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hepatic metabolism

" in MedChemExpress (MCE) Product Catalog:

98

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6

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9

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10

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-114118
    Semaglutide
    Maximum Cited Publications
    35 Publications Verification

    		 GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide
  • HY-13771
    Ursodeoxycholic acid
    Maximum Cited Publications
    26 Publications Verification

    Ursodeoxycholate; Ursodiol; UDCA

    		 G protein-coupled Bile Acid Receptor 1 FXR Angiotensin-converting Enzyme (ACE) Endogenous Metabolite Infection Metabolic Disease Cancer
    Ursodeoxycholic acid (Ursodeoxycholate) is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid can be used for the research of a variety of hepatic and gastrointestinal diseases. Ursodeoxycholic acid also reduces ACE2 expression and is beneficial for reducing SARS-CoV-2 infection. Orally active .
    Ursodeoxycholic acid
  • HY-B1334A
    Perhexiline maleate
    5+ Cited Publications

    		 Carnitine Palmitoyltransferase (CPT) Mitochondrial Metabolism Apoptosis Cardiovascular Disease Cancer
    Perhexiline maleate is an orally active CPT1 and CPT2 inhibitor that reduces fatty acid metabolism. Perhexiline maleate induces mitochondrial dysfunction and apoptosis in hepatic cells. Perhexiline maleate can cross the blood brain barrier (BBB) and shows anti-tumor activity. Perhexiline maleate can be used in the research of cancers, and cardiovascular disease like angina .
    Perhexiline maleate
  • HY-N9933
    Tauro-β-muricholic acid
    4 Publications Verification

    TβMCA

    		 FXR Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC50=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .
    Tauro-β-muricholic acid
  • HY-B1907
    Rifamycin sodium
    2 Publications Verification

    Rifamycin SV sodium

    		 Antibiotic Bacterial DNA/RNA Synthesis Infection Inflammation/Immunology
    Rifamycin sodium (Rifamycin SV monosodium) is an orally active ansamycin antibiotic. Rifamycin sodium inhibits DNA-dependent RNA synthesis. Rifamycin sodium has antibacterial activity against Mycobacterium tuberculosis. Rifamycin sodium interferes with hepatic bile acid metabolism. Rifamycin sodium has anti-inflammatory effects. Rifamycin sodium can be used in the study of Mycobacterium tuberculosis, Bacteroides fragilis infection, and Lipopolysaccharide (HY-D1056B3)-induced inflammation .
    Rifamycin sodium
  • HY-114118B
    Semaglutide acetate
    Maximum Cited Publications
    35 Publications Verification

    		 GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide acetate is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide acetate
  • HY-114118A
    Semaglutide TFA
    Maximum Cited Publications
    35 Publications Verification

    		 GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide TFA
  • HY-125848
    Ginsenoside F2

    		Apoptosis AMPK PPAR p38 MAPK PI3K Akt GSK-3 Reactive Oxygen Species (ROS) SOD Caspase Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota . Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma .
    Ginsenoside F2
  • HY-13771A
    Ursodeoxycholic acid sodium
    Maximum Cited Publications
    26 Publications Verification

    Ursodeoxycholate sodium; Ursodiol sodium; UCDA sodium

    		 G protein-coupled Bile Acid Receptor 1 FXR Endogenous Metabolite Metabolic Disease Inflammation/Immunology Cancer
    Ursodeoxycholic acid (Ursodeoxycholate) sodium is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid sodium acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid sodium can be used for the research of a variety of hepatic and gastrointestinal diseases. Orally active .
    Ursodeoxycholic acid sodium
  • HY-P2917
    Glycerol kinase, microorganism

    GyK

    		 Nuclear Hormone Receptor 4A/NR4A Metabolic Disease Inflammation/Immunology
    Glycerol kinase, microorganism (GyK) acts as a NR4A1 inhibitor with enzymatic activity. It directly binds to and inhibits the transcription factor NR4A1, thereby negatively regulating hepatic gluconeogenesis and reducing blood glucose levels. Glycerol kinase, microorganism positively regulates UCP1 expression via partial dependence on the β-adrenergic receptor-cAMP-CREB pathway, promotes browning of white adipose tissue and thermogenesis, and further modulates intracellular fatty acid composition and energy metabolism. In diabetic mouse models, overexpression of Glycerol kinase effectively antagonizes NR4A1-induced hyperglycemia, demonstrating potential for improving glucose homeostasis. Glycerol kinase, microorganism can be used for studies on diabetes and obesity .
    Glycerol kinase, microorganism
  • HY-B1334
    Perhexiline
    5+ Cited Publications

    		 Carnitine Palmitoyltransferase (CPT) Mitochondrial Metabolism Apoptosis Cardiovascular Disease Cancer
    Perhexiline is an orally active CPT1 and CPT2 inhibitor that reduces fatty acid metabolism. Perhexiline induces mitochondrial dysfunction and apoptosis in hepatic cells. Perhexiline can cross the blood brain barrier (BBB) and shows anti-tumor activity. Perhexiline can be used in the research of cancers, and cardiovascular disease like angina .
    Perhexiline
  • HY-114118CP
    Semaglutide (crude)

    		GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide (crude) is the crude form of Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances Autophagy, inhibits oxidative stress and Apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide (crude)
  • HY-13582
    Carbendazim
    5+ Cited Publications

    		 Environmental Pollutants Fungal Parasite Infection Cancer
    Carbendazim is a potent and orally active broad-spectrum benzimidazole fungicide and can be acts as a pesticide for fungal diseases research, such as Seproria, Fusarium and Sclerotina . Carbendazim is a benzimidazole (HY-Y1825) derivative with antitumor activity and used for cancer research, especially advanced solid tumors and lymphoma .
    Carbendazim
  • HY-114118S3
    Semaglutide-13C6,15N TFA

    		Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Metabolic Disease
    Semaglutide- 13C6, 15N TFA is the 13C- and 15N-labeled Semaglutide TFA (HY-114118A). Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide-13C6,15N TFA
  • HY-N0468
    Rebaudioside D
    1 Publications Verification

    		 FXR Acetyl-CoA Carboxylase Metabolic Disease
    Rebaudioside D is an orally active sweetener that targets and activates FXR, modulates Acetyl-CoA Carboxylase, and inhibits 3-hydroxy-3-methylglutaryl-CoA reductase. Rebaudioside D regulates bile acid homeostasis and lipid metabolism, reduces the synthesis rates of fatty acids and cholesterol, and exerts multiple effects including anti-adipogenesis, hepatoprotection, anti-steatosis, gut microbiota modulation, enhancement of secondary bile acid metabolism, anti-endotoxin activity, regulation of bile acid transport, and inhibition of bile acid efflux. Rebaudioside D also reduces body weight gain, visceral fat accumulation, hepatic triglyceride and cholesterol accumulation, hepatic lipid peroxidation, and decreases the circulating level of lipopolysaccharide-binding protein. Rebaudioside D additionally enhances the secondary bile acid metabolic pathway of intestinal bacteria, upregulates the gene expression of ileal organic solute transporter α, and downregulates the gene expression of hepatic bile salt export pump. Rebaudioside D does not affect glucose homeostasis, alter total caloric intake or fecal energy excretion, induce weight gain, exacerbate obesity, promote hepatic steatosis, impair brown adipose tissue function, nor change skeletal muscle metabolism-related proteins. Rebaudioside D can be used in diet-induced obesity and obesity-related research .
    Rebaudioside D
  • HY-Y1325H
    Sodium acetate trihydrate, meets analytical specification of Ph. Eur. BP USP FCC E262, ≤0.00002% Al
    4 Publications Verification

    		 Environmental Pollutants Fungal Endogenous Metabolite Caspase PPAR AMPK Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Sodium acetate trihydrate is a carboxylic acid and short-chain fatty acid (SCFAs). Sodium acetate trihydrate activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Sodium acetate trihydrate exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Sodium acetate trihydrate regulates energy metabolism. Sodium acetate trihydrate has anticancer activity against gastric cancer. Sodium acetate trihydrate induces writhing reaction and ulcerative colitis. Sodium acetate trihydrate can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain .
    Sodium acetate trihydrate, meets analytical specification of Ph. Eur. BP USP FCC E262, ≤0.00002% Al
  • HY-N0712
    Typhaneoside
    3 Publications Verification

    		 mTOR Akt FXR PI3K Autophagy Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Calcium Channel Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
    Typhaneoside is an orally active activator of PI3K/Akt/mTOR and farnesoid X receptor. Typhaneoside promotes the activation of AMPK and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, cell cycle arrest at the G2/M phase, and reduces cancer cell viability. Typhaneoside improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside can be used in research related to heart failure after myocardial infarction, acute myeloid leukemia, non-alcoholic fatty liver disease and neurological disorders .
    Typhaneoside
  • HY-107582
    JW480

    		Ser/Thr Protease Calcium Channel PKC Cancer
    JW480 is a selective KIAA1363/AADACL1 inhibitor with oral activity, featuring IC50 values of 12 nM against human KIAA1363, 20 nM against mouse KIAA1363. JW480 blocks lipid deacetylase activity to restrain HAG metabolism and lowers retinyl ester hydrolase function in hepatic stellate cells. JW480 reduces MAGE lipid levels and inhibits migration, invasion, survival and tumor growth of prostate cancer cells. JW480 lowers PKCδ phosphorylation, facilitates HAGP accumulation, diminishes platelet aggregation, dense granule secretion and Ca 2+ flux, delays arterial thrombosis and prolongs tail bleeding time in rats. JW480 can be used for the study of prostate cancer and thrombosis .
    JW480
  • HY-106539
    Colesevelam hydrochloride

    		FXR G protein-coupled Bile Acid Receptor 1 GLP Receptor Metabolic Disease Cancer
    Colesevelam hydrochloride is an orally active bile acid sequestrant, lipid-lowering agent, and glycemic control agent. Colesevelam hydrochloride binds bile acids in the gastrointestinal tract to form nonabsorbable complexes, interrupts enterohepatic recirculation and increases fecal bile acid elimination. Colesevelam hydrochloride modulates FXR, TGR5, and Cyp7a1 activity and triggers cAMP signaling and GLP-1 release. Colesevelam hydrochloride alters hepatic lipid and glucose metabolism, suppresses hepatic glycogenolysis, reduces hepatic triglyceride and cholesterol levels, and increases LDL-C (low-density lipoprotein cholesterol) clearance. Colesevelam hydrochloride can be used for the research of type 2 diabetes mellitus, hypercholesterolemia, and alcohol-related liver disease .
    Colesevelam hydrochloride
  • HY-B0859
    MCPA
    1 Publications Verification

    		 Environmental Pollutants Cytochrome P450 Herbicide Metabolic Disease
    MCPA is an orally active phenoxyacetic acid herbicide. MCPA interferes with membrane integrity, energy metabolism (decreases ATP levels), and redox balance in plant cells. MCPA increases hepatic cytochrome P-450 levels and increases aniline hydroxylase and 7-ethoxycoumarin O-deethylase activities. MCPA can be used to control broadleaf weeds .
    MCPA
  • HY-W018587
    TBPH

    		Mitochondrial Metabolism Cytochrome P450 TNF Receptor Interleukin Related HSP LDLR Eukaryotic Initiation Factor (eIF) ClpP Metabolic Disease Inflammation/Immunology
    TBPH is a brominated flame retardant. TBPH enhances hepatic steatosis, inflammation, and fibrosis in mice with nonalcoholic steatohepatitis (NASH). TBPH induces dysregulation of phospholipid metabolism, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH leads to impaired endoplasmic reticulum-mitochondria (ER-Mito) contacts, subsequently causing mitochondrial dysfunction. TBPH induces lung injury through an inflammatory response mediated by mitochondria-derived ds-DNA. TBPH can be used to study the role of MFN2-mediated ER-mitochondria contacts in lipid metabolism homeostasis .
    TBPH
  • HY-Y0319G
    Magnesium acetate tetrahydrate

    		Endogenous Metabolite AMPK Reactive Oxygen Species (ROS) Caspase Fungal PPAR Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Magnesium acetate tetrahydrate is a carboxylic acid and short-chain fatty acid (SCFAs). Magnesium acetate tetrahydrate activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Magnesium acetate tetrahydrate exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Magnesium acetate tetrahydrate regulates energy metabolism. Magnesium acetate tetrahydrate has anticancer activity against gastric cancer. Magnesium acetate tetrahydrate induces writhing reaction and ulcerative colitis. Magnesium acetate tetrahydrate can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain .
    Magnesium acetate tetrahydrate
  • HY-P3016A
    Aspartate aminotransferase, porcine heart

    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-113478S
    Ursodeoxycholic acid-d4

    Ursodeoxycholate-d4; Ursodiol-d4; UDCA-d4

    		 Isotope-Labeled Compounds Infection Metabolic Disease
    Ursodeoxycholic acid-2,2,4,4-d4 is the deuterium labeled Ursodeoxycholic acid (HY-13771). Ursodeoxycholic acid is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid can be used for the research of a variety of hepatic and gastrointestinal diseases. Ursodeoxycholic acid also reduces ACE2 expression and is beneficial for reducing SARS-CoV-2 infection .
    Ursodeoxycholic acid-d4
  • HY-B1134
    Imazalil
    1 Publications Verification

    Enilconazole

    		 Environmental Pollutants Fungal Pregnane X Receptor (PXR) Infection
    Imazalil (Enilconazole) is a fungicide. Imazalil has oral activity and strongly activates mPXR but not mCAR in mouse liver. Imazalil is commonly used to protect various agricultural crops against fungal attack. Imazalil induces developmental abnormalities, gut microbiota dysbiosis, and hepatic metabolism disorder .
    Imazalil
  • HY-112253
    D-Fructose 1-phosphate

    		Endogenous Metabolite Metabolic Disease
    D-Fructose 1-phosphate is a key intermediate metabolite in the fructose metabolic pathway. As a key signaling molecule linking fructose metabolism and glucose metabolic regulation, D-Fructose 1-phosphate acts as an allosteric modulator to counteract the inhibitory effect of the glucokinase-regulatory protein complex, thereby finely regulating the direction of hepatic glucose metabolism at the substrate level .
    D-Fructose 1-phosphate
  • HY-114557
    NSC 90469

    3,5-Diiodo-L-thyronine

    		 JNK NF-κB Sirtuin PGC-1α COX TGF-β Receptor Collagen Metabolic Disease Inflammation/Immunology Endocrinology
    NSC 90469 (3,5-Diiodo-L-thyronine) is an orally active thyroid hormone derivative. NSC 90469 inhibits JNK phosphorylation and NF-κB acetylation, blocks SIRT1 protein expression, induces elevated PGC-1α levels, and stimulates COX activity. NSC 90469 enhances UCP1-mediated thermogenesis, increases hepatic Dio1 activity, inhibits TSH levels and hypothalamic-pituitary-thyroid axis function, enhances lipid metabolism, and regulates energy metabolism via the mitochondrial pathway. NSC 90469 prevents blood glucose reduction, reduces urinary albumin excretion, inhibits renal matrix expansion, decreases TGF-β1 expression, and reduces renal fibronectin and type Ⅳ collagen deposition. NSC 90469 also increases energy expenditure and prevents diet-induced overweight. NSC 90469 can be used in studies related to diabetic nephropathy, hypothyroidism, non-alcoholic fatty liver disease, and diet-induced obesity .
    NSC 90469
  • HY-114118S1
    Semaglutide-d8 tetraTFA

    		Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide-d8 tetraTFA is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide-d8 tetraTFA
  • HY-114118S
    Semaglutide-d8

    		Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide-d8 is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide-d8
  • HY-B0171S
    Antipyrine-d3

    Phenazone-d3; Phenazon-d3

    		 Isotope-Labeled Compounds Inflammation/Immunology
    Antipyrine-d3 is the deuterium labeled Antipyrine. Antipyrine (Phenazone) is an antipyretic and analgesic. Antipyrine can be used as a probe agent for oxidative agent metabolism. Antipyrine has been widely used in assessment of hepatic oxidative capacity .
    Antipyrine-d3
  • HY-112253A
    D-Fructose 1-phosphate disodium
    1 Publications Verification

    		 Endogenous Metabolite Metabolic Disease
    D-Fructose 1-phosphate disodium is a key intermediate metabolite in the fructose metabolic pathway. As a key signaling molecule linking fructose metabolism and glucose metabolic regulation, D-Fructose 1-phosphate disodium acts as an allosteric modulator to counteract the inhibitory effect of the glucokinase-regulatory protein complex, thereby finely regulating the direction of hepatic glucose metabolism at the substrate level .
    D-Fructose 1-phosphate disodium
  • HY-162353
    AZ'9567

    		Cancer
    AZ'9567 is an orally active MAT2a inhibitor with a pIC50 of 9.1. AZ'9567 binds to MAT2a allosterically, reduces the synthesis of SAM, decreases SDMA levels, and exerts antiproliferative effects on MTAP-knockout cells. AZ'9567 depletes SAM, causes methionine accumulation in plasma and tissues, triggers adaptive disorders in one-carbon metabolism, transsulfuration metabolism and lipid metabolism, and induces oxidative stress, hepatic steatosis and lipid homeostasis imbalance. AZ'9567 can be used in studies related to MTAP-deficient/deleted cancers .
    AZ'9567
  • HY-B1907A
    Rifamycin
    2 Publications Verification

    Rifamycin SV

    		 Antibiotic Bacterial DNA/RNA Synthesis Infection
    Rifamycin (Rifamycin SV) is an orally active ansamycin antibiotic. Rifamycin inhibits DNA-dependent RNA synthesis. Rifamycin has antibacterial activity against Mycobacterium tuberculosis. Rifamycin interferes with hepatic bile acid metabolism. Rifamycin has anti-inflammatory effects. Rifamycin can be used in the study of Mycobacterium tuberculosis, Bacteroides fragilis infection, and Lipopolysaccharide (HY-D1056B3)-induced inflammation .
    Rifamycin
  • HY-W001542
    5-Hydroxyoxindole

    		Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Cancer
    5-Hydroxyoxindole is a structural analog of uric acid for its antioxidant. 5-Hydroxyoxindole has DPPH radical scavenging activities and lipid peroxidation-inhibitory activities. 5-Hydroxyoxindole is a product of partial metabolism of tryptophan involving conversion in the gut lumen of tryptophan to indole through the action of bacterial tryptophanase and tryptophan synthase. 5-Hydroxyoxindole is one of the main molecules responsible for the neurological symptoms of hepatic encephalopathy in rats. 5-Hydroxyoxindole can be used for the research of oxidative stress-mediated disorders .
    5-Hydroxyoxindole
  • HY-137967
    Genistein 7-β-D-Glucuronide

    Genistein 7-O-glucuronide

    		 Drug Metabolite Metabolic Disease
    Genistein 7-β-D-Glucuronide (Genistein 7-O-glucuronide) is the primary phase II metabolite of Genistein (HY-14596) in human and rat hepatocytes. Genistein 7-β-D-Glucuronide undergoes distinct deconjugation in different functional assays. Genistein 7-β-D-Glucuronide is produced via hepatic microsomal glucuronidation and shows a mild age-related increase in intrinsic clearance in male F344 rats. Genistein 7-β-D-Glucuronide can be used for research on metabolism .
    Genistein 7-β-D-Glucuronide
  • HY-141645
    IMM-H007

    WS070117

    		 AMPK TGF-β Receptor NF-κB JNK AP-1 Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    IMM-H007 (WS070117) is an orally active and potent AMPK (AMP-activated protein kinase) activator and TGFβ1 (transforming growth factor β1) antagonist. IMM-H007 has protective effects in cardiovascular diseases via activation of AMPK. IMM-H007 negatively regulates endothelium inflammation through inactivating NF-κB and JNK/AP1 signaling. IMM-H007 inhibits ABCA1 degradation. IMM-H007 resolves hepatic steatosis in HFD-fed hamsters by the regulation of lipid metabolism. IMM-H007 can be used for the research of nonalcoholic fatty liver disease (NAFLD) and inflammatory atherosclerosis .
    IMM-H007
  • HY-P3016
    Aspartate aminotransferase, Genetically engineered bacteria

    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-13771R
    Ursodeoxycholic acid (Standard)

    Ursodeoxycholate (Standard); Ursodiol (Standard); UDCA (Standard)

    		 Reference Standards G protein-coupled Bile Acid Receptor 1 FXR Angiotensin-converting Enzyme (ACE) Endogenous Metabolite Infection Metabolic Disease Cancer
    Ursodeoxycholic acid (Standard) is the analytical standard of Ursodeoxycholic acid. This product is intended for research and analytical applications. Ursodeoxycholic acid (Ursodeoxycholate) is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid can be used for the research of a variety of hepatic and gastrointestinal diseases. Ursodeoxycholic acid also reduces ACE2 expression and is beneficial for reducing SARS-CoV-2 infection. Orally active .
    Ursodeoxycholic acid (Standard)
  • HY-156685
    EDI048

    		PI4K Parasite Infection Metabolic Disease Cancer
    EDI048 is an orally active, gut-restricted parasiticidal agent. EDI048 specifically binds to the ATP-binding site of Cryptosporidium phosphatidylinositol 4-kinase (CpPI (4) K), blocks parasite membrane biogenesis, arrests the pathogen at the schizont stage, and thus irreversibly clears the infection. EDI048 is rapidly converted to an inactive carboxylic acid metabolite via hepatic first-pass metabolism, with extremely low systemic exposure, good safety profile, and no cardiotoxicity, genotoxicity or off-target effects. EDI048 is used in studies of intestinal cryptosporidiosis in children .
    EDI048
  • HY-106181
    Rivoglitazone

    R-106056

    		 PPAR Cardiovascular Disease Metabolic Disease
    Rivoglitazone (R-106056) is an orally active, selective PPARγ agonist with an EC50 of 0.22 μM for hPPARγ. Rivoglitazone regulates fatty acid storage and uptake, glucose homeostasis, and cardiac glucose/fatty acid metabolism. Rivoglitazone reduces levels of hyperglycemia, hyperinsulinemia, and hypertriglyceridemia, decreases hepatic glucose production, and accelerates plasma triglyceride clearance. Rivoglitazone induces a reduction in glycated hemoglobin A1C, while causing peripheral edema and weight gain. Rivoglitazone can be used in research related to type 2 diabetes .
    Rivoglitazone
  • HY-13582R
    Carbendazim (Standard)
    5+ Cited Publications

    		 Parasite Fungal Reference Standards Infection Cancer
    Carbendazim (Standard) is the analytical standard of Carbendazim. This product is intended for research and analytical applications. Carbendazim is a potent and orally active broad-spectrum benzimidazole fungicide and can be acts as a pesticide for fungal diseases research, such as Seproria, Fusarium and Sclerotina . Carbendazim is a benzimidazole (HY-Y1825) derivative with antitumor activity and used for cancer research, especially advanced solid tumors and lymphoma .
    Carbendazim (Standard)
  • HY-110260
    LDN-193188

    		Endogenous Metabolite Metabolic Disease
    LDN-193188 is a Phosphatidylcholine transfer protein (PC-TP) inhibitor. LDN-193188 regulates hepatic glucose metabolism, and can be used for study of glucose metabolism .
    LDN-193188
  • HY-168049
    ZLY06

    		PPAR Akt Metabolic Disease
    ZLY06 is an orally active dual agonist of peroxisome proliferator-activated receptor (PPAR) δ and γ (PPAR δ: EC50=341 nM; PPAR γ: EC50=237 nM). ZLY06 induces hepatic lipid accumulation by inhibiting the phosphorylation of AKT1, mediating the upregulation of CD36. In addition, ZLY06 significantly improves glucose and lipid metabolism without increasing body weight, and alleviates fatty liver by promoting β-oxidation of fatty acids and inhibiting hepatic lipogenesis .
    ZLY06
  • HY-W006398S
    Acetic acid-d3 sodium

    Anhydrous sodium acetate-d3

    		 Isotope-Labeled Compounds Neurological Disease Inflammation/Immunology Cancer
    Acetic acid-d3 sodium is the deuterium labeled Acetic acid (HY-Y0319) . Acetic acid is a carboxylic acid and short-chain fatty acid (SCFAs). Acetic acid activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Acetic acid exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Acetic acid regulates energy metabolism. Acetic acid has anticancer activity against gastric cancer. Acetic acid induces writhing reaction and ulcerative colitis. Acetic acid can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain.
    Acetic acid-d3 sodium
  • HY-W020788
    Benoxacor

    CGA 154281

    		 Environmental Pollutants Glutathione S-transferase Estrogen Receptor/ERR Pregnane X Receptor (PXR) FXR Metabolic Disease Cancer
    Benoxacor (CGA 154281) is a herbicide safener and xenobiotic metabolism regulator. Benoxacor protects maize from the toxicity of metolachlor mainly by inducing detoxifying enzymes such as Glutathione S-transferase. Benoxacor also activates FXR, PXR and ERRα, and inhibits aromatase (aromatase). However, Benoxacor exhibits potential subacute oral toxicity and a high risk of hepatotoxicity in animal models. Benoxacor induces reactive oxygen species accumulation, interferes with embryonic heart development, and causes increased liver and kidney weights as well as alterations in gut microbiota in mice. Benoxacor can be used in studies related to hepatic steatosis, infertility, breast cancer and developmental toxicity .
    Benoxacor
  • HY-Y0319D
    Acetic acid lead

    		Endogenous Metabolite AMPK Reactive Oxygen Species (ROS) Caspase Fungal PPAR Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Acetic acid lead is a carboxylic acid and short-chain fatty acid (SCFAs). Magnesium acetate tetrahydrate activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Acetic acid lead exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Acetic acid lead regulates energy metabolism. Acetic acid lead has anticancer activity against gastric cancer. Acetic acid lead induces writhing reaction and ulcerative colitis. Acetic acid lead can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain .
    Acetic acid lead
  • HY-B1134A
    Imazalil sulfate
    1 Publications Verification

    Enilconazolel sulfate

    		 Environmental Pollutants Fungal Pregnane X Receptor (PXR) Infection
    Imazalil (Enilconazole) sulfate is a fungicide. Imazalil sulfate has oral activity and strongly activates mPXR but not mCAR in mouse liver. Imazalil sulfate is commonly used to protect various agricultural crops against fungal attack. Imazalil sulfate induces developmental abnormalities, gut microbiota dysbiosis, and hepatic metabolism disorder .
    Imazalil sulfate
  • HY-P11358
    IRW

    		Angiotensin-converting Enzyme (ACE) Acetyl-CoA Carboxylase Mitochondrial Metabolism Inflammation/Immunology
    IRW is an orally active tripeptide produced from egg white with angiotensin converting enzyme (ACE) inhibitory properties. IRW can prevent high-fat diet (HFD)-induced Non-alcoholic fatty liver disease (NAFLD) by modulating hepatic lipid metabolism and increasing mitochondrial content. IRW decreases hepatic triglyceride content and lipid droplet size. IRW increases the hepatic mitochondrial complexes and citrate synthase activity, phosphorylation of 5’-AMP-activated protein kinase and microsomal triglyceride transfer protein abundance. IRW increases phosphorylated acetyl CoA carboxylase and mitochondrial complexes, IRW can be used for the research of inflammation .
    IRW
  • HY-E70599
    Human CES2 Enzyme

    		Carboxylesterase (CES) Metabolic Disease
    Human CES2 Enzyme is a carboxylesterase involved in drug metabolism and lipid homeostasis. Human CES2 Enzyme hydrolyzes triglycerides, cholesteryl esters and retinyl esters to regulate lipid metabolism and energy homeostasis. Human CES2 Enzyme improves glucose tolerance and insulin sensitivity, reduces hepatic lipid accumulation, alleviates white adipose tissue steatitis, decreases plasma cholesterol levels, and reduces body weight and white adipose tissue weight. Human CES2 Enzyme can be used in the research of metabolic syndrome .
    Human CES2 Enzyme
  • HY-Y0817R
    Acetic acid sodium (Standard)

    Anhydrous sodium acetate (Standard)

    		 Reference Standards Cancer
    Acetic acid sodium (Standard) (Anhydrous sodium acetate (Standard) is the analytical standard of Anhydrous sodium acetate. This product is intended for research and analytical applications. Acetic acid is a carboxylic acid and short-chain fatty acid (SCFAs). Acetic acid activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Acetic acid exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Acetic acid regulates energy metabolism. Acetic acid has anticancer activity against gastric cancer. Acetic acid induces writhing reaction and ulcerative colitis. Acetic acid can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain .
    Acetic acid sodium (Standard)

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