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propionyl-CoA

" in MedChemExpress (MCE) Product Catalog:

12

Inhibitors & Agonists

2

Peptides

4

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Products

1

Isotope-Labeled Compounds

2

Click Chemistry

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-137808
    Succinyl-Coenzyme A sodium
    3 Publications Verification

    Succinyl-CoA sodium

    Endogenous Metabolite Neurological Disease Metabolic Disease
    Succinyl CoA (Succinyl-coenzyme A) sodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA sodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA sodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA sodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA sodium 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) .
    Succinyl-Coenzyme A sodium
  • HY-113092

    Endogenous Metabolite Metabolic Disease
    Propionylcarnitine is metabolized by carnitine acetyltransferase from propionyl-CoA. Increased propionylcarnitine is regarded as a biomarker of vitamin B12 deficiency .
    Propionylcarnitine
  • HY-148285

    Succinyl-coenzyme A; S-(Hydrogen succinyl)coenzyme A

    Endogenous Metabolite Metabolic Disease
    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) .
    Succinyl CoA
  • HY-P5112A

    Azido-PEG3-FLAG TFA

    Biochemical Assay Reagents Others
    Azido-PEG3-DYKDDDDK (azide-PEG3-FLAG) TFA is a multifunctional fusion tag for the purification of recombinant proteins. Azido-PEG3-DYKDDDDK TFA is a click chemistry reagent, it contains an Azide group and can undergo copper-catalyzed azide-alkyne cycloaddition reaction (CuAAc) with molecules containing Alkyne groups. It can also undergo strain-promoted alkyne-azide cycloaddition (SPAAC) reactions with molecules containing DBCO or BCN groups .
    Azido-PEG3-DYKDDDDK TFA
  • HY-P5112

    Azido-PEG3-FLAG

    Biochemical Assay Reagents Others
    Azido-PEG3-DYKDDDDK (azide-PEG3-FLAG) is a multifunctional fusion tag for the purification of recombinant proteins. Azido-PEG3-DYKDDDDK is a click chemistry reagent, it contains an Azide group and can undergo copper-catalyzed azide-alkyne cycloaddition reaction (CuAAc) with molecules containing Alkyne groups. It can also undergo strain-promoted alkyne-azide cycloaddition (SPAAC) reactions with molecules containing DBCO or BCN groups .
    Azido-PEG3-DYKDDDDK
  • HY-164909

    PANK Metabolic Disease
    PZ-3022 is an orally active allosteric agonist of pantothenate kinase (PanK) with an EC50 of 5.3 nM against PanK3. PZ-3022 antagonizes the inhibitory effect of C3-CoA. PZ-3022 increases CoA levels in cells and the liver, upregulates CoASH and C2-CoA, downregulates C3-CoA, and restores impaired TCA cycle and mitochondrial function. PZ-3022 can be used for the research of propionic acidemia and metabolic CoA deficiency .
    PZ-3022
  • HY-B0399A

    DL-Carnitine; DL-Levocarnitine

    Mitochondrial Metabolism Metabolic Disease
    (±)-Carnitine (DL-Carnitine) is an orally effective racemic mixture of L-Carnitine (HY-B0399) and D-Carnitine. (±)-Carnitine elevates the mitochondrial NAD +/NADH ratio in the presence of 1,3-butanediol (HY-77490A). (±)-Carnitine does not increase glucose and urea production from L-glutamine, but stimulates propionate gluconeogenesis in rat renal cortical slices, and significantly reduces hepatic ketone body levels in rats fed a diet containing 30% high fat plus 20% 1,3-butanediol .
    (±)-Carnitine
  • HY-141467S

    Isotope-Labeled Compounds Endogenous Metabolite Metabolic Disease
    Propionyl CoA-d5 is the deuterium labeled Propionyl CoA (HY-141467). Propionyl CoA serves as a common intermediate in the catabolic pathways of 1,2-propanediol and propionate in Salmonella enterica serovar Typhimurium LT2, and also functions as a precursor for 2-methylcitrate. Propionyl CoA is utilized as a substrate for the 2-methylcitrate synthase (PrpC) enzyme to synthesize 2-methylcitrate .
    Propionyl CoA-d5
  • HY-CE00172

    Biochemical Assay Reagents Others
    (3,4-Dihydroxyphenyl)propionyl-CoA is a derivative of Coenzyme A (HY-128851).
    (3,4-Dihydroxyphenyl)propionyl-CoA
  • HY-CE00862

    3-Hydroxy-3-(3-hydroxy-4-methoxyphenyl)propionyl-coenzyme A

    Biochemical Assay Reagents Metabolic Disease
    3-Hydroxy-3-(3-hydroxy-4-methoxyphenyl)propionyl-CoA (3-Hydroxy-3-(3-hydroxy-4-methoxyphenyl)propionyl-coenzyme A) is a coenzyme A derivative.
    3-Hydroxy-3-(3-hydroxy-4-methoxyphenyl)propionyl-CoA
  • HY-W048444

    Endogenous Metabolite Metabolic Disease
    Diaminobiotin is a biotin analog. Diaminobiotin can increase the transcriptional activity of IL-2 and IL-2R genes in Jurkat cells. Diaminobiotin does not affect the abundance of holocarboxylase and the activity of propionyl-CoA carboxylase in Jurkat cells .
    Diaminobiotin
  • HY-148285A

    Succinyl-coenzyme A disodium; S-(Hydrogen succinyl)coenzyme A disodium

    Endogenous Metabolite Metabolic Disease
    Succinyl CoA (Succinyl-coenzyme A) disodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA disodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA disodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA disodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl-Coenzyme A sodium 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) .
    Succinyl CoA disodium

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