| Size | Price | Stock | Qty |
|---|---|---|---|
| 500mg |
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| Other Sizes |
| Targets |
STAT3; NF-κB
Triacetylresveratrol shares the targets of resveratrol, including SIRT1, AMPK, and NF-κB. It also interacts with estrogen receptors and inhibits COX-2. The acetyl groups enhance lipophilicity and membrane permeability. After deacetylation, the active resveratrol exerts its effects. |
|---|---|
| ln Vitro |
The anti-apoptotic Bcl-2 family protein Mcl-1 was considerably down-regulated by triacetyl resveratrol, whereas the pro-apoptotic Bcl-2 family members Bim and Puma were up-regulated. In pancreatic cancer cells, triacetyl resveratrol causes apoptosis and decreases cell viability in a concentration- and time-dependent manner [1].
In vitro, triacetylresveratrol is more potent than resveratrol in some assays due to better uptake. It inhibits the proliferation of cancer cells (e.g., MCF-7, IC50 ~ 10 µM) and reduces LPS-induced NO production (IC50 ~ 5 µM). It shows DPPH scavenging (IC50 ~ 15 µM). It also activates SIRT1 (EC50 ~ 1 µM). |
| ln Vivo |
In vivo, triacetylresveratrol has shown superior oral bioavailability compared to resveratrol. In mice, oral administration of 50 mg/kg resulted in higher plasma levels of resveratrol. It showed efficacy in a mouse model of colon cancer, reducing tumor incidence by 40%. It also improved insulin sensitivity in diabetic mice.
|
| Enzyme Assay |
The in vitro SIRT1 activation assay uses a fluorogenic peptide substrate. Recombinant SIRT1 is incubated with NAD⁺, peptide, and triacetylresveratrol (0.1-10 µM) for 1 h; fluorescence is measured. For anti-inflammatory, RAW 264.7 cells are used. For DPPH, standard radical scavenging assay.
|
| Cell Assay |
Resveratrol (RES) has been studied extensively as an anticancer agent. However, the anticancer effects of triacetylresveratrol (TRES, an acetylated analog of RES) which has higher bioavailability have not been well established. We comparatively evaluated their effects on cell proliferation, apoptosis and the molecular changes in STAT3, NFκB and apoptotic signaling pathways in pancreatic cancer cells. Apoptosis was determined by flow cytometry. The nuclear translocation and interaction of STAT3 and NFκB were detected by Western blotting and immunoprecipitation, respectively. Both TRES and RES inhibited cell viability, and induced apoptosis of pancreatic cancer cells in a concentration and incubation time-dependent manner. TRES, similarly to RES, inhibited the phosphorylation of STAT3 and NFκB, down-regulated Mcl-1, and up-regulated Bim and Puma in pancreatic cancer cells. Remarkably, we, for the first time, observed that both TRES and RES suppressed the nuclear translocation, and interrupted the interaction of STAT3 and NFκB in PANC-1 cells. Comparative anticancer effects of TRES and RES on pancreatic cancer suggested that TRES with higher bioavailability may be a potential agent for pancreatic cancer prevention and treatment. Further in vivo experiments and functional studies are warranted to investigate whether TRES exhibits better beneficial effects than RES in mice and humans.[1]
For in vitro cell-based assays, MCF-7 cells are treated with triacetylresveratrol (1-50 µM) for 48 h. Cell viability is measured by MTT. Apoptosis is evaluated by annexin V/PI. ROS is measured by DCFH-DA. For cancer cell signaling, Western blotting for SIRT1, p53, and NF-κB is performed. |
| Animal Protocol |
In vivo xenograft studies: nude mice with MCF-7 xenografts are treated orally with triacetylresveratrol (25, 50 mg/kg) daily for 21 days. Tumor volumes are measured. For metabolic studies, db/db mice are treated with triacetylresveratrol (30 mg/kg) for 4 weeks; glucose tolerance is assessed.
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| ADME/Pharmacokinetics |
Pharmacokinetic data: in rats, after oral administration of triacetylresveratrol (50 mg/kg), Cmax of resveratrol is 5-fold higher than equimolar resveratrol. Tmax is 1 h, half-life is 3 h. The prodrug is rapidly deacetylated. Bioavailability is ~40%.
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| Toxicity/Toxicokinetics |
Triacetylresveratrol has low toxicity (LD50 > 2000 mg/kg). No significant adverse effects were observed in subchronic studies. It is not mutagenic. Mild gastrointestinal effects may occur at high doses.
|
| References | |
| Additional Infomation |
[4-[2-(3,5-diacetoxyphenyl)vinyl]phenyl]acetate is a stilbene compound.
Triacetylresveratrol is a prodrug of resveratrol with improved pharmacokinetics. It has been studied for chemoprevention and cardiovascular protection. No clinical trials have been conducted. It is available as a research compound. |
| Molecular Formula |
C20H18O6
|
|---|---|
| Molecular Weight |
354.3533
|
| Exact Mass |
354.11
|
| CAS # |
42206-94-0
|
| PubChem CID |
5962587
|
| Appearance |
White to off-white solid powder
|
| Density |
1.2±0.1 g/cm3
|
| Boiling Point |
504.8±50.0 °C at 760 mmHg
|
| Melting Point |
117.0 to 121.0 °C
|
| Flash Point |
221.4±30.2 °C
|
| Vapour Pressure |
0.0±1.3 mmHg at 25°C
|
| Index of Refraction |
1.600
|
| LogP |
2.94
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
6
|
| Rotatable Bond Count |
8
|
| Heavy Atom Count |
26
|
| Complexity |
508
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
CC(=O)OC1=CC=C(C=C1)/C=C/C2=CC(=CC(=C2)OC(=O)C)OC(=O)C
|
| InChi Key |
PDAYUJSOJIMKIS-SNAWJCMRSA-N
|
| InChi Code |
InChI=1S/C20H18O6/c1-13(21)24-18-8-6-16(7-9-18)4-5-17-10-19(25-14(2)22)12-20(11-17)26-15(3)23/h4-12H,1-3H3/b5-4+
|
| Chemical Name |
[4-[(E)-2-(3,5-diacetyloxyphenyl)ethenyl]phenyl] acetate
|
| Synonyms |
triacetylresveratrol; 42206-94-0; Triacetyl resveratrol; trans-Resveratrol triacetate; Acetyl-trans-resveratrol; (E)-5-(4-ACETOXYSTYRYL)-1,3-PHENYLENE DIACETATE; 54443-64-0; 63366-83-6;
|
| HS Tariff Code |
2934.99.9001
|
| 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)
|
| Solubility (In Vitro) |
DMSO : ~125 mg/mL (~352.76 mM)
|
|---|---|
| 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 | 2.8221 mL | 14.1103 mL | 28.2207 mL | |
| 5 mM | 0.5644 mL | 2.8221 mL | 5.6441 mL | |
| 10 mM | 0.2822 mL | 1.4110 mL | 2.8221 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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