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Purity: ≥98%
Diosgenin is a plant steroidal sapogenin which induces apoptosis in colon cancer cell lines and induces apoptosis,cell cycle arrest and COX activity in osteosarcoma cells. It is a steroid sapogenin used in the semi-synthesis of pregnenolone, cortisone, and progesterone. Diosgenin has estrogenic activity and can reduce the level of serum cholesterol.
| Targets |
STAT3 [1]
- 1,25D₃-MARRS/Pdia3/ERp57 [2] - Acetylcholinesterase (AChE), Butyrylcholinesterase (BuChE), Aβ aggregation-related targets [3] - ERβ, PPARγ [4] - miR-19b, ATP-binding Cassette Transporter A1 (ABCA1) [5] |
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| ln Vitro |
Diosgenin demonstrated a modest protective ability at 1 μM in MC65 cells, an AD cell model, and could be a promising option for a bivalent molecule functioning as a steroid moiety to combat AD pathogenesis [3]. Constitutive activation of STAT3 in C3A cells is dose-dependently inhibited, reaching a maximum at approximately 100 μM [1]. The level of miR-19b in foam cells is dramatically decreased by diosgenin (10 μM; 24 h) [5].
Treatment of human hepatocellular carcinoma cells (HepG2, Huh7, Hep3B) with Diosgenin inhibited cell proliferation in a dose-dependent manner, induced G0/G1 cell cycle arrest, and promoted apoptosis. It suppressed STAT3 phosphorylation (Tyr705) and nuclear translocation, downregulated STAT3 downstream target genes (Bcl-2, Cyclin D1, Survivin), and enhanced chemosensitivity to doxorubicin and 5-fluorouracil [1] - Diosgenin acted as an exogenous activator of 1,25D₃-MARRS/Pdia3/ERp57, reduced amyloid-β (Aβ) aggregation, and decreased tau protein phosphorylation in neuronal cells. It also inhibited Aβ-induced neurotoxicity and reactive oxygen species (ROS) production [2] - As a component of bivalent ligands, Diosgenin exhibited inhibitory activity against AChE and BuChE, suppressed Aβ1-42 aggregation, and promoted disaggregation of preformed Aβ fibrils. It also protected neuronal cells from Aβ-induced cytotoxicity [3] - In 3T3-L1 preadipocytes, Diosgenin inhibited adipocyte differentiation by downregulating PPARγ expression and its target genes (aP2, C/EBPα). This effect was mediated through activation of ERβ, as ERβ knockdown reversed the inhibitory role of Diosgenin on PPARγ [4] - Diosgenin upregulated ABCA1 expression in THP-1 macrophage-derived foam cells, promoted cholesterol efflux to apolipoprotein A-I, and reduced intracellular cholesterol accumulation. It suppressed miR-19b expression, and miR-19b overexpression abrogated the Diosgenin-induced upregulation of ABCA1 [5] |
| ln Vivo |
In the IPGTT experiment, diosgenin exhibited a substantial reduction in hypertension when compared to HF diet feeding [4].
In 5XFAD transgenic mice (Alzheimer’s disease model), oral administration of Diosgenin significantly reduced Aβ deposition in the cerebral cortex and hippocampus, decreased tau hyperphosphorylation, and improved spatial learning and memory abilities. It also upregulated 1,25D₃-MARRS/Pdia3/ERp57 expression in brain tissues [2] - In ApoE-/- mice (atherosclerosis model), Diosgenin treatment reduced aortic atherosclerotic plaque area, decreased serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels, and increased high-density lipoprotein cholesterol. It upregulated ABCA1 expression and downregulated miR-19b in aortic tissues and peritoneal macrophages [5] |
| Enzyme Assay |
AChE/BuChE activity assay: Recombinant AChE/BuChE was incubated with different concentrations of Diosgenin (or bivalent ligands containing Diosgenin) and specific substrates. The hydrolysis product was detected by spectrophotometry, and enzyme inhibition rates were calculated [3]
- STAT3 kinase activity assay: Recombinant STAT3 kinase domain was incubated with ATP, substrate peptide, and Diosgenin. Phosphorylated substrate was measured by ELISA, and the inhibitory effect of Diosgenin on STAT3 kinase activity was evaluated [1] |
| Cell Assay |
Hepatocellular carcinoma cell assays: Cells were seeded in 96-well plates and treated with Diosgenin (0-80 μM) for 24-72 hours. Cell viability was detected by MTT assay; cell cycle distribution was analyzed by flow cytometry after propidium iodide staining; apoptosis was assessed by Annexin V-FITC/PI double staining. Western blot and PCR were used to detect STAT3 pathway-related proteins and mRNA levels [1]
- Neuronal cell assays: Neuronal cells were treated with Diosgenin and Aβ1-42. Cell viability was measured by MTT assay; ROS production was detected by fluorescent probe staining; Aβ aggregation was observed by thioflavin T staining. Western blot was used to detect tau phosphorylation and 1,25D₃-MARRS/Pdia3/ERp57 expression [2] - 3T3-L1 adipocyte differentiation assay: Preadipocytes were induced to differentiate in the presence of Diosgenin (0-20 μM). Oil Red O staining was used to quantify lipid accumulation; Western blot and PCR were performed to detect PPARγ, ERβ, aP2, and C/EBPα expression [4] - Macrophage foam cell assay: THP-1 cells were differentiated into macrophages and loaded with oxidized low-density lipoprotein to form foam cells. Cells were treated with Diosgenin, and intracellular cholesterol content was measured by cholesterol assay kit. Western blot and PCR were used to detect ABCA1 and miR-19b expression [5] - Aβ aggregation/disaggregation assay: Diosgenin was incubated with Aβ1-42 peptide. Thioflavin T fluorescence intensity was measured to evaluate Aβ aggregation; atomic force microscopy was used to observe Aβ fibril disaggregation [3] |
| Animal Protocol |
Alzheimer’s disease model: 5XFAD mice (6-month-old) were randomly divided into control and Diosgenin treatment groups. Diosgenin was dissolved in corn oil and administered by oral gavage at a dose of 50 mg/kg once daily for 8 weeks. Behavioral tests (Morris water maze) were performed to evaluate cognitive function. After sacrifice, brain tissues were collected for Aβ deposition analysis (immunohistochemistry) and protein expression detection (Western blot) [2]
- Atherosclerosis model: ApoE-/- mice were fed a high-fat diet to induce atherosclerosis and randomly divided into control and Diosgenin treatment groups. Diosgenin was dissolved in 0.5% carboxymethylcellulose sodium and administered by oral gavage at a dose of 20 mg/kg once daily for 12 weeks. Serum lipid levels were measured; aortic tissues were collected for plaque area analysis (Oil Red O staining) and molecular biological detection [5] |
| Toxicity/Toxicokinetics |
In vitro experiments showed that diosgenin at concentrations up to 80 μM had no significant cytotoxicity to normal hepatocytes (LO2) and normal neurons [1][2]. In vivo experiments showed that administration of diosgenin (50 mg/kg in 5XFAD mice for 8 weeks; 20 mg/kg in ApoE-/- mice for 12 weeks) did not cause significant changes in body weight, organ index, or serum liver and kidney function indicators [2][5].
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| References |
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| Additional Infomation |
Diosgenin is a saponin belonging to the spirostane class of compounds, with a hydroxyl group substituted at the 3β position, a double bond at the 5-6 positions, and an R configuration at the 25 position. It is a natural product found in plants of the genus Dioscorea (wild yam) and is a starting material for the commercial synthesis of various steroidal compounds, including cortisone, pregnenolone, and progesterone. Diosgenin possesses various activities, including inducing apoptosis, antiviral activity, antitumor activity, and as a metabolite. It is a 3β-sterol, spiroacetate, hexagonal triterpenoid, and saponin derived from the hydrogenation of spirostane. Diosgenin has been reported to exist in Allium cernuum, Dioscorea hispida, and other organisms with relevant data. It is a spirostane compound found in the genus Dioscorea and other plants. The 25S isomer is called yam saponin. Solanine is a natural derivative formed by the substitution of a nitrogen atom for a spirocyclic ring, which can rearrange to form solanine. See also: fenugreek seeds (partial); Dioscorea bulbifera tubers (partial). Diosgenin is a steroidal saponin, primarily isolated from plants in the Dioscoreaceae family. Its anticancer effect in hepatocellular carcinoma is mediated by the inhibition of the STAT3 signaling pathway [1]
-Diosgenin's neuroprotective effect in Alzheimer's disease is related to the activation of 1,25D₃-MARRS/Pdia3/ERp57 and the regulation of Aβ metabolism and tau protein phosphorylation [2] -Diosgenin and curcumin divalent ligands exert a synergistic effect on Alzheimer's disease by targeting multiple pathological pathways (AChE/BuChE inhibition, Aβ aggregation inhibition, neuroprotection) [3] -Diosgenin improves metabolic dysfunction by regulating the ERβ-PPARγ signaling pathway, suggesting its potential application value in obesity and metabolic syndrome [4] -Diosgenin's anti-atherosclerotic effect is attributed to its inhibition of miR-19b and upregulation of ABCA1, which can enhance cholesterol efflux and reduce foam cell formation [5] |
| Molecular Formula |
C27H42O3
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| Molecular Weight |
414.62
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| Exact Mass |
414.313
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| CAS # |
512-04-9
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| Related CAS # |
Diosgenin glucoside;14144-06-0
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| PubChem CID |
99474
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| Appearance |
White to off-white solid powder
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| Density |
1.1±0.1 g/cm3
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| Boiling Point |
527.1±50.0 °C at 760 mmHg
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| Melting Point |
205-208°C
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| Flash Point |
272.6±30.1 °C
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| Vapour Pressure |
0.0±3.1 mmHg at 25°C
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| Index of Refraction |
1.564
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| LogP |
5.84
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
0
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| Heavy Atom Count |
30
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| Complexity |
746
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| Defined Atom Stereocenter Count |
11
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| SMILES |
C[C@@H]1CC[C@@]2([C@H]([C@H]3[C@@H](O2)C[C@@H]4[C@@]3(CC[C@H]5[C@H]4CC=C6[C@@]5(CC[C@@H](C6)O)C)C)C)OC1
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| InChi Key |
WQLVFSAGQJTQCK-JJMMJHMNSA-N
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| InChi Code |
InChI=1S/C27H42O3/c1-16-7-12-27(29-15-16)17(2)24-23(30-27)14-22-20-6-5-18-13-19(28)8-10-25(18,3)21(20)9-11-26(22,24)4/h5,16-17,19-24,28H,6-15H2,1-4H3/t16?,17-,19?,20+,21-,22-,23-,24-,25-,26-,27+/m0/s1
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| Chemical Name |
(3β,25R)-spirost-5-en-3-ol
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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: ≥ 0.67 mg/mL (1.62 mM) (saturation unknown) in 10% EtOH + 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 6.7 mg/mL clear EtOH 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: ≥ 0.67 mg/mL (1.62 mM) (saturation unknown) in 10% EtOH + 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 6.7 mg/mL clear EtOH 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: ≥ 0.67 mg/mL (1.62 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 2.5 mg/mL (6.03 mM) in Corn Oil (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4118 mL | 12.0592 mL | 24.1185 mL | |
| 5 mM | 0.4824 mL | 2.4118 mL | 4.8237 mL | |
| 10 mM | 0.2412 mL | 1.2059 mL | 2.4118 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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