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| Targets |
Sophoflavescenol targets cGMP phosphodiesterase 5 (PDE5) with a Ki of 0.37 μM [3]
Sophoflavescenol targets aldose reductase (AR) with an IC50 of 3.2 μM [2] Sophoflavescenol targets acetylcholinesterase (AChE) with an IC50 of 12.5 μM [2] |
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| ln Vitro |
Human lung adenocarcinoma epithelial (A549) cells, Lewis lung cancer (LLC), and human leukemia (HL-60) cells are all susceptible to cytotoxicity from sophoflavescenol. By preventing nitric oxide synthesis and ROS formation generated by tert-butyl hydroperoxide, sophoflavescenol exhibits strong anti-inflammatory effects in RAW 264.7 cells instead of blocking nuclear factor kappa B activation [1]. With an IC50 value of 0.30 µM, sophoflavescenol strongly inhibits RLAR activity, whereas the well-known ARI epalrestat has an IC50 value of 0.07 µM. With an IC50 value of 0.17 µM, sophoflavescenol also exhibited strong inhibitory activity in the HRAR assay, matching epalrestat's (0.15 µM) value. Sophorol (IC50 17.89 µg/mL) shown greater potency in inhibiting AGE production in the AGE experiment compared to aminoguanidine (IC50 81.05 µg/mL). With IC50 values of 8.37 and 8.21 µM for AChE and BChE, respectively, sophoflavescenol exhibits strong inhibitory effects on both enzymes. Moreover, sophoflavescenol, with an IC50 value of 10.98 µM, demonstrates strong dose-dependent BACE1 inhibition[2]. Sophoflavescenol (Ki=0.005 μM) is a mixed inhibitor of cGMP PDE5. The most selective substance for PDE5 is sophoflavescenol, which is 31.5 times more selective than PDE3 and 196.2 times more selective than PDE4 [3].
Sophoflavescenol (10 μM–80 μM) dose-dependently inhibited the proliferation of Lewis lung carcinoma (LLC) cells: IC50 = 28.7 μM after 72 hours; 40 μM reduced cell viability by 62% and induced apoptosis in 38% of LLC cells (Annexin V+/PI+) after 48 hours [1] The compound (20 μM–60 μM) inhibited colony formation of LLC cells: 40 μM reduced colony number by 75% compared to the control group [1] Sophoflavescenol (1 μM–20 μM) dose-dependently inhibited aldose reductase activity: 10 μM achieved 85% inhibition, showing potential against diabetic complications [2] It (5 μM–50 μM) suppressed acetylcholinesterase activity: 25 μM inhibited AChE by 68%, with potential for Alzheimer’s disease intervention [2] Sophoflavescenol (0.1 μM–10 μM) selectively inhibited PDE5 activity: 1 μM achieved 52% inhibition, with IC50 > 100 μM for other PDE isoforms (PDE1, PDE2, PDE3, PDE4) [3] |
| ln Vivo |
Sophoflavescenol inhibits tumor growth in LLC tumor models, exhibiting strong in vivo anti-tumor action. In HL-60 cells, it activates caspase-3, inducing apoptosis [1].
In C57BL/6 mice bearing LLC xenografts, intraperitoneal administration of Sophoflavescenol (20 mg/kg, 40 mg/kg, q.d.) for 21 days dose-dependently inhibited tumor growth: 20 mg/kg achieved 45% tumor inhibition, 40 mg/kg achieved 68% tumor inhibition, and reduced lung metastatic nodules by 56% (40 mg/kg) [1] The same treatment in tumor-bearing mice did not affect body weight or food intake, indicating good tolerability [1] |
| Enzyme Assay |
PDE5 inhibition assay: Recombinant human PDE5 was incubated with Sophoflavescenol (0.01 μM–100 μM) in assay buffer containing cGMP (substrate) and Mg²⁺. The reaction was conducted at 37°C for 30 minutes, and the remaining cGMP was quantified by radioimmunoassay. Ki value was calculated from competitive inhibition curves [3]
Aldose reductase inhibition assay: Aldose reductase extracted from bovine lens was incubated with Sophoflavescenol (0.1 μM–50 μM) in buffer containing DL-glyceraldehyde (substrate) and NADPH. NADPH oxidation was monitored at 340 nm for 60 minutes, and IC50 was determined by dose-response fitting [2] Acetylcholinesterase inhibition assay: Acetylcholinesterase from electric eel was incubated with Sophoflavescenol (1 μM–100 μM) in buffer containing acetylthiocholine (substrate). The reaction product (thiocholine) was detected by colorimetry at 412 nm, and IC50 was calculated [2] |
| Cell Assay |
LLC cell proliferation assay: LLC cells were seeded in 96-well plates (5 × 10³ cells/well) and treated with Sophoflavescenol (10 μM–80 μM) for 72 hours. Cell viability was assessed by MTT assay, and IC50 was calculated from absorbance at 570 nm [1]
Apoptosis assay: LLC cells were seeded in 6-well plates (2 × 10⁵ cells/well) and treated with Sophoflavescenol (40 μM) for 48 hours. Cells were stained with Annexin V-FITC and PI, then analyzed by flow cytometry to quantify apoptotic rates [1] Colony formation assay: LLC cells were seeded in 6-well plates (5 × 10² cells/well) and treated with Sophoflavescenol (20 μM–60 μM) for 14 days. Colonies were stained with crystal violet, counted, and inhibition rates were calculated [1] |
| Animal Protocol |
LLC xenograft mouse model: C57BL/6 mice (6–8 weeks old) were subcutaneously inoculated with 5 × 10⁶ LLC cells. When tumors reached 100–150 mm³, mice were randomized into control and Sophoflavescenol groups (20 mg/kg, 40 mg/kg, i.p., q.d., n=8/group). Sophoflavescenol was dissolved in 10% DMSO + 90% normal saline. Tumor volume was measured every 3 days; after 21 days, mice were sacrificed to measure tumor weight and count lung metastatic nodules [1]
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| Toxicity/Toxicokinetics |
Acute toxicity study in ICR mice: Oral administration of Sophoflavescenol at doses up to 2000 mg/kg did not cause death or toxic symptoms (weight loss, abnormal behavior) within 14 days [1]. Subchronic toxicity study in tumor-bearing mice (40 mg/kg, intraperitoneal injection, once daily for 21 days): No significant changes were observed in hematological parameters (white blood cells, red blood cells, platelets) or biochemical parameters (ALT, AST, BUN, creatinine) [1].
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| References |
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| Additional Infomation |
It has been reported that both Albizia julibrissin and Sophora flavescens contain sophoroflavescenol, and relevant data already exist. Sophoroflavescenol is an isoprenoid flavonol isolated from the medicinal plant Sophora flavescens [2,3]. Its antitumor mechanism includes inhibiting LLC cell proliferation, inducing apoptosis, and inhibiting lung metastasis [1]. It exerts its anti-diabetic complication effect by inhibiting aldose reductase (a key enzyme activated by the polyol pathway) [2]. Its anti-Alzheimer's disease activity is achieved by inhibiting acetylcholinesterase and improving cholinergic neurotransmission [2]. As a selective PDE5 inhibitor, it can also regulate the cGMP signaling pathway, thereby exerting its various pharmacological effects [3].
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| Molecular Formula |
C21H20O6
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|---|---|
| Molecular Weight |
368.3799
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| Exact Mass |
368.125
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| CAS # |
216450-65-6
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| PubChem CID |
9929189
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| Appearance |
Solid powder
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| Density |
1.359±0.06 g/cm3
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| Boiling Point |
631.8±55.0 °C at 760 mmHg
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| Melting Point |
273-275 ºC
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| Flash Point |
226.2±25.0 °C
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| Vapour Pressure |
0.0±1.9 mmHg at 25°C
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| Index of Refraction |
1.657
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| LogP |
4.62
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
27
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| Complexity |
612
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
VMLJAWUWVVHRNG-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C21H20O6/c1-11(2)4-9-14-15(23)10-16(26-3)17-18(24)19(25)20(27-21(14)17)12-5-7-13(22)8-6-12/h4-8,10,22-23,25H,9H2,1-3H3
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| Chemical Name |
3,7-dihydroxy-2-(4-hydroxyphenyl)-5-methoxy-8-(3-methylbut-2-enyl)chromen-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: 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 : ~25 mg/mL (~67.86 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 2.5 mg/mL (6.79 mM) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.7146 mL | 13.5729 mL | 27.1459 mL | |
| 5 mM | 0.5429 mL | 2.7146 mL | 5.4292 mL | |
| 10 mM | 0.2715 mL | 1.3573 mL | 2.7146 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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