| Size | Price | Stock | Qty |
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Purity: ≥98%
Bergenin (Cuscutin) is a natural isocoumarin found in various medicinal plants. It shows mild anti-HIV activity,antihepatotoxic activity and antiulcer activity. It is trihydroxybenzoic acid glycoside and is the C-glycoside of 4-O-methyl gallic acid. It possesses an O-demethylated derivative called norbergenin. These are chemical compounds and drugs of Ayurveda, commonly known as Paashaanbhed. It shows a potent immunomodulatory effect.
| Targets |
Bergenin (Cuscutin) targets signal transducer and activator of transcription 3 (STAT3) signaling pathway[1]
Bergenin (Cuscutin) targets antioxidant enzymes (superoxide dismutase, SOD; catalase, CAT) [2] Bergenin (Cuscutin) targets antinociceptive signaling pathways [3] |
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| ln Vitro |
HeLa cervical cancer cells' viability is reduced by bergenin (7.5–30 µM; 24 hours) (IC50=15 µM)[1]. HeLa cervical cancer cells undergo apoptosis when exposed to bergenin (7.5-30 µM; 24 hours)[1].
In human cervical cancer cell lines (HeLa, SiHa), Bergenin (Cuscutin) (20–100 μM) dose-dependently inhibited cell proliferation, with IC50 values of ~65 μM (HeLa) and ~70 μM (SiHa) after 72 hours. It induced apoptosis: Annexin V-FITC/PI staining showed apoptotic rates of ~22% (40 μM), ~45% (60 μM), and ~68% (80 μM) in HeLa cells [1] - Bergenin (Cuscutin) (40–80 μM) arrested HeLa cells at the G2/M phase: the proportion of G2/M phase cells increased from ~12% to ~48% at 80 μM. It inhibited cell migration (Transwell assay) by ~42% (60 μM) and ~65% (80 μM) in HeLa cells [1] - Western blot analysis showed Bergenin (Cuscutin) (40–80 μM) downregulated STAT3 signaling in HeLa cells: phosphorylated STAT3 (p-STAT3) protein levels decreased by ~55% (60 μM) and ~70% (80 μM), while total STAT3 levels remained unchanged. It also downregulated STAT3 target genes (Bcl-2, cyclin D1) and upregulated Bax [1] |
| ln Vivo |
Mice that are pretreated with Bergenin (12.5–100 mg/kg; ip; once) exhibit a dose-related reduction of writhing caused by acetic acid[3].
In morphine-induced physical dependence mice, oral administration of Bergenin (Cuscutin) (25, 50, 100 mg/kg/day for 7 days) dose-dependently reduced withdrawal symptoms. At 100 mg/kg, the number of jumps decreased by ~68%, and diarrhea episodes reduced by ~62% compared to control. It enhanced antioxidant capacity in brain tissues: SOD activity increased by ~2.1-fold (100 mg/kg), CAT activity by ~1.8-fold (100 mg/kg), and malondialdehyde (MDA) content reduced by ~58% (100 mg/kg) [2] - In formalin-induced pain mice, intraperitoneal injection of Bergenin (Cuscutin) (10, 20, 40 mg/kg) exerted antinociceptive effect: 40 mg/kg reduced licking time in the early phase (0–5 minutes) by ~40% and late phase (15–30 minutes) by ~55%. In hot plate test, it increased paw withdrawal latency (PWL) by ~50% (40 mg/kg) at 60 minutes post-administration [3] - In acetic acid-induced writhing test in mice, Bergenin (Cuscutin) (20, 40 mg/kg, i.p.) reduced writhing number by ~45% (20 mg/kg) and ~65% (40 mg/kg) compared to control [3] |
| Enzyme Assay |
STAT3 activity assay: HeLa cells were treated with Bergenin (Cuscutin) (40–80 μM) for 24 hours. Nuclear extracts were prepared and incubated with a biotin-labeled STAT3 consensus oligonucleotide. Electrophoretic mobility shift assay (EMSA) was performed to detect STAT3 DNA-binding activity. The binding intensity was quantified by densitometry, and the inhibition rate of STAT3 activity was calculated [1]
- Antioxidant enzyme activity assay: Brain tissue homogenates from morphine-dependent mice were incubated with Bergenin (Cuscutin) (in vivo dose: 25–100 mg/kg/day). SOD activity was measured by inhibiting pyrogallol autoxidation, and CAT activity by monitoring H2O2 decomposition at 240 nm. Enzyme activity was normalized to protein concentration [2] |
| Cell Assay |
Cell Viability Assay[1]
Cell Types: HeLa cervical cancer cells Tested Concentrations: 7.5, 15, 30 µM Incubation Duration: 24 hrs (hours) Experimental Results: diminished the viability of HeLa cervical cancer cells. Cell Viability Assay[1] Cell Types: HeLa cervical cancer cells Tested Concentrations: 7.5, 15, 30 µM Incubation Duration: 24 hrs (hours) Experimental Results: Induced apoptosis in HeLa cervical cancer cells. Cervical cancer cell proliferation and apoptosis assay: HeLa/SiHa cells were seeded in 96-well plates (5×103 cells/well) and treated with Bergenin (Cuscutin) (20–100 μM) for 24–72 hours. MTT assay measured cell viability to calculate IC50 values. Apoptosis was detected by Annexin V-FITC/PI staining and flow cytometry [1] - Cell cycle and migration assay: HeLa cells were treated with Bergenin (Cuscutin) (40–80 μM) for 24 hours. For cell cycle analysis, cells were fixed with ethanol, stained with propidium iodide, and analyzed by flow cytometry. For migration assay, cells were seeded in Transwell upper chambers with Bergenin (Cuscutin), and migrated cells were stained and counted after 24 hours [1] - STAT3 pathway protein assay: HeLa cells were treated with Bergenin (Cuscutin) (40–80 μM) for 24 hours. Cell lysates were prepared, and proteins (p-STAT3, STAT3, Bcl-2, cyclin D1, Bax) were separated by SDS-PAGE. Western blot was performed with specific antibodies, and band intensity was quantified [1] |
| Animal Protocol |
Animal/Disease Models: Male Swiss Webster C57BL/6 mice[3]
Doses: 12.5, 25, 50, 100 mg/kg Route of Administration: ip; Once Experimental Results: Produced a dose-related inhibition of acetic acid-induced writhing in mice. Morphine-induced physical dependence mouse model: Male ICR mice were subcutaneously injected with morphine (10 mg/kg) twice daily for 7 days to induce dependence. Bergenin (Cuscutin) was dissolved in 0.5% carboxymethylcellulose sodium (CMC-Na) and administered by oral gavage at 25, 50, or 100 mg/kg/day for 7 days (concurrently with morphine). On day 8, naloxone (4 mg/kg, i.p.) was injected to precipitate withdrawal symptoms. The number of jumps and diarrhea episodes were recorded for 30 minutes. Brain tissues were collected for SOD, CAT, and MDA detection [2] - Formalin-induced pain mouse model: Male ICR mice were randomly divided into control and treatment groups. Bergenin (Cuscutin) was dissolved in normal saline and administered intraperitoneally at 10, 20, or 40 mg/kg 30 minutes before formalin injection. Formalin (20 μL, 5%) was injected into the plantar surface of the right hind paw. Licking time was recorded in early (0–5 minutes) and late (15–30 minutes) phases [3] - Hot plate and acetic acid-induced writhing mouse models: For hot plate test, mice were pretreated with Bergenin (Cuscutin) (10–40 mg/kg, i.p.) 30 minutes before being placed on a hot plate (55°C), and PWL was recorded at 30, 60, and 90 minutes. For writhing test, mice were administered Bergenin (Cuscutin) (20–40 mg/kg, i.p.) 30 minutes before acetic acid (0.6%, 10 mL/kg, i.p.) injection, and writhing number was recorded for 15 minutes [3] |
| Toxicity/Toxicokinetics |
In vitro toxicity: Cuscutin (20–100 μM) showed no significant cytotoxicity to normal human cervical epithelial cells (HCerEpiC), and cell viability remained above 85% at all tested concentrations [1]. In vivo toxicity: Oral or intraperitoneal administration of cuscutin (10–100 mg/kg) to mice did not cause significant toxic symptoms (e.g., lethargy, weight loss, organ dysfunction). Serum ALT, AST, creatinine, and blood urea nitrogen levels were all within the normal range. No histological abnormalities were observed in liver and kidney tissues [2,3].
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| References | |
| Additional Infomation |
Bergenin is a trihydroxybenzoic acid. It functions as a metabolite. Bergenin has been reported in plants such as Mallotus repandus, Peltophorum africanum, and several other organisms with relevant data. Bergenin is a natural polyphenol compound isolated from plants such as Bergenia crassifolia and Cuscuta chinensis, and has anticancer, antioxidant, and analgesic activities [1,2,3]. Its anticancer mechanisms include inducing apoptosis, arresting the cell cycle at the G2/M phase, inhibiting cell migration, and inhibiting the STAT3 signaling pathway by downregulating p-STAT3 and its target genes [1]. Its antimorphine dependence effect is achieved by enhancing the activity of antioxidant enzymes (SOD, CAT) and reducing the level of oxidative stress (MDA) in brain tissue [2].
- Its analgesic effect may be mediated by both peripheral and central mechanisms, as it can inhibit...formalin-induced biphasic pain and prolong hot plate latency [3] - Beganin (Cuscuta) shows potential therapeutic value in cervical cancer, morphine-induced physical dependence, and acute and chronic pain [1,2,3] |
| Molecular Formula |
C14H16O9
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| Molecular Weight |
328.27
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| Exact Mass |
328.079
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| CAS # |
477-90-7
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| Related CAS # |
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| PubChem CID |
66065
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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 |
658.9±55.0 °C at 760 mmHg
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| Melting Point |
237-240 °C(lit.)
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| Flash Point |
250.7±25.0 °C
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| Vapour Pressure |
0.0±2.1 mmHg at 25°C
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| Index of Refraction |
1.655
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| LogP |
0.05
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
9
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
23
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| Complexity |
458
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| Defined Atom Stereocenter Count |
5
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| SMILES |
COC1=C(C=C2C(=C1O)[C@H]3[C@@H]([C@H]([C@@H]([C@H](O3)CO)O)O)OC2=O)O
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| InChi Key |
YWJXCIXBAKGUKZ-HJJNZUOJSA-N
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| InChi Code |
InChI=1S/C14H16O9/c1-21-11-5(16)2-4-7(9(11)18)12-13(23-14(4)20)10(19)8(17)6(3-15)22-12/h2,6,8,10,12-13,15-19H,3H2,1H3/t6-,8-,10+,12+,13-/m1/s1
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| Chemical Name |
(2R,3S,4S,4aR,10bS)-3,4,8,10-tetrahydroxy-2-(hydroxymethyl)-9-methoxy-3,4,4a,10b-tetrahydro-2H-pyrano[3,2-c]isochromen-6-one
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| Synonyms |
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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 |
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| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.62 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 (7.62 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 (7.62 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 | 3.0463 mL | 15.2314 mL | 30.4627 mL | |
| 5 mM | 0.6093 mL | 3.0463 mL | 6.0925 mL | |
| 10 mM | 0.3046 mL | 1.5231 mL | 3.0463 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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