SML0068
CTP Inhibitor
≥98% (HPLC), mitochondrial citrate transport protein inhibitor, powder
Synonym(s):
ZINC Compound 792949; 4-Chloro-3-[[(3-nitrophenyl)amino]sulfonyl]-benzoic acid
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About This Item
Empirical Formula (Hill Notation):
C13H9ClN2O6S
CAS Number:
Molecular Weight:
356.74
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
Product Name
CTP Inhibitor, ≥98% (HPLC)
SMILES string
OC(=O)c1ccc(Cl)c(c1)S(=O)(=O)Nc2cccc(c2)[N+]([O-])=O
InChI key
IIJQJWNGBILZCU-UHFFFAOYSA-N
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)
assay
≥98% (HPLC)
form
powder
color
white to tan
solubility
DMSO: ≥23 mg/mL
storage temp.
2-8°C
Quality Level
Related Categories
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.
CTP inhibitor has been used in mouse to study the transition of endothelial to mesenchymal cells.
Biochem/physiol Actions
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.
CTP inhibitor blocks the exchange of tricarboxylates the key intermediates in anabolism and catabolism by mitochondrial citrate transport protein (CTP).
Storage Class
11 - Combustible Solids
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
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
A metabolic basis for endothelial-to-mesenchymal transition
Xiong J, et al.
Molecular Cell, 69, 689-698 (2018)
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)
Marta Manco et al.
Biomolecules, 14(2) (2024-02-24)
Feline leukemia virus C receptor 1a (FLVCR1a), initially identified as a retroviral receptor and localized on the plasma membrane, has emerged as a crucial regulator of heme homeostasis. Functioning as a positive regulator of δ-aminolevulinic acid synthase 1 (ALAS1), the
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