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SML1517

Sigma-Aldrich

SR9243

≥98% (HPLC)

Synonym(s):

N-(3-Bromophenethyl)-2,4,6-trimethyl-N-((3′-(methylsulfonyl)-[1,1′-biphenyl]-4-yl)methyl)benzenesulfonamide

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About This Item

Empirical Formula (Hill Notation):
C31H32BrNO4S2
CAS Number:
Molecular Weight:
626.62
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 10 mg/mL, clear

storage temp.

2-8°C

SMILES string

CC1=CC(C)=C(S(N(CCC2=CC=CC(Br)=C2)CC3=CC=C(C4=CC(S(C)(=O)=O)=CC=C4)C=C3)(=O)=O)C(C)=C1

InChI

1S/C31H32BrNO4S2/c1-22-17-23(2)31(24(3)18-22)39(36,37)33(16-15-25-7-5-9-29(32)19-25)21-26-11-13-27(14-12-26)28-8-6-10-30(20-28)38(4,34)35/h5-14,17-20H,15-16,21H2,1-4H3

InChI key

FYQFEJFTCLKXTQ-UHFFFAOYSA-N

Biochem/physiol Actions

SR9243 has the ability to reduce liver fibrosis stimulated by BDL (bile-duct ligation) and CCL4 (carbon tetrachloride). It stimulates apoptosis without promoting weight loss, hepatotoxicity and inflammation. SR9243 blocks the initiation of liver-X-receptor (LXR) by increasing LXR-corepressor recruitment.
SR9243 is a selective inverse agonist of the nuclear receptor liver-X-receptor (LXR) that targets the Warburg effect, inhibiting glycolysis and lipogenesis by reducing glycolytic and lipogenic gene expression. SR9243 is believed to enhance corepressor recruitment to LXRs at target-gene promoters, resulting in suppression of gene expression. SR9243 induced apoptosis in tumor cells without harming normal cells. SR9243 reduced prostate, colorectal, and lung cancer cell viability at nanomolar concentrations and also inhibited colon tumor xenograft growth.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Liver X Receptor Inverse Agonist SR9243 Suppresses Nonalcoholic Steatohepatitis Intrahepatic Inflammation and Fibrosis.
Huang P, et al.
BioMed Research International, 2018 (2018)
Colin A Flaveny et al.
Cancer cell, 28(1), 42-56 (2015-06-30)
Malignant cells exhibit aerobic glycolysis (the Warburg effect) and become dependent on de novo lipogenesis, which sustains rapid proliferation and resistance to cellular stress. The nuclear receptor liver-X-receptor (LXR) directly regulates expression of key glycolytic and lipogenic genes. To disrupt

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