Piceatannol

SKU: orb1310449

Description

Piceatannol

Research Area

Cardiovascular Research, Cell Biology, Epigenetics & Chromatin, Metabolism Research, Signal Transduction

Key Properties

• CAS Number: 10083-24-6
• MW: 244.24
• Purity: 99.73%
• Formula: C₁₄H₁₂O₄
• SMILES: C(=C/C1=CC(O)=CC(O)=C1)\C2=CC(O)=C(O)C=C2
• Target: PKA,Syk,PKC,Serine/threonin kinase,Apoptosis,Endogenous Metabolite,Autophagy
• Solubility: DMSO:14.14 mg/mL (57.89 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:4 mg/mL (16.38 mM);Ethanol:24.4 mg/mL (99.9 mM)

Bioactivity

• Target IC50:
  CAK:3 μM|MLCK:12 μM|PKC:8 μM
• In Vivo:
  Oral administration of Piceatannol significantly ameliorates structural damage to the colon in BALB/c mice with dextran sulfate sodium-induced colitis, markedly reducing the production of inflammatory mediators (such as nitric oxide, prostaglandin E2, and pro-inflammatory cytokines), and notably diminishes colonic myeloperoxidase (MPO) activity. In type 2 diabetic db/db mouse models, Piceatannol suppresses early elevation of blood glucose levels and improves impaired glucose tolerance in later stages.
• In Vitro:
  In mast cells, Piceatannol is an effective inhibitor of histamine release, selectively suppressing Syk to block receptor-mediated cellular responses, including inhibition of 1,4,5-IP3 secretion, synthesis, membrane ruffling, and transportation. Piceatannol inhibits Syk activity approximately tenfold more potently than Lyn. When RBL-2H3 cells are treated with Piceatannol, antigen-stimulated phosphorylation of Syk and most other cellular proteins is strongly inhibited. However, it doesn’t affect the phosphorylation of receptor gamma or beta subtypes, presenting a dose-dependent inhibition. Piceatannol also effectively inhibits CDPK, MLCK, PKC, and PKA, with IC50 values of 19 μM, 12 μM, 8 μM, and 3 μM respectively. It selectively inhibits IFNα-induced tyrosine phosphorylation of STAT3/5 without affecting STAT1/2 and selectively inhibits the dephosphorylation of tyrosine on Jak1 and IFNAR1, not affecting Tyk2 and IFNAR2. Piceatannol induces apoptosis in BJAB Burkitt-like lymphoma cells via the activation of caspase-3 and changes in mitochondrial permeability, with an ED50 of 25 μM, independent of the CD95/Fas signaling pathway. It inhibits NF-κB activation induced by TNF, H2O2, PMA, lipopolysaccharides, okadaic acid, and ceramide. Specifically, it inhibits TNF-induced expression of NF-κB-dependent reporter genes (matrix metalloproteinase-9, cyclooxygenase-2, and cyclin D1) by blocking TNF-induced IκBαof phosphorylation, p65 nuclear translocation, and IκB kinase activation, independent of tyrosine kinase. Piceatannol binds to intracellular phosphatidylinositol kinase in an ATP-competitive manner, inhibiting its activity and exhibiting anti-atherosclerotic effects superior to resveratrol. Lastly, Piceatannol suppresses the proliferation of both androgen-dependent and -independent CaP cells and notably reduces the expression of mTOR and its key effectors AKT and eIF4EBP-1.
• Cell Research:
  Cells are exposed to increasing concentrations of Piceatannol. For the determination of cell proliferation, cells are assayed at 72 hours by trypan blue exclusion using a hemocytometer. After 1 week, colonies are stained with 1.25% crystal violet and quantified by measuring the absorbance at 595 nm. (Only for Reference)

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

ALI, cAK, Autophagy, Astringenin, Apoptosis, MLCK, injury, iNOS, trans-Piceatannol, threoninkinase, threonin kinase, Serinekinase, Serine kinase, Piceatannol, PKC, Syk

Compound Identifiers

PubChem CID

667639