| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 25mg | 电议 |
| 100mg | 电议 |
Preparation Method | Screening was performed at approximately 30 ℃ to verify the specificity of the screening by similar experiments in which the experimental compounds( Stattic ) were bound to the SH2 domains of STAT1, STAT5, and Lck |
Reaction Conditions | Stattic and protein for 60min |
Applications | Stattic inhibited binding of a phosphotyrosine-containing peptide derived from the gp130 receptor to the STAT3 SH2 domain in a strongly temperature-dependent manner: while only weak activity was observed at 22℃, the compound displayed moderate activity at 30℃ and high potency at the physiologically relevant temperature of 37℃ (apparent IC50 value after 1 hr of incubation: 5.1 ± 0.8 μM). |
Cell lines | Ly3 cells |
Preparation Method | Ly3 parental cells were plated in the presence of 10% FBS and treated with Stattic at indicated concentrations for 24 or 48 h. Phosphorylated STAT3 levels or cell proliferation were analyzed by flow cytometry or MTS assays, respectively. |
Reaction Conditions | 1/2.5uM Stattic for 24 or 48 h |
Applications | The viability of Ly3 cells cultured in vitro was affected by two inhibitors(STATTIC and S31-201) tested in a dose-dependent manner, and the antiproliferative effect was associated with inhibition of STAT3 phosphorylation. |
Animal models | 4-6-week-old athymic nude mice |
Preparation Method | Ly3 parental tumor-bearing mice were treated daily with vehicle or STATTIC at 3.75mg/kg. Two hours after the last treatment, samples were collected from each group to prepare whole-cell lysates and Western blotting analysis was performed to detect phosphorylated STAT3 levels |
Dosage form | 3.75mg/kg STATTIC for 8 days |
Applications | The effects of both inhibitors were tested in a dose-dependent manner, and the antiproliferative effects were associated with the inhibition of STAT3 phosphorylation. The antilymphoma activity of STATTIC was also observed in the Ly3 NOD/SCID IL2Rnull mouse model, and the inhibition of tumor growth was significant. |
| 产品描述 | Stattic is the first non-peptide small molecule inhibitor of STAT3, which effectively inhibits STAT3 activation and nuclear translocation. Its IC50 is 5.1 µM, and its selectivity on STAT3 is much higher than that on STAT1[1].Stattic inhibits the binding of a high affinity phosphopeptide for the SH2 domain of STAT3[2]. The viability of Ly3 cells cultured in vitro was affected by two inhibitors(STATTIC and S31-201) tested in a dose-dependent manner, and the antiproliferative effect was associated with inhibition of STAT3 phosphorylation[3]. Stattic directly or indirectly reduces histone acetylation and suggest reevaluation of Stattic and related compounds as polypharmacological agents through multipronged cytotoxic effects on cancer cells[5]. Exposure of dendritic cells (DCs) to conditioned media (CM) from cancer cells treated with stattic and/or DOX resulted in secretion of IL-12, which is an indicator of DCs maturation and induction of Th1 response[7]. The effects of both inhibitors(STATTIC and S31-201) were tested in a dose-dependent manner, and the antiproliferative effects were associated with the inhibition of STAT3 phosphorylation. The antilymphoma activity of STATTIC was also observed in the Ly3 NOD/SCID IL2Rnull mouse model, and the inhibition of tumor growth was significant[3].In AC mice, Phosphorylated STAT3 was upregulated in AS kidneys and glomeruli. Treatment with stattic ameliorated the progressive renal dysfunction, such as increased levels of proteinuria, BUN and serum creatinine. Stattic also significantly suppressed the gene expression levels of renal injury markers (Lcn2, Kim-1), pro-inflammatory cytokines (Il-6, KC), pro-fibrotic genes (Tgf-β, Col1a1, α-Sma) and Mmp9. Stattic treatment decreased the renal fibrosis congruently with the decrease of transforming growth factor beta (TGF-β) protein and increase of antifibrosis-associated markers p-Smad1, 5 and 8, which are negative regulators of TGF-β signaling[4]. To investigate the effects of STAT3 here, LPS/d-GalN-induced hepatic damage was induced in mice, the STAT3 inhibitor Stattic was administered, and the degree of liver injury, inflammation, and hepatocyte apoptosis were investigated[6]. References: |
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