|Description:||1. Triacetylresveratrol inhibits the phosphorylation of STAT3 and NFκB, down-regulates Mcl-1, and up-regulates Bim and Puma in pancreatic cancer cells, it may be a potential agent for pancreatic cancer prevention and treatment. |
2. Triacetylresveratrol can significantly inhibit intracranial tumor growth and prolong survival in these mouse models, it may as a drug with novel glioblastoma tissue disrupting effects and validate the importance of preclinical screens designed to address tumor tissue function rather than the mechanisms of autonomous tumor cell growth.
|Targets:||STAT | NF-kB|
|Source:||The rhizomes of Polygonum cuspidatum Sieb. et Zucc.|
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.8217 mL||14.1084 mL||28.2167 mL||56.4334 mL||70.5418 mL|
|5 mM||0.5643 mL||2.8217 mL||5.6433 mL||11.2867 mL||14.1084 mL|
|10 mM||0.2822 mL||1.4108 mL||2.8217 mL||5.6433 mL||7.0542 mL|
|50 mM||0.0564 mL||0.2822 mL||0.5643 mL||1.1287 mL||1.4108 mL|
|100 mM||0.0282 mL||0.1411 mL||0.2822 mL||0.5643 mL||0.7054 mL|
Sci Rep. 2016 Aug 19;6:31672.
|In vitro comparative studies of resveratrol and triacetylresveratrol on cell proliferation, apoptosis, and STAT3 and NFκB signaling in pancreatic cancer cells.[Pubmed: 27539371]|
|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.|
Oncotarget. 2015 Jul 30;6(21):18282-92.
|Novel chemical library screen identifies naturally occurring plant products that specifically disrupt glioblastoma-endothelial cell interactions.[Pubmed: 26286961]|
|Three candidate PVN-disrupting agents, Iridin, Tigogenin and Triacetylresveratrol (TAR), were identified and evaluated in secondary in vitro screens against a panel of primary GBM isolates as well as in two different in vivo intracranial models. Iridin and TAR significantly inhibited intracranial tumor growth and prolonged survival in these mouse models. Together these data identify Iridin and TAR as drugs with novel GBM tissue disrupting effects and validate the importance of preclinical screens designed to address tumor tissue function rather than the mechanisms of autonomous tumor cell growth.|