SML1517
SR9243
≥98% (HPLC)
동의어(들):
N-(3-Bromophenethyl)-2,4,6-trimethyl-N-((3′-(methylsulfonyl)-[1,1′-biphenyl]-4-yl)methyl)benzenesulfonamide
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모든 사진(1)
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5 MG
₩149,510
About This Item
실험식(Hill 표기법):
C31H32BrNO4S2
CAS Number:
Molecular Weight:
626.62
MDL number:
UNSPSC 코드:
12352200
PubChem Substance ID:
NACRES:
NA.77
추천 제품
Quality Level
분석
≥98% (HPLC)
양식
powder
색상
white to beige
solubility
DMSO: 10 mg/mL, clear
저장 온도
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
생화학적/생리학적 작용
SR9243 has the ability to reduce liver fibrosis stimulated by BDL (bile-duct ligation) and CCL4 (carbon tetrachloride).[1] It stimulates apoptosis without promoting weight loss, hepatotoxicity and inflammation.[2] SR9243 blocks the initiation of liver-X-receptor (LXR) by increasing LXR-corepressor recruitment.[2]
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.
SR9243 is a selective inverse agonist of the nuclear receptor liver-X-receptor (LXR).
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
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시험 성적서(COA)
Lot/Batch Number
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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