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Key Documents

SML0068

Sigma-Aldrich

CTP Inhibitor

≥98% (HPLC)

Sinonimo/i:

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

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About This Item

Formula empirica (notazione di Hill):
C13H9ClN2O6S
Numero CAS:
Peso molecolare:
356.74
Numero MDL:
Codice UNSPSC:
12352200
ID PubChem:
NACRES:
NA.77

Livello qualitativo

Saggio

≥98% (HPLC)

Forma fisica

powder

Colore

white to tan

Solubilità

DMSO: ≥23 mg/mL

Temperatura di conservazione

2-8°C

Stringa SMILE

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)
IIJQJWNGBILZCU-UHFFFAOYSA-N

Applicazioni

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.

Azioni biochim/fisiol

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.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

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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