1. Metabolic Enzyme/Protease
  2. Endogenous Metabolite
  3. Succinyl CoA

Succinyl CoA  (Synonyms: Succinyl-coenzyme A; S-(Hydrogen succinyl)coenzyme A)

Cat. No.: HY-148285
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Succinyl CoA (Succinyl-coenzyme A) is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis).

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No. CAS : 604-98-8

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Top Publications Citing Use of Products

    Succinyl CoA purchased from MedChemExpress. Usage Cited in: Cell Rep. 2024 Dec 13;43(12):115060.  [Abstract]

    FLAG-TBK1 was overexpressed in HEK293T cells and immunoprecipitated using an anti-FLAG antibody. The immunoprecipitates were then treated with 2 mM Succinyl-Coenzyme A sodium (succinyl-CoA) for 15 min, followed by detection of TBK1 succinylation. The results showed that succinyl-coenzyme A sodium, a well-known precursor for protein succinylation, markedly induced succinylation of FLAG-tagged TBK1 in vitro.

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    Descripciòn

    Succinyl CoA (Succinyl-coenzyme A) is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis)[1][2][3].

    In Vitro

    Succinyl CoA acts as a substrate for rat liver δ-aminolevulinic acid synthase-1 with a Michaelis constant (Km) of 6-120 μmol/L[2].
    Succinyl CoA does not bind to recombinant NLRX1 in an in vitro pull-down assay[2].

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

    Peso molecular

    867.61

    Fòrmula

    C25H40N7O19P3S

    No. CAS
    SMILES

    O[C@@H]1[C@H](OP(O)(O)=O)[C@@H](COP(OP(OCC(C)(C)[C@@H](O)C(NCCC(NCCSC(CCC(O)=O)=O)=O)=O)(O)=O)(O)=O)O[C@H]1N2C=NC3=C(N)N=CN=C32

    Initial Source
    Envío

    Room temperature in continental US; may vary elsewhere.

    Almacenamiento

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

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    Nombre del producto:
    Succinyl CoA
    Cat. No.:
    HY-148285
    Cantidad:
    MCE Japan Authorized Agent: