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SML0068

Sigma-Aldrich

CTP Inhibitor

≥98% (HPLC)

Sinónimos:

ZINC Compound 792949; 4-Chloro-3-[[(3-nitrophenyl)amino]sulfonyl]-benzoic acid

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About This Item

Fórmula empírica (notación de Hill):
C13H9ClN2O6S
Número de CAS:
412940-35-3
Peso molecular:
356.74
MDL number:
MFCD01122300
UNSPSC Code:
12352200
PubChem Substance ID:
329825132
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to tan

solubility

DMSO: ≥23 mg/mL

storage temp.

2-8°C

SMILES string

OC(=O)c1ccc(Cl)c(c1)S(=O)(=O)Nc2cccc(c2)[N+]([O-])=O

InChI

1S/C13H9ClN2O6S/c14-11-5-4-8(13(17)18)6-12(11)23(21,22)15-9-2-1-3-10(7-9)16(19)20/h1-7,15H,(H,17,18)

InChI key

IIJQJWNGBILZCU-UHFFFAOYSA-N

Application

CTP inhibitor may be used in cell signaling studies.
CTP inhibitor has been used in mouse to study the transition of endothelial to mesenchymal cells.

Biochem/physiol Actions

CTP inhibitor blocks the exchange of tricarboxylates the key intermediates in anabolism and catabolism by mitochondrial citrate transport protein (CTP).
CTP Inhibitor is an inhibitor of mitochondrial citrate transport protein, was the first purely competitive inhibitor to be discovered and is more potent than BTC.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

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Jiakang Sun et al.
Molecular and cellular pharmacology, 2(3), 101-110 (2010-08-06)
Cytoplasmic citrate is the prime carbon source for fatty acid, triacylglycerol, and cholesterol biosyntheses, and also regulates glucose metabolism via its allosteric inhibition of phosphofructokinase. It originates either via the efflux of citrate from the mitochondrial matrix on the inner
A metabolic basis for endothelial-to-mesenchymal transition
Xiong J, et al.
Molecular Cell, 69, 689-698 (2018)
Kishore S Malyavantham et al.
Chromosoma, 117(6), 553-567 (2008-07-05)
To study when and where active genes replicated in early S phase are transcribed, a series of pulse-chase experiments are performed to label replicating chromatin domains (RS) in early S phase and subsequently transcription sites (TS) after chase periods of
Bowen Wu et al.
Cell metabolism, 32(6), 967-980 (2020-12-03)
Autoimmune T cells in rheumatoid arthritis (RA) have a defect in mitochondrial oxygen consumption and ATP production. Here, we identified suppression of the GDP-forming β subunit of succinate-CoA ligase (SUCLG2) as an underlying abnormality. SUCLG2-deficient T cells reverted the tricarboxylic acid (TCA)
Ali Burak Ozkaya et al.
Anti-cancer agents in medicinal chemistry, 15(3), 374-381 (2014-12-17)
Lipogenesis is considered to be a very important aspect of cancer metabolism and targeting de novo lipid synthesis or related pathways are among novel approaches to treat cancer. Many targets of the pathway including ATP-citrate lyase (ACLY), acetyl-CoA carboxylase and

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