatives), dehydrogenation, hydroxylation, and conjugation reactions (glucuronidation and sulfation). The major metabolites detected in plasma and urine include desugarized, dehydrogenated, hydrogenated, dehydroxylated, 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 Epmedin C in plasma is approximately 2-4 hours, and the compound is primarily excreted in the urine and feces as metabolites. The compound exhibits good stability when stored as a powder at 2-8°C or -20°C, protected from light and moisture. For in vivo administration, Epmedin C can be formulated in 0.5% CMC, saline, or other suitable vehicles, with sonication or heating to enhance solubility. Further studies are needed to fully characterize the pharmacokinetic profile of Epmedin C in different species and to investigate potential drug-drug interactions involving cytochrome P450 enzymes and drug transporters.
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| Toxicity/Toxicokinetics |
Toxicological data for Epmedin C are limited but generally indicate a favorable safety profile at pharmacologically relevant doses. In acute toxicity studies in mice, the oral LD₅₀ of Epmedin C has been estimated to be greater than 2000 mg/kg, indicating low acute toxicity. In subacute toxicity studies, mice administered Epmedin C at doses of 10-100 mg/kg/day for 28 days showed no significant changes in body weight, organ weights, hematological parameters (complete blood count), or serum biochemical parameters (ALT, AST, BUN, creatinine, glucose, total protein, albumin), compared to vehicle controls. Histopathological examination of major organs (liver, kidneys, heart, lungs, spleen, thymus, and reproductive organs) revealed no treatment-related abnormalities. No significant genotoxicity was observed in the Ames test (with or without metabolic activation) or in the mouse micronucleus assay at doses up to 500 mg/kg. However, at very high doses (≥200 mg/kg), mild gastrointestinal disturbances, including soft stools and reduced appetite, have been reported, likely due to the osmotic effects of the glycosylated compound in the intestinal lumen. As a flavonoid glycoside, Epmedin C may exhibit estrogenic activity at high concentrations, which could theoretically lead to hormone-related adverse effects in sensitive individuals, 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, including the use of gloves, lab coats, and safety glasses, should be followed when handling Epmedin C.
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| References | |
| Additional Infomation |
Epimedin C belongs to the flavonoid and glycoside classes. It has been reported that Epimedin C is found in Epimedium brevicornu, Epimedium truncatum, and other organisms with relevant data.
Epmedin C is a research-use only compound and has not been approved for clinical applications by any regulatory authority. It is also known as 淫羊霍定C in Chinese and is one of the major bioactive flavonoid glycosides isolated from plants of the Epimedium genus, including Epimedium brevicornum, Epimedium sagittatum, and Epimedium koreanum. 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 C₃₉H₅₀O₁₉ and a molecular weight of 822.80 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 ≥95% (HPLC). Epmedin C 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, oncology, and traditional medicine, and ongoing studies continue to explore its mechanisms of action, therapeutic potential, and safety profile. 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 |
C₃₉H₅₀O₁₉
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|---|---|
| Molecular Weight |
822.80
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| Exact Mass |
822.294
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| CAS # |
110642-44-9
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| PubChem CID |
5748394
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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 |
1062.1±65.0 °C at 760 mmHg
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| Melting Point |
147 °C(dec.)
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| Flash Point |
322.2±27.8 °C
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| Vapour Pressure |
0.0±0.3 mmHg at 25°C
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| Index of Refraction |
1.678
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| LogP |
3.19
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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 |
58
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| Complexity |
1450
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| Defined Atom Stereocenter Count |
15
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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=C(OC4=C(C3=O)C(=CC(=C4CC=C(C)C)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO)O)O)O)O)C6=CC=C(C=C6)OC)C)O)O)O)O)O
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| InChi Key |
ULZLIYVOYYQJRO-JIYCBSMMSA-N
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| InChi Code |
InChI=1S/C39H50O19/c1-14(2)6-11-19-21(54-38-32(50)29(47)26(44)22(13-40)55-38)12-20(41)23-27(45)35(33(56-34(19)23)17-7-9-18(51-5)10-8-17)57-39-36(30(48)25(43)16(4)53-39)58-37-31(49)28(46)24(42)15(3)52-37/h6-10,12,15-16,22,24-26,28-32,36-44,46-50H,11,13H2,1-5H3/t15-,16-,22+,24-,25-,26+,28+,29-,30+,31+,32+,36+,37-,38+,39-/m0/s1
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| Chemical Name |
3-(((2S,3R,4R,5R,6S)-4,5-dihydroxy-6-methyl-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-(4-methoxyphenyl)-8-(3-methylbut-2-en-1-yl)-7-(((2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl)oxy)-4H-chromen-4-one
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| Synonyms |
Baohuoside-VI Epimedin-CBaohuoside VI
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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 : ~250 mg/mL (~303.84 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (2.53 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 (2.53 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.2154 mL | 6.0768 mL | 12.1536 mL | |
| 5 mM | 0.2431 mL | 1.2154 mL | 2.4307 mL | |
| 10 mM | 0.1215 mL | 0.6077 mL | 1.2154 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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