1. Metabolic Enzyme/Protease
  2. Endogenous Metabolite
  3. Acetyl Coenzyme A trisodium

Acetyl Coenzyme A trisodium (Synonyms: Acetyl-CoA trisodium)

Cat. No.: HY-113596
Handling Instructions

Acetyl Coenzyme A trisodium (Acetyl-CoA trisodium) is a central metabolic intermediate. Acetyl Coenzyme A trisodium is the actual molecule through which glycolytic pyruvate enters the tricarboxylic acid (TCA) cycle, is a key precursor of lipid synthesis, and is the sole donor of the acetyl groups for acetylation. Acetyl Coenzyme A trisodium acts as a potent allosteric activator of pyruvate carboxylase (PC).

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Acetyl Coenzyme A trisodium Chemical Structure

Acetyl Coenzyme A trisodium Chemical Structure

CAS No. : 102029-73-2

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Description

Acetyl Coenzyme A trisodium (Acetyl-CoA trisodium) is a central metabolic intermediate. Acetyl Coenzyme A trisodium is the actual molecule through which glycolytic pyruvate enters the tricarboxylic acid (TCA) cycle, is a key precursor of lipid synthesis, and is the sole donor of the acetyl groups for acetylation. Acetyl Coenzyme A trisodium acts as a potent allosteric activator of pyruvate carboxylase (PC)[1].

In Vitro

Acetyl-coenzyme A (Acetyl-CoA) is a membrane-impermeant molecule constituted by an acetyl moiety (CH3CO) linked to coenzyme A (CoA), a derivative of vitamin B5 and cysteine, through a thioester bond. As thioester bonds are energy rich, the chemical structure of acetyl-CoA facilitates the transfer of the acetyl moiety to a variety of acceptor molecules, including amino groups on proteins[1].
In most mammalian cells, Acetyl-coenzyme A (Acetyl-CoA) is predominantly generated in the mitochondrial matrix by various metabolic circuitries, namely glycolysis, β-oxidation, and the catabolism of branched amino acids. Cytosolic Acetyl-coenzyme A is the precursor of multiple anabolic reactions that underlie the synthesis of fatty acids and steroids, as well as specific amino acids including glutamate, proline, and arginine[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Mice deprived of food (but with access to water ad libitum) for 24 hr exhibit a significant reduction in total Acetyl-coenzyme A (Acetyl-CoA) levels in several organs, including the heart and muscles, corresponding to a decrease in protein acetylation levels. However, the same experimental conditions have no major effects on Acetyl-coenzyme A concentrations in the brain and actually increase hepatic Acetyl-coenzyme A and protein acetylation levels. Ethanol intake augments Acetyl-coenzyme A levels in hepatic mitochondria[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Clinical Trial
Molecular Weight

875.52

Formula

C₂₃H₃₅N₇Na₃O₁₇P₃S

CAS No.

102029-73-2

SMILES

O[[email protected]]1[[email protected]@H](O[[email protected]](COP(OP(OCC(C)([[email protected]@H](O)C(NCCC(NCCSC(C)=O)=O)=O)C)(O[Na])=O)(O)=O)[[email protected]]1OP(O[Na])(O[Na])=O)N2C3=C(C(N)=NC=N3)N=C2

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Please store the product under the recommended conditions in the Certificate of Analysis.

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Keywords:

Acetyl Coenzyme A trisodiumAcetyl-CoA trisodiumEndogenous MetabolitePyruvatecarboxylasesecondmessengerintermediateTCAprecursorInhibitorinhibitorinhibit

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Acetyl Coenzyme A trisodium
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