Stattic

STAT3 inhibitor,small-molecule and potent CAS# 19983-44-9

Stattic

Catalog No. BCC1176----Order now to get a substantial discount!

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Quality Control of Stattic

Number of papers citing our products

Chemical structure

Stattic

3D structure

Chemical Properties of Stattic

Cas No. 19983-44-9 SDF Download SDF
PubChem ID 2779853 Appearance Powder
Formula C8H5NO4S M.Wt 211.19
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : 50 mg/mL (236.75 mM; Need ultrasonic)
Chemical Name 6-nitro-1-benzothiophene 1,1-dioxide
SMILES C1=CC(=CC2=C1C=CS2(=O)=O)[N+](=O)[O-]
Standard InChIKey ZRRGOUHITGRLBA-UHFFFAOYSA-N
Standard InChI InChI=1S/C8H5NO4S/c10-9(11)7-2-1-6-3-4-14(12,13)8(6)5-7/h1-5H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Stattic

DescriptionSmall molecule inhibitor of STAT3. Inhibits binding of tyrosine-phosphorylated peptide motifs to STAT3 SH2 domain and inhibits STAT3 activation, dimerization and nuclear translocation. Displays selectivity over STAT1, STAT5, c-Myc/Max, Jun/Jun and Lck. Induces apoptosis in STAT3-dependent cancer cell lines.

Stattic Dilution Calculator

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Stattic Molarity Calculator

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Preparing Stock Solutions of Stattic

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.7351 mL 23.6754 mL 47.3507 mL 94.7015 mL 118.3768 mL
5 mM 0.947 mL 4.7351 mL 9.4701 mL 18.9403 mL 23.6754 mL
10 mM 0.4735 mL 2.3675 mL 4.7351 mL 9.4701 mL 11.8377 mL
50 mM 0.0947 mL 0.4735 mL 0.947 mL 1.894 mL 2.3675 mL
100 mM 0.0474 mL 0.2368 mL 0.4735 mL 0.947 mL 1.1838 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Stattic

Stattic is a small molecule inhibitor of STAT3 with IC50 values of 2.562 ± 0.409 μM, 3.481 ± 0.953 μM, 2.282 ± 0.423 μM and 2.648 ± 0.542 μM, respectively, in UM-SCC-17B, OSC-19, Cal33 and UM-SCC-22B cell lines [1].

Stattic is reported to selectively inhibit dimerization, activation and nuclear translocation of STAT3. It can also induce the apoptosis of STAT3-dependent breast cancer cell lines [2].

The inhibition of STAT3 by Stattic results in decreased STAT3-mediated HIF-1 expression and subsequent radiosensitization of HNSCC cells. Inhibiting the STAT3 signaling pathway may represent an effective strategy in the treatment of HNSCC. The evidence of Stattic activity in vivo has also been found. Stattic pre-treatment sensitizes orthotopic xenograft HNSCC tumors to radiation, wich results in significantly reduced tumor growth, although this effect was not as dramatic as anticipated by the in vitro studies [1].

References:
[1] Makoto Adachi, Caixia Cui, Cristina T. Dodge, Mihir K. Bhayani, Stephen Y. Lai. Targeting STAT3 inhibits growth and enhances radiosensitivity in head and neck squamous cell carcinoma. Oral Oncology. 2012 July(48):1220-1226.

[2] Jochen Schust, Bianca Sperl, Angela Hollis, Thomas U. Mayer, and Thorsten Berg. Stattic: A Small-Molecule Inhibitor of STAT3 Activation and Dimerization. Chemistry & Biology. 2006(13):1235-1242.

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References on Stattic

Stattic and metformin inhibit brain tumor initiating cells by reducing STAT3-phosphorylation.[Pubmed:28030813]

Oncotarget. 2017 Jan 31;8(5):8250-8263.

Glioblastoma (GBM) is the most common and malignant type of primary brain tumor and associated with a devastating prognosis. Signal transducer and activator of transcription number 3 (STAT3) is an important pathogenic factor in GBM and can be specifically inhibited with Stattic. Metformin inhibits GBM cell proliferation and migration. Evidence from other tumor models suggests that metformin inhibits STAT3, but there is no specific data on brain tumor initiating cells (BTICs).We explored proliferation and migration of 7 BTICs and their differentiated counterparts (TCs) after treatment with Stattic, metformin or the combination thereof. Invasion was measured in situ on organotypic brain slice cultures. Protein expression of phosphorylated and total STAT3, as well as AMPK and mTOR signaling were explored using Western blot. To determine functional relevance of STAT3 inhibition by Stattic and metformin, we performed a stable knock-in of STAT3 in selected BTICs.Inhibition of STAT3 with Stattic reduced proliferation in all BTICs, but only in 4 out of 7 TCs. Migration and invasion were equally inhibited in BTICs and TCs. Treatment with metformin reduced STAT3-phosphorylation in all investigated BTICs and TCs. Combined treatment with Stattic and metformin led to significant additive effects on BTIC proliferation, but not migration or invasion. No additive effects on TCs could be detected. Stable STAT3 knock-in partly attenuated the effects of Stattic and metformin on BTICs.In conclusion, metformin was found to inhibit STAT3-phosphorylation in BTICs and TCs. Combined specific and unspecific inhibition of STAT3 might represent a promising new strategy in the treatment of glioblastoma.

Combined Treatment with Stattic and Docetaxel Alters the Bax/Bcl-2 Gene Expression Ratio in Human Prostate Cancer Cells[Pubmed:28032735]

Asian Pac J Cancer Prev. 2016 Nov 1;17(11):5031-5035.

Docetaxel, recognized as a stabilizing microtubule agent, is frequently administrated as a first line treatment for prostate cancers. Due to high side effects of monotherapy, however, combinations with novel adjuvants have emerged as an alternative strategy in cancer therapy protocols. Here, we investigated the combined effects of Stattic and docetaxel on the DU145 prostate cancer cell line. Cytotoxicity was evaluated by MTT assay. To understand molecular mechanisms of Stattic action, apoptotic related genes including Bcl-2, Mcl-1, Survivin and Bax were evaluated by real-time RT-PCR. Alteration in the expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 genes and Bax/Bcl-2 ratio were investigated via the 2DeltaDeltaCT method. The IC50 values for docetaxel and Stattic were 3.7 +/- 0.9 nM and 4.6+/-0.8 muM, respectively. Evaluation of key gene expression levels revealed a noticeable decrease in antiapoptotic Bcl-2 and Mcl-1 along with an increase in pro-apoptotic Bax mRNA levels (p<0.05). Our results suggest that combination of a STAT3 inhibitor with doctaxel can be considered as a potent strategy for induction of apoptosis via increasing Bax mRNA expression.

STAT3 inhibitor stattic enhances radiosensitivity in esophageal squamous cell carcinoma.[Pubmed:25492480]

Tumour Biol. 2015 Mar;36(3):2135-42.

The radioresistance of esophageal squamous cell carcinoma (ESCC) remains an obstacle for the effective radiotherapy of ESCC. This study aimed to investigate the radiosensitization of ESCC by signal transducer and activator of transcription 3 (STAT3) inhibitor Stattic. ECA109, TE13, and KYSE150 cell lines were exposed to hypoxia and treated with Stattic or radiation, alone or in combination. Cell proliferation, colony formation, apoptosis, and double-stranded DNA breaks (DSBs) were examined. In addition, ECA109 cells were xenografted into nude mice and treated with radiation and/or Stattic. The levels of STAT3, p-STAT3, hypoxia-inducible factor 1alpha (HIF-1alpha), and vascular endothelial growth factor (VEGF) in ESCC cells and xenografts were detected by Western blot and immunohistochemical analysis. Our results showed that Stattic efficiently radiosensitized ESCC cells and xenografts, especially under hypoxia. Moreover, Stattic inhibited STAT3 activation and downregulated HIF-1alpha and VEGF expression. In conclusion, Stattic confers radiosensitivity in ESCC cells in vitro and in vivo and is a potential adjuvant for the radiotherapy of ESCC in the clinical setting.

Stattic: a small-molecule inhibitor of STAT3 activation and dimerization.[Pubmed:17114005]

Chem Biol. 2006 Nov;13(11):1235-42.

Signal transducers and activators of transcription (STATs) are a family of latent cytoplasmic transcription factors that transmit signals from the cell membrane to the nucleus. One family member, STAT3, is constitutively activated by aberrant upstream tyrosine kinase activities in a broad spectrum of cancer cell lines and human tumors. Screening of chemical libraries led to the identification of Stattic, a nonpeptidic small molecule shown to selectively inhibit the function of the STAT3 SH2 domain regardless of the STAT3 activation state in vitro. Stattic selectively inhibits activation, dimerization, and nuclear translocation of STAT3 and increases the apoptotic rate of STAT3-dependent breast cancer cell lines. We propose Stattic as a tool for the inhibition of STAT3 in cell lines or animal tumor models displaying constitutive STAT3 activation.

Description

Stattic is a potent STAT3 inhibitor. Stattic inhibits STAT3 phosphorylation (at Y705 and S727).

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