Catalog No.S1155 Synonyms: NSC 74859
Molecular Weight(MW): 365.36
S3I-201 shows potent inhibition of STAT3 DNA-binding activity with IC50 of 86 μM in cell-free assays, and low activity towards STAT1 and STAT5.
Cited by 23 Publications
9 Customer Reviews
On day 1, 5-week-old female NOD/SCID mice were injected with 1 x 108 cells of the NOD/SCID repopulating T315I BCR-ABL1-positive leukemia UPN1 cells. On day 2, these mice were treated with either vehicle (n = 6), vismodegib (20 mg/kg per os; q.d.; n = 6), ponatinib (30 mg/kg; q.d.; n = 6), vismodegib (20 mg/kg per os; q.d.) + ponatinib (30 mg/kg; q.d.; n = 6) for each group. On day 28, mice were sacrificed for evaluation. CD19-positive cells from peripheral blood from each mouse have been shown. Histopathologic analysis of the bone marrow cavity from each treated mouse with UPN1 transplantation. Similar results were obtained in 2 independent experiments. H&E, hematoxylin and eosin.
Clin Cancer Res 2013 19(6), 1422-32. S3I-201 purchased from Selleck.
Inhibition of JAK1/2 with AG490 or STAT3 with S3I-201 leads to reduced STAT3 activation and reduced WASF3 levels. In contrast, treatment with Dasatinib (SRC inhibitor) or Gefitinib (EGFR inhibitor) does not significantly affect activated STAT3 or WASF3 levels.
Carcinogenesis 2013 34(9), 1994-9. S3I-201 purchased from Selleck.
A. Representative images and quantifications B. of tube formation of human lymphatic endothelial cells (HLECs) cultured with conditioned medium derived from LoVo cells. DMSO was used as vehiche control. Scale bars: 50μm. C. Immunoprecipitation using anti-BRG1 or anti-STAT3 antibodies was performed in LoVo cells, followed by immunoblotting with the indicated antibodies. D. (Left) Western blot analysis of BRG1, STAT3, p-STAT3 expression after transfection with siNC and siBRG1 in the presence or absence of S3I-201 (STAT3-specific inhibitor) in SW480 cells. (Right) Quantitative expression analysis of VEGFC protein levels by ELISA in the supernatants of SW480 cells after transfection with siNC and siBRG1 in the presence or absence of S3I-201 (STAT3-specific inhibitor) in SW480 cells. *p<0.05, **p<0.01. E. The luciferase activity fold change of STAT3 pathway reporter in LoVo and SW480 cells.
Oncotarget, 2016, 7(24):36501-36509. S3I-201 purchased from Selleck.
The inhibitors U0126, PP1 and S3I-201 reduce the colony-forming ability of KIF5B-RET positive cells. A549 cells carrying KIF5B-RET were diluted and seeded in 6-well plates, treated with DMSO, U0126 (MEK inhibitor) 10 uM, PP1 (SRC inhibitors) 5 uM or S3I-201(STAT3 inhibitors) 100 uM for 14 days. The total numbers of colonies, each containing more than 40 cells, were determined. (*P < 0.05, **P < 0.01, ***P < 0.001, Student's t test).
Mol Cancer 2014 13:176. S3I-201 purchased from Selleck.
The survival phenotype of A549 cells dependents on transiently activation of STAT3 signaling pathway. A549 cells were mock-invaded (A549, medium alone as control) following treatment with or without NSC 74859 for 24 h. DMSO was used for control. Cell lysates were analyzed by immunoblotting with antibodies to pSTAT3, STAT3 (2 h), and β-actin.
Microbes Infect 2014 16(1), 17-27. S3I-201 purchased from Selleck.
(A) The expression and phosphorylation of STAT3 in DCs after inhibition by NSC74859 was measured by western blot. β-Actin was measured as an internal control. The results are representative of three independent experiments. The expression of PD-L1 in DCs after STAT3 inhibition by NSC74859. DCs were seeded at a density of 2 x 106per well in 6-well plates. NSC74859 (100 uM) and TGF-β (10 ng/ml) were added on day 4 of DC culture. Cells were harvested on day 6, and the expression of PD-L1 was analyzed by western blot and flow cytometry. (B) The expression of PD-L1 was measured by western blot. (C) Densitometric analysis from the above immunoblots is shown as a bar chart. Data are shown as the means ± SD from 3 replicate experiments. **P < 0.01 vs. control DCs; ##P < 0.01 vs. stimulated with TGF-β only.
Int Immunopharmacol 2014 20(1), 117-23. S3I-201 purchased from Selleck.
Effects of LPS on RANKL mRNA expression. aP<0.05. (A) MLO-Y4 cells were incubated with various concentrations of LPS for 4 h. RANKL expression significantly increased after LPS stimulation at 100, 500, and 1000 ng/mL compared to the control, and there were no significant differences among the three groups. (B) The cells were incubated with or without 100 ng/mL LPS for 0.5, 1, 2, 4, and 8 h. RANKL expression increased significantly after 1 h of LPS treatment and reached a peak at 4 h. (C) The cells were pretreated with U0126 (10 μM) and S3I-201 (100 μM) separately or simultaneously for 1 h and then treated with 100 ng/mL of LPS for 4 h. RANKL expression was significantly decreased in presence of U0126 compared to that in the group with only LPS treatment but was still higher than that in the control. However in the presence of S3I-201 with or without U0126, RANKL expression was the lowest, but there was no significant difference compared to the control.
Cell Biol Int, 2017, 41(1):84-92. S3I-201 purchased from Selleck.
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Choose Selective STAT Inhibitors
|Description||S3I-201 shows potent inhibition of STAT3 DNA-binding activity with IC50 of 86 μM in cell-free assays, and low activity towards STAT1 and STAT5.|
|Features||A chemical probe inhibitor of Stat3 activity.|
S3I-201 inhibits growth and induces apoptosis preferentially in tumor cells that contain persistently activated Stat3 by inhibiting Stat3·Stat3 complex formation and Stat3 DNA-binding and transcriptional activitie. Moreover, S3I-201 also inhibits the expression of the Stat3-regulated genes encoding cyclin D1, Bcl-xL, and survivin.  S3I-201 inhibits breast carcinoma MDA-MB-435, MDA-MB-453 and MDA-MB-231 cell lines with IC50 of 100 μM. In addition, the cells with impaired TGF-β signaling are four times as sensitive to the STAT3 inhibitor S3I-201.  A recent study shows that S3I-201 potentiates the antiproliferative effect of cetuximab in HepG2 and Huh-7 cells via the STAT3 signalling pathway. 
|In vivo||S3I-201 (5 mg/kg, i.v. every 2 or every 3 days) shows the antitumor efficacy in mouse models with human breast tumor xenografts that harbor constitutively active Stat3.  S3I-201 treatment reduces Varicella-zoster virus (VZV) replication on the basis of the bioluminescence signal and the number of positive skin xenografts compared with DMSO-treated mice by inhibiting STAT3 phosphorylation. |
In vitro Stat3 DNA-binding assay and EMSA analysis :Briefly, 100 mL of biotinyl-e-Ac-EPQpYEEIEL-OH (in 50 mM Tris/150 mM NaCl, pH 7.5) is added to each well of streptavidin-coated 96-well microtiter plates and incubated with shaking at 4 °C overnight. Then plates are rinsed with PBS/Tween 20 and then two times with 200 mL of BSA-T-PBS (0.2% BSA/0.1% Tween 20/PBS). Then 50 mL of Lck-SH2-GST fusion protein (6.4 ng/ml in BSA-T-PBS) is added to each well of the 96-well plate in the presence and absence of 50 mL of S3I-201 (for 30 and 100 mM final concentrations), and the plate is shaken at room temperature for 4 hours. After solutions are removed, each well is rinsed four times with BSA-T-PBS (200 mL), and 100 mL of polyclonal rabbit anti-GST antibody (100 ng/mL in BSA-T-PBS) is added to each well and incubated at 4 °C overnight. After washing with BSA-T-PBS, 100 mL of 200 ng/mL BSA-T-PBS horseradish peroxidase-conjugated mouse anti-rabbit antibody is added to each well and incubated for 45 minutes at room temperature. After four washing steps with BSA-T-PBS and three washing steps with PBS-T, 100 mL of peroxidase substrate is added to each well and incubated for 5-15 minutes. The peroxidase reaction is stopped by adding 100 mL of 1 M sulfuric acid solution, and absorbance is read at 450 nm with an ELISA plate rea
|In vitro||DMSO||73 mg/mL (199.8 mM)|
|In vivo||5% DMSO+corn oil||6mg/mL|
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