| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| Other Sizes |
| Targets |
Estrogen receptor α (ERα) and estrogen receptor β (ERβ): activates ER‑dependent transcription in transfected cells [1].
α‑glucosidase: IC50 = 48.13 ± 1.5 μg/mL [4]. α‑amylase: IC50 = 153.31 ± 1.5 μg/mL [4]. Influenza A/PR/8/34 (H1N1): CPE inhibition IC50 = 18.7 μM [2]. Other influenza strains (CPE inhibition): A/PR/8/34 (H1N1) IC50 = 24.5±4.5 μM, A/FM/1/47 (H1N1) IC50 = 39.8±11.5 μM, A/Aichi/2/68 (H3N2) IC50 = 16.3±2.3 μM, B/Lee/1940 IC50 = 13.4±4.1 μM [2]. Plaque reduction assay (H1N1, H3N2): IC50 values 19.0–29.8 μM [2]. |
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| ln Vitro |
In HeLa cells co‑transfected with ERE‑luciferase and ERα/ERβ, Pinoresinol 4-O-glucoside (10⁻⁷–10⁻⁴ M) increased luciferase activity; this was suppressed by ICI 182,780 (10⁻⁷ M) [1].
In MCF‑7 cells, it induced pS2 mRNA expression (dose‑dependent, 24 h), blocked by 0.1 μM ICI 182,780 [1]. In MCF‑7 cells (ERα+), it enhanced proliferation: RPE = 151±6.19% (10⁻⁶ M), 140±9.42% (10⁻⁵ M), 139±8.11% (10⁻⁴ M); effect blocked by 10⁻⁵ M ICI [1]. In MDA‑MB‑231 cells (ERα–), it inhibited proliferation at 10⁻⁴ M (RPE = 86.8±2.68%), not blocked by ICI [1]. Induced ERα nuclear translocation in MCF‑7 cells (immunofluorescence) [1]. Antioxidant: ABTS radical scavenging IC50 = 34.5±5.9 μg/mL, TAC = 1091.3±18.43 μmol/g ascorbic acid equivalents; FRAP TAC = 418.47±0.54 μmol/g ascorbic acid equivalents [4]. Anti‑influenza (CPE): inhibited human strains but not avian (IC50 >138.1 μM for H6N2, H7N3, H9N2) [2]. Anti‑influenza (plaque reduction): reduced plaques on MDCK cells [2]. Time‑of‑addition (A/PR/8/34 H1N1, MDCK): Pinoresinol 4-O-glucoside (134.3 μM) reduced viral titers at 0‑4 h post‑infection (CPE and real‑time PCR) [2]. In A549 cells infected with H1N1, it inhibited virus‑induced NF‑κB activation (37.5‑150 μM, dose‑dependent) and blocked nuclear translocation of p65 [2]. Blocked nuclear export of viral ribonucleoprotein (RNP) complexes in infected A549 cells [2][4]. |
| ln Vivo |
In male Swiss albino mice with CCl₄‑induced hepatotoxicity, oral Pinoresinol 4-O-glucoside (50 mg/kg b.w., 20 days) lowered serum AST (‑33.94%), ALT (‑3.01%), and lipid peroxides (‑49.96%); raised CAT (+130%), SOD (+90.45%), and TAS (+61.39%) versus CCl₄ control [4].
In STZ‑induced diabetic mice, oral Pinoresinol 4-O-glucoside (50 mg/kg b.w., 10 days) lowered serum glucose (‑37.83%), raised insulin (+25.37%), reduced lipid peroxides (‑51.77%), and increased CAT (+93.02%), SOD (+70.79%), TAS (+101.90%) [4]. |
| Enzyme Assay |
α‑Glucosidase inhibition: measured colorimetrically at 405 nm using a microplate reader; % inhibition = (A405 control – A405 sample) × 100; IC50 determined graphically [4].
α‑Amylase inhibition: calorimetric assay at 405 nm; % inhibition = (Abs control – Abs sample) × 100 [4]. Western blot for NF‑κB/ERK: A549 cells lysed, protein quantified, separated by SDS‑PAGE, transferred to PVDF, blocked, probed with anti‑phospho‑NF‑κB p65, anti‑NF‑κB p65, anti‑phospho‑ERK1/2, anti‑ERK1/2, then HRP‑secondary antibodies and chemiluminescence [2]. |
| Cell Assay |
Transient transfection and reporter assay: HeLa cells in 24‑well plates with CD‑FBS, co‑transfected with ERE‑TK‑Luc, ERα/β expression vectors, and pRL‑TK (control) using lipofectamine; after 18 h treated with compound for 24 h; lysates measured for luciferase and Renilla activity [1].
pS2 mRNA expression: MCF‑7 cells in phenol red‑free DMEM + 3% CD‑FBS, treated 24 h, RNA purified with TRIzol, DNase I treated, cDNA synthesized, qPCR with SYBR Green for pS2 and GAPDH; data by comparative Ct method [1]. Cell proliferation (MTT): Cells seeded in 24‑well plates (5% FBS), next day medium replaced with 1% CD‑FBS + compound, incubated 5 days (medium changed every 2 days), MTT added, OD at 570 nm [1]. Immunofluorescence (ERα): MCF‑7 on coverslips fixed in 4% paraformaldehyde, blocked with BSA, rabbit anti‑ERα primary, TRITC‑labelled anti‑rabbit secondary, nuclei stained with propidium iodide, confocal microscopy [1]. Indirect immunofluorescence (NF‑κB, RNP): A549 on coverslips infected with H1N1, treated with compound, fixed, permeabilized, blocked, incubated with anti‑phospho‑NF‑κB p65 or anti‑viral NP, FITC‑labelled secondary, DAPI nuclear stain, fluorescence microscopy [2]. |
| Animal Protocol |
Hepatoprotective study: Male Swiss albino mice (27‑30 g) divided into 4 groups (n=10). Group 1: normal saline. Group 2: CCl₄ (1 ml/kg in paraffin oil). Group 3: CCl₄ + oral silymarin (50 mg/kg) for 20 days. Group 4: CCl₄ + oral Pinoresinol 4-O-glucoside (50 mg/kg) for 20 days. Blood collected from optical vein on final day, serum separated [4].
Antihyperglycaemic study: Diabetes induced by single i.p. STZ (60 mg/kg) in citrate buffer (pH 4.5). Groups (n=10): normal control (citrate buffer), diabetic control (STZ), positive control (STZ + oral glibenclamide 5 mg/kg for 10 days), test (STZ + oral Pinoresinol 4-O-glucoside 50 mg/kg for 10 days). Blood collected on day 11 [4]. Pharmacokinetic study in rats: Male Sprague‑Dawley rats (220‑240 g) fasted 12 h, then orally given E. ulmoides extract (4.8 g/kg equivalent to 49.92 mg/kg of Pinoresinol 4-O-glucoside in saline). Blood from caudal vein at 0, 0.083, 0.25, 0.5, 0.75, 1, 2, 3.5, 5, 7, 9, 11, 13, 24, 30 h post‑dose. Plasma separated and stored at ‑20°C [5]. |
| ADME/Pharmacokinetics |
Pharmacokinetics in rats after oral administration of E. ulmoides extract (dose of Pinoresinol 4-O-glucoside = 49.92 mg/kg) [5]:
Cmax = 143.42 ± 20.31 μg/L [5]. Tmax = 0.54 ± 0.10 h [5]. t₁/₂ = 2.75 ± 0.76 h [5]. AUC₀₋ₜ = 143.70 ± 24.91 μg/L·h [5]. CLz/F = 9221.89 ± 2829.47 μg/L·h [5]. Vz/F = 36336.10 ± 12884.54 μg/L·h [5]. |
| References |
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| Additional Infomation |
(+)-Pinoresinol 4-O-glucoside is a lignan and glycoside. (2S,3R,4S,5S,6R)-2-[4-[(3S,3aR,6S,6aR)-3-(4-hydroxy-3-methoxyphenyl)-1,3,3a,4,6,6a-hexahydrofurano[3,4-c]furan-6-yl]-2-methoxyphenoxy]-6-(hydroxymethyl)oxacyclohexane-3,4,5-triol has been reported in Ipomoea purpurea, Daphne odora, and other organisms with available data.
Biotechnological production: The endophytic fungus Phomopsis sp. XP‑8 produces Pinoresinol 4-O-glucoside (PMG). In mung bean polysaccharide medium (35 g/L) with fungal cells (100 g/L), PMG reached 5.60 mg/L after 56 h; production is induced by arabinose and galactose. A defined monosaccharide mixture (glucose 10 g/L, arabinose 5 g/L, galactose 6 g/L, xylose 8 g/L, mannose 2 g/L) gave 5.9 mg/L PMG after 56 h [6]. Selective estrogen receptor modulation: Pinoresinol 4-O-glucoside is one of several phytoestrogens from Eucommia ulmoides acting as a SERM [1]. Anti‑inflammatory activity: It inhibits NF‑κB activation and contributes to anti‑influenza effects [2][4]. |
| Molecular Formula |
C26H32O11
|
|---|---|
| Molecular Weight |
520.5257
|
| Exact Mass |
520.194
|
| CAS # |
69251-96-3
|
| PubChem CID |
486614
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| Appearance |
White to light yellow solid
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| Density |
1.4±0.1 g/cm3
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| Boiling Point |
752.5±60.0 °C at 760 mmHg
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| Flash Point |
408.9±32.9 °C
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| Vapour Pressure |
0.0±2.6 mmHg at 25°C
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| Index of Refraction |
1.619
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| LogP |
-0.69
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
11
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
37
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| Complexity |
741
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| Defined Atom Stereocenter Count |
9
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| SMILES |
O1C([H])([H])[C@@]2([H])[C@@]([H])(C3C([H])=C([H])C(=C(C=3[H])OC([H])([H])[H])O[H])OC([H])([H])[C@]2([H])[C@]1([H])C1C([H])=C([H])C(=C(C=1[H])OC([H])([H])[H])O[C@]1([H])[C@@]([H])([C@@]([H])([C@@]([H])([C@@]([H])(C([H])([H])O[H])O1)O[H])O[H])O[H]
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| InChi Key |
QLJNETOQFQXTLI-WMYFGKAISA-N
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| InChi Code |
InChI=1S/C26H32O11/c1-32-18-7-12(3-5-16(18)28)24-14-10-35-25(15(14)11-34-24)13-4-6-17(19(8-13)33-2)36-26-23(31)22(30)21(29)20(9-27)37-26/h3-8,14-15,20-31H,9-11H2,1-2H3/t14-,15-,20+,21+,22-,23+,24+,25+,26+/m0/s1
|
| Chemical Name |
(2S,3R,4S,5S,6R)-2-[4-[(3S,3aR,6S,6aR)-3-(4-hydroxy-3-methoxyphenyl)-1,3,3a,4,6,6a-hexahydrofuro[3,4-c]furan-6-yl]-2-methoxyphenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol
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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: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| 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 (~192.11 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.80 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 (4.80 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 (4.80 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 | 1.9211 mL | 9.6056 mL | 19.2112 mL | |
| 5 mM | 0.3842 mL | 1.9211 mL | 3.8422 mL | |
| 10 mM | 0.1921 mL | 0.9606 mL | 1.9211 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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