| 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 |
Purity: =99.4%
| Targets |
N-Myc; RKIP
Didymin targets multiple pathways involved in cancer cell survival and apoptosis. It inhibits N-Myc expression and upregulates RKIP in neuroblastoma cells, leading to apoptosis induction. It also induces the Fas-mediated apoptotic pathway in non-small-cell lung cancer cells. The compound possesses antioxidant properties, reducing ROS production and increasing superoxide dismutase (SOD) activity. It may also act as a p53 modulator. |
|---|---|
| ln Vitro |
Human non-small cell lung cancer cells cannot proliferate when didymin (1–20 μM) is applied for 48 hours [1]. A549 and H460 cells undergo apoptosis when exposed to didymin (10–20 μM) for 12–48 hours, but cell cycle division is unaffected [1].
In vitro, Didymin (1-20 μM; 48 h) inhibits cell proliferation in human non-small-cell lung cancer cells. It induces apoptosis by inhibiting N-Myc and upregulating RKIP in neuroblastoma, killing p53 wild-type as well as drug-resistant p53-mutant neuroblastoma cells. The compound also induces the Fas-mediated apoptotic pathway in non-small-cell lung cancer cells. It reduces hydrogen peroxide-induced ROS production and cell death and increases SOD activity. |
| ln Vivo |
Didymin (6 mg/kg/day; i.p.; once daily for 28 days) delays tumor growth in nude mice [1].
In vivo, Didymin induces the Fas-mediated apoptotic pathway in human non-small-cell lung cancer cells. Specific in vivo efficacy data in animal models are limited, but the compound's in vitro anticancer activity and ability to induce apoptosis through multiple pathways suggest potential for in vivo efficacy studies in xenograft models of neuroblastoma, lung cancer, and other malignancies. Its antioxidant properties also suggest potential for neuroprotection studies. |
| Enzyme Assay |
N-Myc promoter-reporter assay[2]
CHLA-90 and SMS-KCNR cells were cultured as adherent monolayers in a 96-well plate at a density of 2 × 104 cells per well. The Firefly luciferase reporter construct (0.4 ug, pEB-Luc-N-Myc), kindly gifted by Prof William L Carroll, M.D., New York University Medical Center, NY, was co-transfected with 100 ng of Renilla luciferase construct (thymidine kinase promoter-driven Renilla luciferase; pTK-RL) by Lipofectamine Reagent according to the manufacturer's instructions (Invitrogen, Carlsbad, CA). After 24 h of incubation, transfected cells were treated with 50 μM of Didymin. At 24 h post-treatment, promoter activity was measured as luciferase activity by mixing cells with 50 μl of passive lysis buffer followed by 15 min of shaking at room temperature. On a luminometer plate, 20 μl of the lysate was then mixed with 100 μl of luciferase assay reagent followed by 100 μl of Stop N' Glo Buffer. Luciferase activity was then determined as a ratio of Firefly to Renilla luciferase. Renilla luciferase activity was thus used as an internal control. The anticancer activity is assessed using cell viability assays. Cancer cell lines such as neuroblastoma and non-small-cell lung cancer cells are cultured in appropriate media and treated with Didymin at various concentrations (e.g., 1-20 μM for 48 h). Cell viability is measured using MTT, SRB, or CellTiter-Glo assays. Apoptosis is assessed by measuring caspase-3/7 activity, Annexin V/PI staining, and DNA fragmentation. N-Myc and RKIP protein levels are analyzed by Western blot. |
| Cell Assay |
Cell proliferation assay [1]
Cell Types: A549 and H460 cells Tested Concentrations: 1μM, 5μM, 10μM, 20μM Incubation Duration: 48h Experimental Results: Inhibition of cell proliferation of human non-small cell lung cancer cells. Apoptosis analysis [1] Cell Types: A549 and H460 cells Tested Concentrations: 10 μM, 20 μM Incubation Duration: 12 h, 24 h, 48 h Experimental Results: Induced apoptosis of A549 and H460 cells without affecting cell cycle distribution. For cellular studies, neuroblastoma and non-small-cell lung cancer cell lines are cultured in appropriate media supplemented with 10% FBS at 37°C in 5% CO₂. Cells are treated with Didymin at various concentrations for 24-72 hours. Cell viability is assessed using MTT or similar assays. Apoptosis is evaluated by flow cytometry. Protein expression of N-Myc, RKIP, and apoptosis-related proteins is analyzed by Western blot. ROS production is measured using DCFH-DA. |
| Animal Protocol |
Animal/Disease Models: Male nude mouse [6 weeks old; 28 days old]. BALB/cA-nu (nu/nu)] injection of A549 cells [1]
Doses: 6 mg/kg/day Route of Administration: intraperitoneal (ip) injection; one time/day for 28 days Experimental Results: Inhibited tumor growth in nude mice. In vivo efficacy studies for Didymin would be conducted in mouse xenograft models. Neuroblastoma or lung cancer cells would be implanted subcutaneously into immunodeficient mice. Once tumors reach a certain size, Didymin would be administered via oral gavage or intraperitoneal injection. Tumor volumes would be measured twice weekly, and body weights monitored for toxicity. At study termination, tumors would be harvested for histological analysis and assessment of apoptosis markers and signaling pathways. |
| ADME/Pharmacokinetics |
Specific pharmacokinetic data for Didymin are not extensively reported. The compound has a molecular weight of 594.56 g/mol. As a flavonoid glycoside, it is expected to have limited oral bioavailability due to poor membrane permeability and extensive intestinal metabolism (deglycosylation). The aglycone (isosakuranetin) may be absorbed and undergo further metabolism. Pharmacokinetic studies would be required to determine the compound's absorption, distribution, metabolism, and excretion profile.
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| Toxicity/Toxicokinetics |
Didymin is a natural product from citrus fruits and is generally considered to have a favorable safety profile at dietary intake levels. However, comprehensive toxicology studies for therapeutic use have not been reported. The compound's ability to induce apoptosis in cancer cells and its antioxidant properties suggest potential for cancer and neuroprotection research. It should be handled with appropriate safety precautions.
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| References |
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| Additional Infomation |
Didimine is a flavonoid compound belonging to the glycoside class. It has been reported to exist in citrus (Citrus reticulata), Cyclotrichium niveum, and other organisms with relevant data. See also: Orange peel (partial).
Didymin is a dietary flavonoid glycoside from citrus fruits with antioxidant and anticancer properties. It induces apoptosis by inhibiting N-Myc and upregulating RKIP in neuroblastoma and induces the Fas-mediated apoptotic pathway in non-small-cell lung cancer. It reduces ROS production and increases SOD activity. No clinical trials or approvals exist. For research use only. |
| Molecular Formula |
C28H34O14
|
|---|---|
| Molecular Weight |
594.5612
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| Exact Mass |
594.194
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| CAS # |
14259-47-3
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| PubChem CID |
16760075
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| Appearance |
White to yellow solid
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| Density |
1.6±0.1 g/cm3
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| Boiling Point |
896.6±65.0 °C at 760 mmHg
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| Melting Point |
211-213ºC
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| Flash Point |
295.3±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 |
2.72
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| Hydrogen Bond Donor Count |
7
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| Hydrogen Bond Acceptor Count |
14
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
42
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| Complexity |
900
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| Defined Atom Stereocenter Count |
11
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| SMILES |
O1[C@]([H])([C@@]([H])([C@]([H])([C@@]([H])([C@@]1([H])C([H])([H])O[C@@]1([H])[C@@]([H])([C@@]([H])([C@]([H])([C@]([H])(C([H])([H])[H])O1)O[H])O[H])O[H])O[H])O[H])O[H])OC1=C([H])C(=C2C(C([H])([H])[C@@]([H])(C3C([H])=C([H])C(=C([H])C=3[H])OC([H])([H])[H])OC2=C1[H])=O)O[H]
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| InChi Key |
RMCRQBAILCLJGU-HIBKWJPLSA-N
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| InChi Code |
InChI=1S/C28H34O14/c1-11-21(31)23(33)25(35)27(39-11)38-10-19-22(32)24(34)26(36)28(42-19)40-14-7-15(29)20-16(30)9-17(41-18(20)8-14)12-3-5-13(37-2)6-4-12/h3-8,11,17,19,21-29,31-36H,9-10H2,1-2H3/t11-,17-,19+,21-,22+,23+,24-,25+,26+,27+,28+/m0/s1
|
| Chemical Name |
(2S)-5-hydroxy-2-(4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxy-2,3-dihydrochromen-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: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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 (~420.48 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.17 mg/mL (3.65 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 21.7 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: ≥ 2.17 mg/mL (3.65 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 21.7 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: ≥ 2.17 mg/mL (3.65 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 | 1.6819 mL | 8.4096 mL | 16.8192 mL | |
| 5 mM | 0.3364 mL | 1.6819 mL | 3.3638 mL | |
| 10 mM | 0.1682 mL | 0.8410 mL | 1.6819 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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