| Size | Price | Stock | Qty |
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| 1mg |
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| Other Sizes |
| Targets |
Tricin 7-O-beta-D-glucopyranoside exerts its effects by modulating key inflammatory and cell survival signaling pathways. Its primary molecular targets appear to be within the NF-kappaB pathway. It significantly decreases the expression of TNF-alpha-induced phosphor-kappaB-alpha (the phosphorylated inhibitor of NF-kappaB) and phosphor-NF-kappaB (the active transcription factor), leading to a reduction in NF-kappaB transcriptional activity. It also decreases the expression of high mobility group box 1 (HMGB1), a pro-inflammatory cytokine. By inhibiting these targets, the compound reduces neuroinflammation. It is also an inducer of apoptosis.
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| ln Vitro |
After 3 hours of hypoxic glucose induction and 12 hours of incubation, SH-SY5Y cells undergo dose-dependent apoptosis in response to tricin 7-O-β-D-glucopyranoside (4-64 µM; 12 hours). [1]. In SH-SY5Y cells, TNF-α (20 ng/ml, 30 min)-induced phospho-κB-α, phospho-NF, and κB and HMGB1 expression is reduced by tricin 7-O-β-D-glucopyranoside (16, 32 µM; 12 h)[1].
In vitro, Tricin 7-O-beta-D-glucopyranoside has been demonstrated to effectively suppress TNF-alpha-induced inflammatory responses. In cellular assays, treatment with the compound leads to a decrease in the expression levels of phosphor-kappaB-alpha, phosphor-NF-kappaB, and HMGB1, as measured by Western blotting, indicating inhibition of the NF-kappaB signaling pathway. It also possesses neuroprotective activity, likely as a result of its anti-inflammatory and antioxidant properties. The compound has been shown to induce apoptosis in certain cell types. The exact IC₅0 values are not specified but the compound is described as "potent". Effective concentrations are likely in the low micromolar range. |
| ln Vivo |
In rats undergoing ischemia and reperfusion (I/R), tricin 7-O-β-D-glucopyranoside (50, 100, 200, and 400 mg/kg; oral) exhibits neuroprotective properties[1].
In vivo, Tricin 7-O-beta-D-glucopyranoside has been shown to possess significant neuroprotective potential. In a rat model of ischemia and reperfusion (I/R), which simulates stroke damage, the compound was administered orally. Doses of 50, 100, 200, and 400 mg/kg were tested, and the results demonstrated a clear neuroprotective effect. This suggests the compound can cross the blood-brain barrier and exert anti-inflammatory and anti-apoptotic effects in the brain. The study highlights the therapeutic potential of this naturally occurring compound for treating acute neurological injuries and chronic neurodegenerative conditions where neuroinflammation plays a key role. |
| Enzyme Assay |
A typical non-cellular assay is an ELISA-based NF-kappaB DNA-binding assay to measure direct inhibition of NF-kappaB p65 binding to its consensus sequence. Nuclear extracts are prepared from TNF-alpha-stimulated cells. Using a commercial TransAM NF-kappaB p65 kit, 5-20 ug of nuclear extract is added to a 96-well plate coated with an NF-kappaB oligonucleotide. After incubation, an anti-p65 antibody and HRP-conjugated secondary antibody are added. Absorbance at 450 nm is measured. The compound can be added directly to the nuclear extract to test direct inhibition. Alternatively, a DPPH radical scavenging assay can be performed: 0.1 mM DPPH in methanol is mixed with various concentrations of the compound (1-100 ug/mL), incubated 30 min, and absorbance at 517 nm measured.
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| Cell Assay |
Apoptosis Analysis[1]
Cell Types: SH-SY5Y cells Tested Concentrations: 2, 4, 8, 16, 32, 64 µM Incubation Duration: 12 h Experimental Results: Induced cell apoptosis after oxygen-glucose deprivation for 3 h followed by 12 h incubation with neurobasal medium with the apoptosis rate of 35.6%. Western Blot Analysis[1] Cell Types: SH-SY5Y cells Tested Concentrations: 16, 32 µM Incubation Duration: 12 h Experimental Results: Blocked TNF-α (20 ng/ml for 30 min) induced IκB-α and NF-κB phosphorylation, and diminished HMGB1 expression. A standard in vitro cell-based assay uses human neuroblastoma SH-SY5Y cells to study neuroprotection against TNF-alpha-induced inflammation. Cells are cultured in DMEM/F12 with 10% FBS at 37degC, 5% CO2. Cells are seeded in 6-well plates at 5 × 10⁵ cells/well. After 24 h, cells are pre-treated with the compound (0.1-25 uM) for 1 h, then 10 ng/mL TNF-alpha is added for 24 h. Cell viability is measured by MTT. Protein lysates are analyzed by Western blotting for phosphor-kappaB-alpha, phosphor-NF-kappaB p65, and HMGB1, with GAPDH as loading control. Band intensities are quantified by densitometry. The compound decreases these markers concentration-dependently. |
| Animal Protocol |
Animal/Disease Models: Adult male SD (Sprague-Dawley) rats[1]
Doses: 50, 100, 200 and 400 mg/kg Route of Administration: Po Experimental Results: diminished neurological deficit scores, decreased brain infarct volume and brain water content, inhibited NF-κB activation and decreased HMGB1 expression. An in vivo animal study is performed in a rat model of cerebral ischemia/reperfusion (I/R). Adult male Sprague-Dawley rats (250-300 g) are used. I/R injury is induced by the intraluminal suture method to occlude the middle cerebral artery (MCAO) for 2 hours, followed by reperfusion. The compound is suspended in 0.5% carboxymethyl cellulose (CMC) and administered orally at doses of 50, 100, 200, and 400 mg/kg once daily for 7 days before MCAO, with the last dose given 1 hour before ischemia. After 24 h reperfusion, brains are sectioned and stained with 2% TTC. Infarct volume is measured. Neurological scores are assessed. All procedures require IACUC approval. |
| ADME/Pharmacokinetics |
The pharmacokinetic (PK) properties of Tricin 7-O-beta-D-glucopyranoside have not been extensively reported. It is described as "orally active" in a rat model of cerebral ischemia, indicating sufficient oral bioavailability to reach therapeutic concentrations in the brain. As a flavonoid glycoside, it is likely hydrolyzed in the gut to its aglycone (tricin), which is then absorbed. The compound has a molecular weight of 476.43 g/mol and is moderately lipophilic. No specific PK parameters (Cmax, Tmax, half-life) are publicly available. Human PK data is not available.
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| Toxicity/Toxicokinetics |
Toxicological data for Tricin 7-O-beta-D-glucopyranoside is not publicly available. As a flavonoid isolated from various plant sources, it is generally considered to have low toxicity. In the reported in vivo neuroprotection study, the compound was administered at doses up to 400 mg/kg orally in rats with no reported adverse effects such as significant weight loss or behavioral abnormalities. However, a formal toxicological evaluation has not been published. Standard laboratory safety precautions (gloves, lab coat, eye protection) should be used when handling this compound. For research use only; not for human administration.
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| References | |
| Additional Infomation |
Trihydroxyflavone 7-O-β-D-glucoside is a glycosyloxyflavone with the structure 3',5'-di-O-methyltrihydroxyflavone (trihydroxyflavone), in which the phenolic hydroxyl hydrogen at position 7 is replaced by a β-D-glucopyranoyl group. It is a plant metabolite, a free radical scavenger, and a metabolite of exogenous substances. It is a β-D-glucoside, dihydroxyflavone, dimethoxyflavone, glycosyloxyflavone, monosaccharide derivative, and polyphenol. Its function is related to 3',5'-di-O-methyltrihydroxyflavone. Trihydroxyflavone 7-glucoside has been reported in watercress (Hyparrhenia hirta), buttercup (Ranunculus sieboldii), and several other organisms with relevant data.
Tricin 7-O-beta-D-glucopyranoside is not an approved drug and has no clinical development history. It is a natural product used as a research tool for studying neuroprotection, particularly in the context of cerebral ischemia (stroke). Its mechanism involves inhibition of the NF-kappaB inflammatory pathway and reduction of HMGB1 expression. It also induces apoptosis. The compound is of interest for its potential therapeutic use in treating stroke, traumatic brain injury, and other neurodegenerative diseases. No clinical trials have been registered for this compound. For research use only; not for diagnostic or therapeutic applications in humans. |
| Molecular Formula |
C23H24O12
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| Molecular Weight |
492.43
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| Exact Mass |
492.127
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| CAS # |
32769-01-0
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| PubChem CID |
5322022
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| Appearance |
Typically exists as solid at room temperature
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| LogP |
0.067
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| Hydrogen Bond Donor Count |
6
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| Hydrogen Bond Acceptor Count |
12
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
35
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| Complexity |
762
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| Defined Atom Stereocenter Count |
5
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| SMILES |
COC1=CC(=CC(=C1O)OC)C2=CC(=O)C3=C(C=C(C=C3O2)OC4C(C(C(C(O4)CO)O)O)O)O
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| InChi Key |
JGXFMIJHKASCIZ-LDBVRRDLSA-N
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| InChi Code |
InChI=1S/C23H24O12/c1-31-15-3-9(4-16(32-2)19(15)27)13-7-12(26)18-11(25)5-10(6-14(18)34-13)33-23-22(30)21(29)20(28)17(8-24)35-23/h3-7,17,20-25,27-30H,8H2,1-2H3/t17-,20-,21+,22-,23-/m1/s1
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| Chemical Name |
5-hydroxy-2-(4-hydroxy-3,5-dimethoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-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 |
| 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) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.0307 mL | 10.1537 mL | 20.3075 mL | |
| 5 mM | 0.4061 mL | 2.0307 mL | 4.0615 mL | |
| 10 mM | 0.2031 mL | 1.0154 mL | 2.0307 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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