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573102

Sigma-Aldrich

STAT3 Inhibitor VI, S3I-201

STAT3 Inhibitor VI, S3I-201, CAS 501919-59-1, is a cell-permeable compound that binds Stat3-SH2 domain and blocks Stat3 phosphorylation, dimerization, DNA-binding, & Stat3-dependent transcription.

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Synonym(s):
STAT3 Inhibitor VI, S3I-201, 2-Hydroxy-4-(((4-methylphenyl)sulfonyloxy)acetyl)amino)-benzoic acid, NSC 74859
Empirical Formula (Hill Notation):
C16H15NO7S
CAS Number:
Molecular Weight:
365.36
MDL number:

Quality Level

Assay

≥95% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

light beige

solubility

DMSO: 10 mg/mL (Use only fresh, anhydrous DMSO.)

shipped in

ambient

storage temp.

−20°C

InChI

1S/C16H15NO7S/c1-10-2-5-12(6-3-10)25(22,23)24-9-15(19)17-11-4-7-13(16(20)21)14(18)8-11/h2-8,18H,9H2,1H3,(H,17,19)(H,20,21)

InChI key

HWNUSGNZBAISFM-UHFFFAOYSA-N

General description

A cell-permeable amidosalicylic acid compound that binds Stat3-SH2 domain and prevents Stat3 phosphorylation/activation, dimerization, DNA-binding, and Stat3-dependent transcription. Shown to arrest Stat3-dependent tumor growth both in cultures in vitro (effective conc. ≤100 µM) and in a murine xenograft model in vivo (5 mg/kg, i.v.). Also available as a 50 mM solution in DMSO (Cat. No. 573130).

Packaging

Packaged under inert gas

Warning

Toxicity: Regulatory Review (Z)

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Supriya Murthy et al.
Cell death & disease, 13(1), 53-53 (2022-01-14)
The danger signal extracellular calcium is pathophysiologically increased in the synovial fluid of patients with rheumatoid arthritis (RA). Calcium activates the NLRP3-inflammasome via the calcium-sensing receptor in monocytes/macrophages primed by lipopolysaccharide, and this effect is mediated by the uptake of
Mutation-Driven S100A8 Overexpression Confers Aberrant Phenotypes in Type 1 CALR-Mutated MPN.
Wang, et al.
International Journal of Molecular Sciences, 24 (2023)
Kentaro Kajiwara et al.
Life science alliance, 4(4) (2021-02-13)
Compensatory growth of organs after loss of their mass and/or function is controlled by hepatocyte growth factor (HGF), but the underlying regulatory mechanisms remain elusive. Here, we show that CUB domain-containing protein 1 (CDCP1) promotes HGF-induced compensatory renal growth. Using

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