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Piceatannol (Astringenin; NSC-622471; trans-Piceatannol)

Alias: NSC 622471; NSC-622471; Piceatannol; NSC622471.
Cat No.:V0654 Purity: ≥98%
Piceatannol (also known as Astringenin; NSC-622471; trans-Piceatannol), a naturally occuring stilbene, is a potent and selective Syk inhibitor and shows ~10-fold selectivity for Srk over Lyn.
Piceatannol (Astringenin; NSC-622471; trans-Piceatannol)
Piceatannol (Astringenin; NSC-622471; trans-Piceatannol) Chemical Structure CAS No.: 10083-24-6
Product category: Syk
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Piceatannol (also known as Astringenin; NSC-622471; trans-Piceatannol), a naturally occuring stilbene, is a potent and selective Syk inhibitor and shows ~10-fold selectivity for Srk over Lyn. It has anti-inflammatory, immunomodulatory and antiproliferative activities. Piceatannol demonstrated high in vivo anti-inflammatory activity in female BALB/c mice with dextran sulfate sodium (DSS)-induced colitis. It inhibits p56lck and syk protein tyrosine kinases and inhibits TNF-induced NF-κB activation and gene expression. Synthesis results from conversion of resveratrol by cytochrome P450 1B1.

Biological Activity I Assay Protocols (From Reference)
Targets
Syk
ln Vitro
One metabolite of resveratrol is piceatannol [2]. Six diffuse large B-cell lymphoma (DLBCL) cell lines (SUDHL-6, U2392, DOHH2, Karpas 422, VAL, OCI Ly19) have their cell growth inhibited by the SYK inhibitor Piceatannol (3.125, 6.25, 12.5, 25 and 50 μM; 72 hours); the IC50 values for these cell lines are 18 μM, 25 μM, 37 μM, 48 μM, and >50 μM, respectively [3].
Piceatannol, a polyphenolic compound present in grapes and wine, has been reported to exhibit anticancer properties. Recently, it has been demonstrated to exert antiproliferative and proapoptotic effects in various human cancer types. The aim of our study was to investigate whether piceatannol induces autophagy and apoptosis in MOLT-4 human leukemia cells. Our results revealed that piceatannol activated autophagy in MOLT-4 cells, as evidenced by the detection of an increased level of LC3-II protein and a concomitant decrease in p62/SQSTM1 protein level. Moreover, piceatannol induced apoptosis in MOLT-4 cells which was accompanied by phosphatidylserine externalization, caspase-3 activation, disruption of mitochondrial membrane potential, internucleosomal DNA fragmentation, PARP1 cleavage, chromatin condensation, and fragmentation of cell nuclei. However, the toxic effects exerted by piceatannol in MOLT4 cells diminished after longer periods of exposure to the compound. Our findings imply that MOLT-4 cells may acquire resistance to piceatannol toxicity, which may result from the induction of efflux transporters such as P-glycoprotein. The present study provides new data showing that the use of piceatannol as a potential chemotherapeutic agent in the treatment of leukemia may be associated with the risk of multidrug resistance. [4]
ln Vivo
Piceatannol (10, 20 and 40 mg/kg) suppresses the infiltration of inflammatory cells generated by lipopolysaccharide and prevents pulmonary edema [1]. In lung tissue, piceatannol (10, 20, and 40 mg/kg) reduces myeloperoxidase activity and prevents the synthesis of iNOS and COX-2 expression that is produced by lipopolysaccharide [1]. By preventing the activation of the TLR/NF-κB signaling pathway in lung tissue, piceatannol (10, 20, and 40 mg/kg; intraperitoneally injected for 1 hour) therapy decreased the inflammatory response during LPS-induced acute lung injury (ALI) [1].
Enzyme Assay
Caspase-3 activity assay [4]
Caspase-3 activity was measured using FITC-conjugated Monoclonal Active Caspase-3 Antibody Apoptosis Kit I. MOLT-4 cells were exposed to piceatannol at the IC90 concentration for 48 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (5 × 105 cells per sample) were collected and stained with FITC-conjugated anti-active caspase-3 antibody according to the manufacturer's protocol. Analysis of mitochondrial membrane potential [4]
Changes in mitochondrial membrane potential were examined using JC-1 dye as described previously. MOLT-4 cells were exposed to piceatannol at the IC90 concentration for 48 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (5 × 105 cells per sample) were collected, stained with JC-1, and analyzed by flow cytometry.
Rhodamine 123 uptake/retention assay [4]
MOLT-4 cells were exposed to piceatannol at the IC90 concentration for 96 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (5 × 105 cells per sample) were collected, centrifuged, and supernatants were discarded. After washing with RPMI 1640 medium, cells were suspended in RPMI 1640 containing 0.1 μg/ml rhodamine 123 and incubated for 1 h at 37 °C in the dark in the presence or absence of an appropriate ABC-transporter's inhibitor. Cyclosporin A (2 μM, 5 μM, and 10 μM) was used for P-gp activity analysis. Ko143 (5 μM and 10 μM) was used to study the activity of BCRP, whereas MK571 (10 μM, 20 μM, and 50 μM) was used for MRP1 activity analysis. Following incubation, cells were washed twice with ice-cold rhodamine 123-free culture medium with or without an appropriate inhibitor. Next, cells were incubated in rhodamine 123-free medium for 45 min at 37 °C, in the presence or absence of an appropriate inhibitor. After centrifugation (300 g/5 min/4 °C) supernatants were discarded, whereas cells were suspended in the culture medium containing 0.5 μg/ml PI and incubated in the presence or absence of an appropriate inhibitor (10 min at RT in the dark). Following incubation, samples were kept on ice and immediately analyzed by flow cytometry. PI-positive cells, corresponding to non-viable cells, were excluded from data analysis. RPMI 1640 medium, used in all steps of the experiment did not contain phenol red and was supplemented by 10% FBS, 2 mM l-glutamine, and antibiotics.
Detection of P-gp [4]
MOLT-4 cells were exposed to piceatannol at the IC90 concentration for 96 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (5 × 105 cells per sample) were collected, centrifuged, and supernatants were discarded. Next, cells were washed with cold Stain Buffer and incubated on ice for 30 min in the dark with FITC-conjugated mouse monoclonal antibody against P-gp (UIC2) or FITC-conjugated mouse IgG2a isotype control antibody. The final concentration of the UIC2 antibody was 5 μg/ml (0.5 μg per 5 × 105 cells in 100 μl) and was equal to the final concentration of the isotype control antibody. After incubation, cells were washed with cold Stain Buffer and incubated with 2.5 μg/ml PI for 10 min at RT in the dark. Afterwards, samples were kept on ice and immediately analyzed by flow cytometry. PI-positive cells, corresponding to non-viable cells, were excluded from data analysis. Results were expressed as the ratio of the mean fluorescence intensity (MFI) of the UIC2 antibody and the isotype control antibody (MFI shift).
Detection of MRP1 [4]
MOLT-4 cells were exposed to piceatannol at the IC90 concentration for 96 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (5 × 105 cells per sample) were collected, centrifuged, and supernatants were discarded. Next, cells were washed with cold PBS, suspended in Cytofix/Cytoperm™ solution, and incubated on ice for 20 min. Following washing with Perm/Wash™ Buffer, cells were incubated for 30 min at 4 °C in the dark with FITC-conjugated mouse monoclonal antibody against MRP1 (QCRL-3) or FITC-conjugated mouse IgG2a isotype control antibody. The final concentration of the QCRL-3 antibody was 3 μg/ml (0.3 μg per 5 × 105 cells in 100 μl) and was equal to the final concentration of the isotype control antibody. After subsequent washing with Perm Wash Buffer, samples were kept on ice and immediately analyzed by flow cytometry. Results were expressed as the ratio of MFI of the QCRL-3 antibody and the isotype control antibody (MFI shift).
Detection of BCRP [4]
MOLT-4 cells were exposed topiceatannol at the IC90 concentration for 96 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (5 × 105 cells per sample) were collected, centrifuged, and supernatants were discarded. Next, cells were washed with cold PBS and incubated on ice for 30 min in the dark with PE-conjugated mouse monoclonal antibody against BCRP (5D3) or PE-conjugated mouse IgG2b isotype control antibody. The final concentration of the 5D3 antibody was 5 μg/ml (0.5 μg per 5 × 105 cells in 100 μl) and was equal to the final concentration of the isotype control antibody. After incubation, cells were washed with cold FCM Wash Buffer and incubated with 2.5 μg/ml 7AAD for 10 min at RT in the dark. Afterwards, samples were kept on ice and immediately analyzed by flow cytometry. 7AAD-positive cells, corresponding to non-viable cells, were excluded from data analysis. Results were expressed as the ratio of MFI of the 5D3 antibody and the isotype control antibody (MFI shift).
Cell Assay
Cell Cytotoxicity Assay[3]
Cell Types: Six DLBCL cell lines (Karpas 422, VAL, SUDHL-6, OCI Ly19, U2392 and DOHH2)
Tested Concentrations: 3.125, 6.25, 12.5, 25, and 50 μM
Incubation Duration: 72 hrs (hours)
Experimental Results: The IC50s were 18 μM in SUDHL-6, 25 μM in U2392, 37 mM in DOHH2, 48 μM in Karpas 422 and higher than 50 μM in OCI-Ly19 and in VAL.
Cytotoxicity assay [4]
The cytotoxic effect of piceatannol on MOLT-4 cells was determined using the neutral red uptake assay. MOLT-4 cells (7.5 × 104 cells/5 ml of the culture medium) were treated with piceatannol at concentrations of 0.05 μM, 15 μM, 25 μM, 50 μM, and 100 μM for 48 h (approximately three population doublings of MOLT-4 cells). MOLT-4 cells not exposed to piceatannol, but treated with DMSO (solvent) alone, were used as control. In all samples, DMSO concentration was equal to 0.1% (v/v) and did not affect the cell growth. Cells were stained with neutral red as described previously (Siedlecka-Kroplewska et al., 2012). Absorbance was measured at λ = 540 nm using a microplate reader. A dose-response curve was plotted to calculate the concentration of piceatannol required to inhibit cell growth by 50% (IC50) and 90% (IC90).
Cell cycle analysis [4]
MOLT-4 cells were treated with piceatannol at the concentration corresponding to the IC90 value (45.5 μM) for 6, 12, 24, and 48 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (2 × 106 cells per sample) were collected, stained with propidium iodide (PI), and analyzed by flow cytometry (Becton Dickinson FACScan, USA), as described previously (Siedlecka-Kroplewska et al., 2012).
Annexin V-FITC/PI assay [4]
Phosphatidylserine externalization and loss of plasma membrane integrity was examined using Annexin V-FITC Apoptosis Detection Kit. MOLT-4 cells were treated with piceatannol at the IC90 concentration for 12, 24, 48, 72, and 96 h or exposed to three repeated treatment cycles, each lasting 96 h (3 × 96 h). MOLT-4 cells not exposed to piceatannol were used as control. Experiments based on the exposure of cells to repeated treatment cycles were performed as follows. Cells (5 × 105 cells) were exposed to piceatannol (IC90). After each 96 h treatment period, cells were collected, washed, re-planted into a new flask, and then re-exposed to piceatannol for further 96 h. After treatment, cells (5 × 105 cells per sample) were collected and stained with FITC-conjugated annexin V and PI according to the manufacturer's protocol. Samples were analyzed by flow cytometry.
DNA fragmentation assay [4]
DNA fragmentation was examined by agarose gel electrophoresis. MOLT-4 cells were exposed to piceatannol at the IC90 concentration for 12, 24, and 48 h. MOLT-4 cells not exposed to piceatannol were used as control. After treatment, cells (2 × 106 cells per sample) were collected and DNA isolation was performed as described previously (Augustin et al., 2006). DNA fragments were fractionated by electrophoresis on 1.8% agarose gels, stained with ethidium bromide, and photographed using Gel Doc 2000 (Bio-Rad, Italy).
Detection of intracellular reactive oxygen species [4]
MOLT-4 cells (5 × 105 cells per sample) were incubated with piceatannol at the IC90 concentration for 45 min, 2 h, 4 h, and 6 h. Simultaneously, control cells were incubated in the absence of piceatannol. Thirty minutes before the end of incubation with piceatannol, H2DCFDA (final concentration 10 μM) was added. Cells were then collected, washed, and suspended in ice-cold PBS (Phosphate-Buffered Saline). Samples were analyzed for DCF fluorescence by flow cytometry.
Western blotting analysis of LC3, p62 and PARP1 [4]
MOLT-4 cells were incubated with piceatannol at the IC90 concentration. MOLT-4 cells not exposed to piceatannol were used as control. Cell lysates were prepared using Mammalian Cell Extraction Kit. The total concentration of proteins in cell lysates was determined using the Bradford protein assay. Protein samples (65 μg of total protein per sample) were separated electrophoretically by SDS-PAGE (12% for LC3 and p62, 10% for PARP1) and transferred onto a PVDF membrane. The membrane was then incubated with 5% non-fat dry milk in TBS (Tris-Buffered Saline) for 1 h at RT (room temperature). Following washing with TBST (0.1% Tween20 in TBS), the membrane was incubated with primary antibodies: rabbit anti-LC3 (1:4000) or mouse anti-p62 (1:200) or rabbit anti-PARP1 (1:1000) at 4 °C overnight, and after subsequent washing, incubated with appropriate horseradish peroxidase-conjugated secondary antibodies (1:10,000) for 2 h at RT. The membrane was also incubated with horseradish peroxidase-conjugated anti-GAPDH antibody (1:50,000, 1 h at RT) or horseradish peroxidase-conjugated anti-β-actin antibody (1:50,000, 45 min at RT) for loading control. The bound antibodies were detected by the enhanced chemiluminescence method using the Chemiluminescent Peroxidase Substrate. The densitometric analysis of immunoreactive protein bands was performed using Quantity One Software.
Immunofluorescent analysis [4]
The immunofluorescent analysis was performed as described previously (Siedlecka-Kroplewska et al., 2013). MOLT-4 cells were exposed to piceatannol at the IC90 concentration for 6, 12, 24, 48, 72, and 96 h. MOLT-4 cells not exposed to piceatannol were used as control. Cells were incubated with rabbit anti-LC3 primary antibody (1:500) for 1 h at RT, and subsequently with Cy3-conjugated anti-rabbit secondary antibody (1:600) for 1 h at RT in the dark. Afterwards, cells were stained with 1 μg/ml Hoechst 33342 for 15 min at RT in the dark. The mounting step of slides' preparation was performed using the Permafluor mounting medium. Slides were examined by the fluorescence microscope. The images were obtained using × 60 oil immersion objective lens.
Animal Protocol
Animal/Disease Models: Male C57BL/6 mice (40-50 g)[1]
Doses: 10, 20, and 40 mg/kg
Route of Administration: Intraperitoneally 1 h before LPS challenge
Experimental Results: Dramatically decreased the pulmonary edema induced by LPS.
Animals and Experimental Establishment Male C57BL/6 mice (40–50 g) were were kept in a temperature and humidity-controlled room with an artificial light/dark cycle and allowed to adapt the new environment for 1 week. Briefly, total 50 mice were randomly divided into five groups (n = 10), including the control, LPS, piceatannol (10, 20, and 40 mg/kg) + LPS groups. To establish ALI model, LPS (5 mg/kg) was intraperitoneal injection in mice as previous described (Yu et al., 2019). The mice of piceatannol group were received intraperitoneally with 10, 20, and 40 mg/kg 1 h before LPS challenge while control group mice were injected by the equal volume of saline. Twenty-four hours later, mice were euthanized and the biological samples were collected for subsequent determination.
References
[1]. Protective Effect of Piceatannol Against Acute Lung Injury Through Protecting the Integrity of Air-Blood Barrier and Modulating the TLR4/NF-κB Signaling Pathway Activation. Front Pharmacol. 2020 Jan 22;10:1613.
[2]. The Therapeutic Potential of Piceatannol, a Natural Stilbene, in Metabolic Diseases: A Review. J Med Food. 2017 May;20(5):427-438.
[3]. In vitro efficacy of tyrosine kinase inhibitors: SYK and BCR-ABL inhibitors in lymphomas.Hematol Oncol. 2011 Sep;29(3):164-6.
[4]. Induction of autophagy, apoptosis and aquisition of resistance in response to piceatannol toxicity in MOLT-4 human leukemia cells. Toxicol In Vitro. 2019 Sep;59:12-25.
Additional Infomation
Piceatannol is a stilbenol that is trans-stilbene in which one of the phenyl groups is substituted by hydroxy groups at positions 3 and 4, while the other phenyl group is substituted by hydroxy groups at positions 3 and 5. It has a role as a protein kinase inhibitor, a tyrosine kinase inhibitor, an antineoplastic agent, a plant metabolite, a hypoglycemic agent, an apoptosis inducer and a geroprotector. It is a stilbenol, a member of resorcinols, a member of catechols and a polyphenol. It derives from a hydride of a trans-stilbene.
Piceatannol has been reported in Malus, Caragana tibetica, and other organisms with data available.
Piceatannol is a polyhydroxylated stilbene extract from the seeds of Euphorbia lagascae, which inhibits protein tyrosine kinase Syk and induces apoptosis. (NCI)
Piceatannol is a metabolite found in or produced by Saccharomyces cerevisiae.
See also: Wine grape (part of); Robinia pseudoacacia whole (part of); Tsuga canadensis bark (part of).
Acute lung injury (ALI) is a common and complex inflammatory lung syndrome with higher morbidity and mortality rate. Piceatannol (PIC) has anti-inflammation and anti-oxidant properties. The study was designed to explore the effect and the action mechanisms of PIC on lipopolysaccharide (LPS)-induced ALI. Twenty-four hours after LPS challenge, mice from different treatment groups were euthanized, and the bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected. Then the degree of pulmonary edema, lung pathological changes, myeloperoxidase (MPO) activity, and the production of pro-inflammatory cytokines were detected. Additionally, the messenger RNA (mRNA) expressions associated with cell adhesion molecules and tight junction were analyzed through quantitative real-time (qRT)-PCR, and the TLR4/NF-κB activation was examined by western blot. The results showed that PIC significantly inhibited LPS-induced lung edema, histopathological damage, MPO activity, cell infiltration, and pro-inflammatory cytokines production. Moreover, PIC notably suppressed mRNA expressions associated with inflammation and cell adhesion molecules. Furthermore, PIC also alleviated LPS-induced damage of air-blood barrier through reducing the levels of total proteins in BALF and recovering the expression of occludin and ZO-1 in the lung tissues. We also found that PIC remarkably restrained the LPS-induced TLR4/NF-κB pathway activation in lung tissues. In conclusion, PIC may be potential to treat LPS-induced acute lung injury (ALI) via regulating air-blood barrier and TLR4/NF-κB signaling pathway activation.[1]
Metabolic disease comprises a set of risk factors highly associated with obesity and insulin resistance and is a consequence of central adiposity, hyperglycemia, and dyslipidemia. Furthermore, obesity increases the risk of the development of metabolic disease due to ectopic fat deposition, low-grade inflammation, and systemic energy disorders caused by dysregulated adipose tissue function. Piceatannol is a naturally occurring polyphenolic stilbene found in various fruits and vegetables and has been reported to exhibit anticancer and anti-inflammatory properties. In addition, recently reported beneficial effects of piceatannol on hypercholesterolemia, atherosclerosis, and angiogenesis underscore its therapeutic potential in cardiovascular disease. However, investigation of its role in metabolic disease is still in its infancy. This review intensively summarizes in vitro and in vivo studies supporting the potential therapeutic effects of piceatannol in metabolic disease, including inhibition of adipogenesis and lipid metabolism in adipocytes, and regulation of hyperlipidemia, hyperglycemia, insulin resistance, and fatty acid-induced inflammation and oxidative stress. [2]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C14H12O4
Molecular Weight
244.24
Exact Mass
244.073
Elemental Analysis
C, 68.85; H, 4.95; O, 26.20
CAS #
10083-24-6
Related CAS #
10083-24-6
PubChem CID
667639
Appearance
Light yellow to khaki solid powder
Density
1.5±0.1 g/cm3
Boiling Point
507.3±38.0 °C at 760 mmHg
Melting Point
223-227ºC
Flash Point
252.2±21.4 °C
Vapour Pressure
0.0±1.4 mmHg at 25°C
Index of Refraction
1.801
LogP
2.69
Hydrogen Bond Donor Count
4
Hydrogen Bond Acceptor Count
4
Rotatable Bond Count
2
Heavy Atom Count
18
Complexity
282
Defined Atom Stereocenter Count
0
SMILES
O([H])C1=C(C([H])=C([H])C(=C1[H])/C(/[H])=C(\[H])/C1C([H])=C(C([H])=C(C=1[H])O[H])O[H])O[H]
InChi Key
CDRPUGZCRXZLFL-OWOJBTEDSA-N
InChi Code
InChI=1S/C14H12O4/c15-11-5-10(6-12(16)8-11)2-1-9-3-4-13(17)14(18)7-9/h1-8,15-18H/b2-1+
Chemical Name
(E)-4-[2-(3,5Dihydroxyphenyl)ethenyl]1,2-benzenediol, 3,3′,4,5′-Tetrahydroxy-trans-stilbene
Synonyms
NSC 622471; NSC-622471; Piceatannol; NSC622471.
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 Data
Solubility (In Vitro)
DMSO: 48 mg/mL (196.5 mM)
Water:<1 mg/mL
Ethanol:<48 mg/mL (196.5 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (10.24 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 25.0 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: ≥ 2.5 mg/mL (10.24 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 25.0 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.

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Solubility in Formulation 3: 1% DMSO+30% polyethylene glycol+1% Tween 80: 30mg/mL


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Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 4.0943 mL 20.4717 mL 40.9433 mL
5 mM 0.8189 mL 4.0943 mL 8.1887 mL
10 mM 0.4094 mL 2.0472 mL 4.0943 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.

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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.

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT06127381 Not yet recruiting Drug: Glycolic acid tetrasubstituted
piceatannol (TGKP)
Acute Respiratory Distress
Syndrome (ARDS)
Gamaleya Research Institute of
Epidemiology and Microbiology, Health
Ministry of the Russian Federation
November 2023 Phase 1
NCT04983017 Recruiting Dietary Supplement: Dietary supplement
Other: Placebo
Chronic Inflammation
Inflammaging
Edifice Health August 10, 2021 Not Applicable
Biological Data
  • Piceatannol

    Int Immunopharmacol.2008 Dec 10;8(12):1695-702.

  • Piceatannol

    Int Immunopharmacol. 2008 Dec 10;8(12):1695-702.

  • Piceatannol

    Int Immunopharmacol. 2008 Dec 10;8(12):1695-702.

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