1. Search Result
Search Result
Pathways Recommended: Metabolic Enzyme/Protease
Results for "

metabolic abnormality

" in MedChemExpress (MCE) Product Catalog:

38

Inhibitors & Agonists

9

Screening Libraries

16

Natural
Products

6

Isotope-Labeled Compounds

1

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-123033A
    Nicotinamide riboside chloride
    Maximum Cited Publications
    25 Publications Verification

    Sirtuin Endogenous Metabolite Neurological Disease Metabolic Disease Cancer
    Nicotinamide riboside Chloride, an orally active NAD + precursor, increases NAD + levels and activates SIRT1 and SIRT3. Nicotinamide riboside Chloride is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities . Nicotinamide riboside Chloride reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease .
    Nicotinamide riboside chloride
  • 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-113166
    Dodecanoylcarnitine
    1 Publications Verification

    (-)-Lauroylcarnitine

    Endogenous Metabolite Metabolic Disease Inflammation/Immunology
    Dodecanoylcarnitine ((-)-Lauroylcarnitine) is a medium long-chain acylcarnitine, an intermediate product in key energy metabolic pathways of fatty acid β-oxidation and amino acids catabolism. The abnormal decrease in the Dodecanoylcarnitine levels indicats that mitochondrial fuel metabolism, including fatty acid oxidation is significantly disturbed. Changes in plasma concentrations of Dodecanoylcarnitine are not only associated with type II diabetes, but also with pre-diabetes status. Dodecanoylcarnitine is present in fatty acid oxidation disorders such as long-chain acyl CoA dehydrogenase deficiency, carnitine palmitoyltransferase I/II deficiency, and is also associated with celiac disease. Dodecanoylcarnitine deomonstrates high sensitivities and specificities in predicting asthma. Combined model of Decanoylcarnitine (HY-113069), Dodecanoylcarnitine, PC (16:0/0:0), and Asp Arg Pro can be used as a potential biomarker for the diagnosis of Yin-deficiency-heat syndrome .
    Dodecanoylcarnitine
  • HY-N3021

    Endogenous Metabolite NF-κB TNF Receptor FOXO Microtubule/Tubulin Metabolic Disease
    D-chiro-Inositol is a stereoisomer of inositol that exhibits activities such as improving glucose metabolism, anti-tumor effects, anti-inflammatory properties, and antioxidant activity. D-chiro-Inositol effectively alleviates cholestasis by enhancing bile acid secretion and reducing oxidative stress. D-chiro-Inositol improves insulin resistance, lowers hyperglycemia and circulating insulin levels, reduces serum androgen levels, and ameliorates some metabolic abnormalities associated with X syndrome by mimicking the action of insulin. Additionally, D-chiro-Inositol can induce a reduction in pro-inflammatory factors (such as Nf-κB) and cytokines (such as TNF-α), thereby exerting anti-inflammatory effects. D-chiro-Inositol may be used in the study of liver cirrhosis, breast cancer, type 2 diabetes, and polycystic ovary syndrome .
    D-chiro-Inositol
  • HY-123033

    Sirtuin Endogenous Metabolite Neurological Disease Metabolic Disease Cancer
    Nicotinamide riboside, an orally active NAD + precursor, increases NAD + levels and activates SIRT1 and SIRT3. Nicotinamide riboside is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities . Nicotinamide riboside reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease .
    Nicotinamide riboside
  • HY-34596

    Biochemical Assay Reagents Amyloid-β Neurological Disease Metabolic Disease
    4-Hydroxyindole is a type of hydroxyindole in which the 1H-indole at position 4 is substituted by a hydroxyl group. 4-Hydroxyindole serves as an important raw material or intermediate in the synthesis of pharmaceutical products and industrial polymers. 4-Hydroxyindole inhibits amyloid fibrillization and induces liver function impairment, thyroid abnormalities, and blood glucose fluctuations in mice. 4-Hydroxyindole holds potential for research in neurodegenerative diseases and metabolic disorders .
    4-Hydroxyindole
  • HY-P3016A

    EC 2.6.1.1, porcine heart; GOT, porcine heart; AST, porcine heart

    Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), porcine heart is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, porcine heart comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, porcine heart also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, porcine heart is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, porcine heart
  • HY-123033AR

    Reference Standards Sirtuin Endogenous Metabolite Neurological Disease Metabolic Disease Cancer
    Nicotinamide riboside (chloride) (Standard) is the analytical standard of Nicotinamide riboside (chloride). This product is intended for research and analytical applications. Nicotinamide riboside Chloride, an orally active NAD+ precursor, increases NAD+ levels and activates SIRT1 and SIRT3. Nicotinamide riboside Chloride is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities[1]. Nicotinamide riboside Chloride reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease[2].
    Nicotinamide riboside chloride (Standard)
  • HY-123033C
    Nicotinamide riboside malate
    Maximum Cited Publications
    25 Publications Verification

    Sirtuin Endogenous Metabolite Neurological Disease Metabolic Disease Cancer
    Nicotinamide riboside malate, an orally active NAD + precursor, increases NAD + levels and activates SIRT1 and SIRT3. Nicotinamide riboside malate is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities . Nicotinamide riboside malate reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease .
    Nicotinamide riboside malate
  • HY-W036120

    2,2′,4,4′-Tetrahydroxybenzophenone

    Environmental Pollutants Glycosidase Estrogen Receptor/ERR Pregnane X Receptor (PXR) Metabolic Disease Endocrinology
    Benzophenone-2 (2,2',4,4'-Tetrahydroxybenzophenone) is an organic ultraviolet absorber that is widely used in personal care products and industrial products such as plastics and coatings. Benzophenone-2 is an endocrine disruptor that can interfere with estrogen receptors (ERα receptor) and pregnane X receptor (PXR receptor) activity, leading to reproductive toxicity, immune disorders, and metabolic abnormalities. Benzophenone-2 can inhibit the activity of α-glucosidase (IC50 = 49.72 μM), and can be used for research on diabetes .
    Benzophenone-2
  • HY-135700

    Calcineurin Ras HMG-CoA Reductase (HMGCR) Metabolic Disease Inflammation/Immunology
    Mevalonolactone is an intermediate metabolite in the eukaryotic mevalonate pathway, serving as the stable δ-lactone form of mevalonate with oral activity. Mevalonolactone exhibits binding affinity for ZNF384 (Ka = 12.6 μM) and inhibitory activity against aconitase (aconitase). Mevalonolactone promotes the nuclear localization of ZNF384 and enhances its binding to the GGPPS promoter. Mevalonolactone induces insulin resistance, disrupts glucose and lipid metabolism, enhances the isoprenylation of K-Ras, and inhibits the activation of the insulin signaling pathway. Mevalonolactone inhibits polypeptide synthesis of HMG-CoA reductase in isolated rat hepatocytes, promotes its degradation, and reduces its enzymatic activity. Mevalonolactone impairs mitochondrial function in rat brains. Mevalonolactone promotes the development of metabolically unhealthy obesity. Mevalonolactone can be used in research related to metabolically abnormal obesity, mevalonic aciduria, HMGCR-related limb-girdle myopathy, and statin-induced myopathy .
    Mevalonolactone
  • HY-P3016

    EC 2.6.1.1; GOT; AST

    Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), Genetically engineered bacteria is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Genetically engineered bacteria comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Genetically engineered bacteria also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Genetically engineered bacteria is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, Genetically engineered bacteria
  • HY-120657

    CGRP Receptor NF-κB Neurological Disease Metabolic Disease Inflammation/Immunology
    9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
    9-PAHSA
  • 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-B1120
    Temephos
    2 Publications Verification

    Temefos

    Insecticide Cholinesterase (ChE) Dengue Virus Flavivirus Infection
    Temephos (Temefos) is an orally active, blood-brain barrier-permeable organophosphate insecticide and AChE inhibitor. By irreversibly inhibiting AChE to induce cholinergic overactivation, Temephos effectively blocks larval development of Aedes aegypti (yellow fever mosquito) and Aedes albopictus (Asian tiger mosquito), and is commonly used in studies related to Dengue Virus, Zika Virus and other relevant pathogens. Temephos exhibits genotoxicity and neurodevelopmental toxicity, and may also cause liver injury, reproductive system abnormalities and cholinergic poisoning symptoms in mammals. Temephos tends to accumulate in adipose tissues and aquatic organisms, and is excreted via feces after metabolism through oxidation and hydrolysis. Note that CYP-mediated metabolic detoxification may reduce the actual larvicidal efficacy of Temephos against some mosquito species. Temephos can be used in research related to dengue fever, Zika virus disease, chikungunya and dracunculiasis .
    Temephos
  • HY-123033B
    Nicotinamide riboside tartrate
    Maximum Cited Publications
    25 Publications Verification

    Sirtuin Endogenous Metabolite Neurological Disease Metabolic Disease Cancer
    Nicotinamide riboside tartrate, an orally active NAD + precursor, increases NAD + levels and activates SIRT1 and SIRT3. Nicotinamide riboside tartrate is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities . Nicotinamide riboside tartrate reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease .
    Nicotinamide riboside tartrate
  • HY-B1080A
    Tilorone
    2 Publications Verification

    Influenza Virus Akt Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Tilorone is an orally active antiviral agent and interferon inducer that also has potential antineoplastic, immunomodulatory, and metabolic modulating effects. Tilorone induces an abnormally delayed interferon response and primarily stimulates interferon production in lymphoid tissue. Thus, Tilorone exerts antiviral effects and can be used as a chemotherapeutic agent. Tilorone has the potential to inhibit type 2 diabetes by increasing glucose uptake in vivo and in skeletal muscle cells by enhancing Akt2/AS160 signaling and glucose transporter levels .
    Tilorone
  • HY-122963

    Adenosine Receptor Metabolic Disease
    Danshenol B is a diterpenoid. Danshenol B has strong aldose reductase (AR) inhibitory activity with IC50 value of 0.042μM. Danshenol B can be used for the research of diabetic related complication resulted by metabolic abnormality, such as cataracts, retinopathy, neuropathy, and nephropathy .
    Danshenol B
  • HY-W018004S

    Isotope-Labeled Compounds Endogenous Metabolite Metabolic Disease
    L-Homocitrulline-d3 is the deuterium labeled L-Homocitrulline. L-Homocitrulline is metabolized to homoarginine through homoargininosuccinate via the urea cycle pathway and its metabolic abnormality could lead to Lysinuric Protein Intolerance (LPI).
    L-Homocitrulline-d3
  • HY-123033D

    Endogenous Metabolite Sirtuin Neurological Disease Metabolic Disease Cancer
    Nicotinamide riboside triflate, an orally active NAD + precursor, increases NAD + levels and activates SIRT1 and SIRT3. Nicotinamide riboside triflate is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities . Nicotinamide riboside triflate reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease .
    Nicotinamide riboside triflate
  • HY-W018004R

    Reference Standards Endogenous Metabolite Metabolic Disease
    L-Homocitrulline is metabolized to homoarginine through homoargininosuccinate via the urea cycle pathway and its metabolic abnormality could lead to Lysinuric Protein Intolerance (LPI).
    L-Homocitrulline (Standard)
  • HY-P3016B

    EC 2.6.1.1, Human liver; GOT, Human liver; AST, Human liver

    Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), Human liver is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Human liver comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Human liver also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Human liver is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, Human liver
  • HY-N3021R

    Reference Standards Endogenous Metabolite NF-κB TNF Receptor FOXO Microtubule/Tubulin Metabolic Disease
    D-chiro-Inositol is a stereoisomer of inositol that exhibits activities such as improving glucose metabolism, anti-tumor effects, anti-inflammatory properties, and antioxidant activity. D-chiro-Inositol effectively alleviates cholestasis by enhancing bile acid secretion and reducing oxidative stress. D-chiro-Inositol improves insulin resistance, lowers hyperglycemia and circulating insulin levels, reduces serum androgen levels, and ameliorates some metabolic abnormalities associated with X syndrome by mimicking the action of insulin. Additionally, D-chiro-Inositol can induce a reduction in pro-inflammatory factors (such as Nf-κB) and cytokines (such as TNF-α), thereby exerting anti-inflammatory effects. D-chiro-Inositol may be used in the study of liver cirrhosis, breast cancer, type 2 diabetes, and polycystic ovary syndrome .
    D-chiro-Inositol (Standard)
  • HY-W770410

    Isotope-Labeled Compounds CGRP Receptor NF-κB Others
    9-PAHSA- 13C4 is 13C-labeled 9-PAHSA. 9-PAHSAis an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSAsignificantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSAinduces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSAregulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSAdoes not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSAcan be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
    9-PAHSA-13C4
  • HY-178912

    Reactive Oxygen Species (ROS) Bacterial ClpP Infection Inflammation/Immunology
    Anti-MRSA agent 39 is an orally active ClpX modulator that binds Staphylococcus aureus caseinolytic protease X (SaClpX) with high affinity (Kd = 3.6 μM). Anti-MRSA agent 39 exerts antibacterial effects through temperature-dependent inhibition of cell division. Anti-MRSA agent 39 elicits profound metabolic dysregulation in methicillin-resistant Staphylococcus aureus (MRSA), manifesting as significantly reduced ATP levels, elevated reactive oxygen species (ROS), and decreased NAD+/NADH ratio, and accelerates bacterial lysis rates in MRSA ATCC 33591. Anti-MRSA agent 39 significantly increases the proportion of MRSA cells in the mitotic phase, and the cells exhibit obvious morphological abnormalities. Anti-MRSA agent 39 can be used for the study of invasive MRSA infections .
    Anti-MRSA agent 39
  • HY-120657S

    Isotope-Labeled Compounds CGRP Receptor NF-κB Others
    9-PAHSA-d4 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
    9-PAHSA-d4
  • 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
  • HY-B1120R

    Temefos (Standard)

    Reference Standards Insecticide Cholinesterase (ChE) Dengue Virus Flavivirus Infection
    Temephos (Standard) is the analytical standard of Temephos. This product is intended for research and analytical applications. Temephos (Temefos) is an orally active, blood-brain barrier-permeable organophosphate insecticide and AChE inhibitor. By irreversibly inhibiting AChE to induce cholinergic overactivation, Temephos effectively blocks larval development of Aedes aegypti (yellow fever mosquito) and Aedes albopictus (Asian tiger mosquito), and is commonly used in studies related to Dengue Virus, Zika Virus and other relevant pathogens. Temephos exhibits genotoxicity and neurodevelopmental toxicity, and may also cause liver injury, reproductive system abnormalities and cholinergic poisoning symptoms in mammals. Temephos tends to accumulate in adipose tissues and aquatic organisms, and is excreted via feces after metabolism through oxidation and hydrolysis. Note that CYP-mediated metabolic detoxification may reduce the actual larvicidal efficacy of Temephos against some mosquito species. Temephos can be used in research related to dengue fever, Zika virus disease, chikungunya and dracunculiasis .
    Temephos (Standard)
  • HY-B1120S

    Temefos-d12

    Cholinesterase (ChE) Dengue Virus Flavivirus Parasite Infection
    Temephos-d12 is the deuterium labeled Temephos. Temephos (Temefos) is an orally active, blood-brain barrier-permeable organophosphate insecticide and AChE inhibitor. By irreversibly inhibiting AChE to induce cholinergic overactivation, Temephos effectively blocks larval development of Aedes aegypti (yellow fever mosquito) and Aedes albopictus (Asian tiger mosquito), and is commonly used in studies related to Dengue Virus, Zika Virus and other relevant pathogens. Temephos exhibits genotoxicity and neurodevelopmental toxicity, and may also cause liver injury, reproductive system abnormalities and cholinergic poisoning symptoms in mammals. Temephos tends to accumulate in adipose tissues and aquatic organisms, and is excreted via feces after metabolism through oxidation and hydrolysis. Note that CYP-mediated metabolic detoxification may reduce the actual larvicidal efficacy of Temephos against some mosquito species. Temephos can be used in research related to dengue fever, Zika virus disease, chikungunya and dracunculiasis .
    Temephos-d12
  • HY-113166R

    (-)-Lauroylcarnitine (Standard)

    Reference Standards Endogenous Metabolite Metabolic Disease Inflammation/Immunology
    Dodecanoylcarnitine (Standard) is the analytical standard of Dodecanoylcarnitine (HY-113166). This product is intended for research and analytical applications. Dodecanoylcarnitine ((-)-Lauroylcarnitine) is a medium long-chain acylcarnitine, an intermediate product in key energy metabolic pathways of fatty acid β-oxidation and amino acids catabolism. The abnormal decrease in the Dodecanoylcarnitine levels indicats that mitochondrial fuel metabolism, including fatty acid oxidation is significantly disturbed. Changes in plasma concentrations of Dodecanoylcarnitine are not only associated with type II diabetes, but also with pre-diabetes status. Dodecanoylcarnitine is present in fatty acid oxidation disorders such as long-chain acyl CoA dehydrogenase deficiency, carnitine palmitoyltransferase I/II deficiency, and is also associated with celiac disease. Dodecanoylcarnitine deomonstrates high sensitivities and specificities in predicting asthma. Combined model of Decanoylcarnitine (HY-113069), Dodecanoylcarnitine, PC (16:0/0:0), and Asp Arg Pro can be used as a potential biomarker for the diagnosis of Yin-deficiency-heat syndrome .
    Dodecanoylcarnitine (Standard)
  • HY-120657R

    Reference Standards CGRP Receptor NF-κB Cardiovascular Disease Inflammation/Immunology
    Flumethrin (Standard) is the analytical standard of Flumethrin. This product is intended for research and analytical applications. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
    9-PAHSA (Standard)
  • HY-144026S

    CGRP Receptor NF-κB Inflammation/Immunology
    9-PAHSA-d9 is the deuterium labeled 9-PAHSA (HY-120657). 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
    9-PAHSA-d9
  • HY-120657S1

    Isotope-Labeled Compounds CGRP Receptor NF-κB Others
    9-PAHSA-d31 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
    9-PAHSA-d31
  • HY-107387

    PI3K Metabolic Disease Inflammation/Immunology
    PF-376304 is an orally active non-specific class I phosphoinositide 3-kinase (PI3K) inhibitor with an IC50 of 0.197 μM against PI3Kγ. PF-376304 induces dose-dependent glucose and lipid metabolic disorders in rats, causes rapid death at high doses, and leads to metabolic abnormalities that are self-reversible at low doses. PF-376304 is applicable to the research of metabolic and inflammatory diseases .
    PF-376304
  • HY-180341

    Platelet-activating Factor Receptor (PAFR) Inflammation/Immunology
    UR-12633 is a platelet-activating factor (PAF) antagonist. UR-12633 can effectively reverse hypotension, inhibit coagulation abnormalities, increased vascular permeability, and metabolic disorders in rodent models of endotoxic shock. UR-12633 can be used for research on endotoxic shock .
    UR-12633
  • HY-182456

    KMO Neurological Disease
    CHDI-340246 is an orally active kynurenine monooxygenase (KMO) inhibitor. CHDI-340246 blocks KMO activity, alters the metabolic flux of the kynurenine pathway, inhibits the production of 3-hydroxykynurenine and quinolinic acid, elevates the levels of kynurenine and kynurenic acid, and restores electrophysiological abnormalities in transgenic mouse models of Huntington's disease. CHDI-340246 can be used in studies related to Huntington's disease .
    CHDI-340246
  • HY-P3016C

    EC 2.6.1.1, Human (HEK293); GOT, Human (HEK293); AST, Human (HEK293)

    Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), Human (HEK293) is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Human (HEK293) comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Human (HEK293) also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Human (HEK293) is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, Human (HEK293)
  • HY-W783351

    Coppersensor 790 acetoxymethyl ester

    Fluorescent Dye Metabolic Disease
    CS790AM (Coppersensor 790 acetoxymethyl ester) is a cell-permeable, Cu +-targeted near-infrared fluorescent probe (λabs=760 nm, λem=790 nm) applicable to live cells. CS790AM can cross lipophilic cell membranes, and is converted into negatively charged CS790 under the action of intracellular esterases to be retained, thus enabling highly sensitive, reversible "turn-on" detection of labile Cu + pools in live cells and mice. CS790AM possesses excellent biocompatibility and selectivity, avoids interference from other metal ions, shows no obvious toxicity, and can be rapidly cleared. CS790AM allows long-term longitudinal monitoring of individual mice, visualizes copper levels in internal organs and isolated livers, and effectively evaluates abnormal copper accumulation in Wilson's disease models (Atp7b -/-) as well as dynamic changes after chelator treatment. CS790AM can be used for research on Wilson's disease and related copper metabolic disorders .
    CS790AM

Inquiry Online

Your information is safe with us. * Required Fields.

Salutation

 

Country or Region *

Applicant Name *

 

Organization Name *

Department *

     

Email Address *

 

Product Name *

Cat. No.

 

Requested quantity *

Phone Number *

     

Remarks

Inquiry Online

Inquiry Information

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent: