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Succinyl-CoA

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Amyloid-β (2) Biochemical Assay Reagents (6) Caspase (1) Endogenous Metabolite (5) Mitochondrial Metabolism (5) Nuclear Hormone Receptor 4A/NR4A (1) Parasite (1) PERK (1) Pyroptosis (1) Reactive Oxygen Species (ROS) (3)
By Research Areas:	Cancer (1) Infection (1) Inflammation/Immunology (3) Metabolic Disease (10) Neurological Disease (4)

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Recombinant Proteins

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) .

HY-12688A

Succinyl phosphonate trisodium salt 10+ Cited Publications	Mitochondrial Metabolism Reactive Oxygen Species (ROS) Amyloid-β	Neurological Disease Inflammation/Immunology
Succinyl phosphonate trisodium salt is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate trisodium salt protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate trisodium salt corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate trisodium salt reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate trisodium salt improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate trisodium salt can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .

HY-E70121

Succinyl-CoA synthetase	Endogenous Metabolite Mitochondrial Metabolism	Neurological Disease Metabolic Disease Inflammation/Immunology
Succinyl-CoA synthetase is a mitochondrial matrix enzyme and catalyst. Succinyl-CoA synthetase supports TCA, ketone and heme metabolism and is activated by mitochondrial phosphate. Succinyl-CoA synthetase distributes broadly across mammalian tissues with distinct substrate-related biochemical features. Succinyl-CoA synthetase gains structural stability after phosphorylation and relies on SUCLG1-encoded subunit for activity. Succinyl-CoA synthetase malfunction links to metabolic and neurological disorders. Succinyl-CoA synthetase serves as a research tool for mitochondrial hepatoencephalomyopathy .

HY-173527

PSSI-51	Mitochondrial Metabolism	Metabolic Disease
PSSI-51 is an orally active, peripherally selective inhibitor of succinyl-CoA:3-ketoacid-CoA transferase (SCOT). PSSI-51 inhibits SCOT activity in peripheral tissues (such as muscle and kidney) but does not affect SCOT activity in brain tissue. PSSI-51 reduces ketone body oxidation by inhibiting SCOT, thereby improving obesity-related hyperglycemia. PSSI-51 can be used in the study of type 2 diabetes (T2D) and has the potential to improve obesity-related metabolic disorders .

HY-126791A

Methylmalonyl-CoA tetralithium IsoSuccinyl coenzyme A tetralithium; Methylmalonyl coenzyme tetralithium	Endogenous Metabolite	Others
Methylmalonyl-CoA (Methylmalonyl coenzyme A) tetralithium is a catabolite of valine, isoleucine, methionine, threonine, odd-chain fatty acids, and cholesterol. Methylmalonyl-CoA tetralithium is converted to succinyl-CoA by enzymatic reaction of methylmalonyl-CoA mutase (MCM) with coenzyme vitamin B12 .

HY-148285

*Succinyl CoA* 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) .

HY-12688

Succinyl phosphonate	Mitochondrial Metabolism Reactive Oxygen Species (ROS) Amyloid-β	Neurological Disease Inflammation/Immunology
Succinyl phosphonate is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .

HY-W973644

LY-266500	Mitochondrial Metabolism Parasite	Infection
LY-266500 is a succinyl CoA synthetase (SCS) specific inhibitor. LY-266500 has inhibitory effects on various parasites, such as Trypanosoma brucei brucei (IC₅₀ =0.6 μM) and Leishmania donovani (IC₅₀ =2.86 μM). LY-266500 can be used for research on parasitic infections .

HY-CE00006

(1-Methylpentyl)succinyl-CoA (1-Methylpentyl)Succinyl-coenzyme A	Biochemical Assay Reagents	Others
(1-Methylpentyl)succinyl-CoA ((1-Methylpentyl)succinyl-coenzyme A) is a a higher alkylsuccinyl-CoA .

HY-CE00290

(R,S)-(Hydroxy(phenyl)methyl)succinyl-CoA (2S)-2-((R)-Hydroxybenzyl)Succinyl-coenzyme A	Biochemical Assay Reagents	Metabolic Disease
(R,S)-(Hydroxy(phenyl)methyl)succinyl-CoA ((2S)-2-((R)-Hydroxybenzyl)succinyl-coenzyme A) is a [hydroxy(phenyl)methyl]succinyl-CoA.

HY-148285A

Succinyl CoA disodium 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) .

HY-CE01911

[Hydroxy(phenyl)methyl]succinyl-CoA [Hydroxy(phenyl)methyl]Succinyl-coenzyme A	Biochemical Assay Reagents	Metabolic Disease
[Hydroxy(phenyl)methyl]succinyl-CoA ([Hydroxy(phenyl)methyl]succinyl-coenzyme A) is a coenzyme A derivative .

HY-CE00712

2-(2-Naphthylmethyl)succinyl-CoA Naphthyl-2-methyl-Succinyl-CoA	Biochemical Assay Reagents	Metabolic Disease
2-(2-Naphthylmethyl)succinyl-CoA (Naphthyl-2-methyl-succinyl-CoA) is a coenzyme A derivative.

HY-CE01613

Naphthyl-2-methylene-succinyl-CoA Naphthyl-2-methylene-Succinyl-coenzyme A	Biochemical Assay Reagents	Metabolic Disease
Naphthyl-2-methylene-succinyl-CoA (Naphthyl-2-methylene-succinyl-coenzyme A) is a coenzyme A derivative .

HY-CE01614

Naphthyl-2-oxomethyl-succinyl-CoA Naphthyl-2-oxomethyl-Succinyl-coenzyme A	Biochemical Assay Reagents	Metabolic Disease
Naphthyl-2-oxomethyl-succinyl-CoA (Naphthyl-2-oxomethyl-succinyl-coenzyme A) is a coenzyme A derivative .

HY-180786

DdBIC	Nuclear Hormone Receptor 4A/NR4A Pyroptosis Reactive Oxygen Species (ROS) PERK Caspase	Cancer
DdBIC is a pyroptosis inducer. DdBIC binds to Nur77 and triggers its translocation to mitochondria, activates SDHA to deplete succinyl-CoA, disrupts heme homeostasis, induces electron leakage, and elicits mitochondrial ROS production. DdBIC induces mitochondrial ROS that oxidatively activates OMA1, promotes OPA1 cleavage and its release into the cytoplasm, activates the integrated stress response via PERK, and ultimately activates granzyme B to cleave GSDMC. DdBIC can be used for the study of melanoma .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-137808

Succinyl-Coenzyme A sodium 3 Publications Verification Succinyl-CoA sodium	Structural Classification Natural Products Neurological Disease Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
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) .

HY-12688A

Succinyl phosphonate trisodium salt 10+ Cited Publications	Structural Classification Classification of Application Fields Ketones, Aldehydes, Acids Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification Cancer	Mitochondrial Metabolism Reactive Oxygen Species (ROS) Amyloid-β
Succinyl phosphonate trisodium salt is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate trisodium salt protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate trisodium salt corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate trisodium salt reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate trisodium salt improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate trisodium salt can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .

HY-126791A

Methylmalonyl-CoA tetralithium IsoSuccinyl coenzyme A tetralithium; Methylmalonyl coenzyme tetralithium	Natural Products Human Gut Microbiota Metabolites Classification of Application Fields Other Diseases Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
Methylmalonyl-CoA (Methylmalonyl coenzyme A) tetralithium is a catabolite of valine, isoleucine, methionine, threonine, odd-chain fatty acids, and cholesterol. Methylmalonyl-CoA tetralithium is converted to succinyl-CoA by enzymatic reaction of methylmalonyl-CoA mutase (MCM) with coenzyme vitamin B12 .

HY-148285

*Succinyl CoA* Succinyl-coenzyme A; S-(Hydrogen Succinyl)coenzyme A	Human Gut Microbiota Metabolites Microorganisms Endogenous metabolite Source Classification	Endogenous Metabolite
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) .

HY-12688

Succinyl phosphonate	Structural Classification Neurological Disease Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Disease Research Fields Source Classification	Mitochondrial Metabolism Reactive Oxygen Species (ROS) Amyloid-β
Succinyl phosphonate is a α-Ketoglutarate Dehydrogenase Complex (KGDHC) modulator with neuroprotective activity. Succinyl phosphonate protects this complex, reduces cellular succinyl-CoA concentration, downregulates protein succinylation levels, and inhibits the activity of the α-ketoglutarate dehydrogenase complex. Succinyl phosphonate corrects hypoxic or ethanol-induced behavioral impairments, modulates exploratory behavior and emotional stress responses, and improves hypoxia tolerance. Succinyl phosphonate reduces glutamate excitotoxicity, restores the activity of the α-ketoglutarate dehydrogenase complex, reverses the changes in glutamate dehydrogenase and glutamine synthetase activities induced by β-amyloid (Amyloid-β), modulates cognitive function, and prevents β-amyloid-induced neuronal damage. Succinyl phosphonate improves microglial senescence, alleviates neuroinflammation, reactive oxygen species (ROS) production, lipid peroxidation, and the expression of proinflammatory cytokines. Succinyl phosphonate can be used in the research of Alzheimer's disease, aging-related neuroinflammation, and Parkinson's disease .

Cat. No.	Compare	Product Name	Species	Source	Image

HY-P702784

	OXCT1 Protein, Human (His) 3 oxoacid CoA transferase 1; 3-oxoacid CoA-transferase 1; OXCT; Oxct1; SCOT; Scot S; Scot-S; Somatic-type Succinyl-CoA:3-oxoacid CoA-transferase (SCOT-s)	Human	E. coli
	OXCT1 Protein, Human (His) is the recombinant human-derived OXCT1, expressed by E. coli , with N-6*His labeled tag. ,

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Succinyl-CoA

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