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Results for "

Hepatic glucose

" in MedChemExpress (MCE) Product Catalog:

77

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2

Biochemical Assay Reagents

6

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23

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3

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2

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Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-113402
    Gamma-glutamylcysteine
    4 Publications Verification

    γ-Glu-Cys

    		 Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine
  • HY-142114
    SRI-37330
    5 Publications Verification

    		 Arrestin Metabolic Disease
    SRI-37330 is an orally bioavailable thioredoxin-interacting protein (TXNIP) inhibitor. SRI-37330 inhibits glucagon secretion and function, reduces hepatic glucose production and reverses hepatic steatosis. SRI-37330 can be used for type 2 diabetes research .
    SRI-37330
  • HY-141623
    SRI-37330 hydrochloride
    5 Publications Verification

    		 Arrestin Metabolic Disease
    SRI-37330 hydrochloride is an orally bioavailable thioredoxin-interacting protein (TXNIP) inhibitor. SRI-37330 hydrochloride inhibits glucagon secretion and function, reduces hepatic glucose production and reverses hepatic steatosis. SRI-37330 hydrochloride can be used for type 2 diabetes research .
    SRI-37330 hydrochloride
  • 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-113402A
    Gamma-glutamylcysteine TFA
    4 Publications Verification

    γ-Glu-Cys TFA

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine TFA
  • HY-109500
    Masoprocol

    meso-Nordihydroguaiaretic acid; meso-NDGA

    		 Lipoxygenase Metabolic Disease Cancer
    Masoprocol (meso-Nordihydroguaiaretic acid) is a potent and orally active lipoxygenase inhibitor. Masoprocol shows antihyperglycemic activity. Masoprocol decreases the glucose concentration and hepatic triglyceride in vivo. Masoprocol has the potential for the research of type II diabetes .
    Masoprocol
  • HY-42680
    D-Tagatose

    D-(-)-Tagatose

    		 Endogenous Metabolite Metabolic Disease Inflammation/Immunology Cancer
    D-Tagatose (D-(-)-Tagatose) is a natural low-calorie rare sugar. D-Tagatose inhibits the activities of sucrase, maltase and intestinal disaccharidases, reduces the digestion of sucrose and starch, and blocks the absorption of sucrose, maltose and glucose. D-Tagatose promotes glucokinase activity and inhibits glycogen phosphorylase activity via tagatose-1-phosphate, regulates the synthesis and decomposition of hepatic glycogen, reduces postprandial and fasting blood glucose levels, and improves hyperinsulinemia. D-Tagatose regulates lipid profiles, stimulates GLP-1 secretion, and exhibits prebiotic effects. D-Tagatose is a bulking sweetener. D-Tagatose can be used in research related to diabetes, hyperlipidemia, dental caries, atherosclerosis and type 2 diabetes .
    D-Tagatose
  • 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-N15721
    Tryptophan-cholic acid

    Trp-CA

    		 Orphan GPCR GLP Receptor Metabolic Disease
    Tryptophan-cholic acid (Trp-CA) is a microbial amino acid-conjugated bile acid that acts as an endogenous ligand and agonist (EC50=9.6 μM) for the orphan G protein-coupled receptor (GPCR) MRGPRE (Mas-related G protein-coupled receptor family member E). Tryptophan-cholic acid is orally effective but has poor oral absorption and does not cross the blood-brain barrier. Tryptophan-cholic acid promotes the secretion of glucagon-like peptide GLP-1, thereby improving glucose tolerance in diabetic mice. Tryptophan-cholic acid improves glucose tolerance, promotes insulin secretion, and alleviates high-fat diet-induced hepatic steatosis without causing pruritus side effects. Tryptophan-cholic acid is primarily used in research on type 2 diabetes (T2D) .
    Tryptophan-cholic acid
  • HY-N0712
    Typhaneoside
    3 Publications Verification

    		 Autophagy mTOR Akt FXR Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
    Typhaneoside is an orally bioavailable signal modulator and cellular regulator. Typhaneoside regulates the PI3K/Akt/mTOR autophagy transduction pathway. Typhaneoside promotes the activation of AMP-activated protein kinase and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, and cell cycle arrest at the G2/M phase, and reduces cancer cell viability. Typhaneoside activates the farnesoid X receptor signaling pathway, improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside is applicable to research related to post-myocardial infarction heart failure, acute myeloid leukemia, non-alcoholic fatty liver disease, and neurological disorders .
    Typhaneoside
  • 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-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-B2099A
    Buformin hydrochloride
    3 Publications Verification

    1-Butylbiguanide hydrochloride

    		 AMPK Cancer
    Buformin hydrochloride (1-Butylbiguanide hydrochloride), a potent AMPK activator, acts as an orally active biguanide antidiabetic agent. Buformin hydrochloride decreases hepatic gluconeogenesis and lowers blood glucose production in vivo. Buformin hydrochloride also has anti-cancer activities and is applied in cancer study (such as, cervical cancer and breast cancer, et al) .
    Buformin hydrochloride
  • HY-P10302A
    GLP-1R/GIPR agonist-1 (soduim)

    		GLP Receptor Metabolic Disease Inflammation/Immunology
    GLP-1R/GIPR agonist-1 sodium is a dual GLP-1/GIP receptor agonist, with an EC50 of 0.57 nM for GLP-1R and an EC50 of 0.75 nM for GIPR. GLP-1R/GIPR agonist-1 sodium reduces food intake, inhibits weight gain, repairs islet damage, improves glucose tolerance, regulates serum lipid and liver enzyme levels, ameliorates hepatic vacuolization, reduces hepatic fat accumulation, delays the progression of hepatic fibrosis, and exhibits long-lasting hypoglycemic activity. GLP-1R/GIPR agonist-1 sodium can be used in research related to type 2 diabetes, obesity, and non-alcoholic steatohepatitis .
    GLP-1R/GIPR agonist-1 (soduim)
  • HY-108615
    CP-316819

    GPi 819

    		 Phosphorylase Cardiovascular Disease Neurological Disease Metabolic Disease
    CP-316819 (GPi 819) is a blood-brain barrier permeable glycogen phosphorylase inhibitor. CP-316819 inhibits hepatic glycogenolysis, safely reduces blood glucose in type 2 diabetes, and rarely induces hypoglycemia. CP-316819 increases brain glycogen reserves, protects neurons, alleviates hypoglycemic brain injury, and inhibits excessive platelet activation, exerting both neuroprotective and vasculoprotective effects. CP-316819 can be used in research related to hypoglycemia, thrombosis, autoimmune inflammatory diseases, and type 2 diabetes .
    CP-316819
  • HY-110390
    GR148672X

    		Carboxylesterase (CES) Free Fatty Acid Receptor Reactive Oxygen Species (ROS) Mitochondrial Metabolism Ferroptosis Apoptosis Cardiovascular Disease Cancer
    GR148672X is an inhibitor of carboxylesterase 1 (CES1) and hepatic microsomal triglyceride hydrolase (TGH). GR148672X blocks the catalytic activity of CES1, impairs the functions of triglyceride and cholesteryl ester lipase, reduces triglyceride mobilization and secretion, and decreases apolipoprotein B-100 secretion in primary rat hepatocytes. Under low-glucose conditions, GR148672X inhibits the survival of colorectal cancer cells by reducing free fatty acid availability, inducing toxic triglyceride accumulation, ROS production, mitochondrial damage, ferroptosis and apoptosis. GR148672X can be used in studies related to colorectal cancer and atherosclerosis .
    GR148672X
  • 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-153617
    FOXO1-IN-3
    1 Publications Verification

    		 FOXO Metabolic Disease
    FOXO1-IN-3 is a highly-selective and orally active FOXO1 inhibitor. FOXO1-IN-3 reduces hepatic glucose production in mice. FOXO1-IN-3 improves insulin sensitivity and glucose control in db/db mice without causing weight gain .
    FOXO1-IN-3
  • 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-P2989
    Pyruvate carboxylase

    		Endogenous Metabolite Metabolic Disease Cancer
    Pyruvate carboxylase is a key mitochondrial anaplerotic enzyme that catalyzes the conversion of pyruvate to oxaloacetate. Pyruvate carboxylase not only maintains tricarboxylic acid cycle activity and redox homeostasis, but also drives hepatic gluconeogenesis and fatty acid synthesis. The activity of Pyruvate carboxylase is upregulated in insulin-resistant states, exacerbating hepatic glucose production. Pyruvate carboxylase also shows significantly enhanced expression in early-stage non-small cell lung cancer (NSCLC). Pyruvate carboxylase promotes tumor proliferation by supporting nucleotide and lipid synthesis, and its functional deficiency cannot be compensated by glutaminolysis. Pyruvate carboxylase can be used in the research of prediabetes type 2 and NSCLC .
    Pyruvate carboxylase
  • HY-W009417
    Cedryl acetate

    		Environmental Pollutants Glycosidase Metabolic Disease
    Cedryl acetate is an orally active α-glucosidase inhibitor with an IC50 of 94 μM against yeast α-glucosidase. Cedryl acetate reduces high-fat diet-induced body weight gain, visceral fat pad weight, adipocyte hypertrophy, hepatic lipid accumulation, glucose intolerance, insulin resistance and gluconeogenesis. Cedryl acetate can be used in the research of obesity and obesity-related metabolic syndrome .
    Cedryl acetate
  • HY-120103
    PF-06649298
    1 Publications Verification

    		 Sodium Channel Metabolic Disease
    PF-06649298 is a sodium-coupled citrate transporter (NaCT or SLC13A5) inhibitor. PF-06649298 specifically interacts with NaCT with an IC50 value of 16.2 μM to inhibits the transport of citrate in human hepatocytes. PF-06649298 can be used for the research of regulating glucose metabolism and lipid metabolism .
    PF-06649298
  • 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-129297
    CMPF

    		Endogenous Metabolite Metabolic Disease
    CMPF can be found in trace constituent of urine and blood. CMPF is a biomarker of type 2 diabetes. CMPF can act on the β cell and induces impaired mitochondrial function. CMPF decreases glucose-induced ATP accumulation, and induces oxidative stress. CMPF reverses hepatic lipid accumulation and improves insulin sensitivity in obese mice .
    CMPF
  • HY-125539
    Roridin E

    		Antibiotic Phosphatase Fungal Infection
    Roridin E is a glucose-6-phosphatase (G6Pase) inhibitor and antibiotic, and is a metabolic byproduct of Roridin A (HY-N9599). Roridin E induces significant oxidative stress, characterized by depletion of glutathione in vivo, induction of hepatic lipid peroxidation, and inhibition of renal superoxide dismutase activity. Roridin E reduces blood glucose levels in rats, but exhibits acute toxicity (which is enhanced when co-administered with linoleic acid (HY-N0729)) and causes hepatotoxicity in male albino mice. Roridin E induces a decrease in total blood protein and increases in the levels of total lipids, γ-glutamyltransferase, alkaline phosphatase, and 5'-nucleotidase. Roridin E can be isolated from molds, and possesses cytostatic and antifungal activities similar to those of Verrucarin A (HY-107426) and Roridin A. Roridin E exhibits in vivo activity in rodents and is commonly used in hepatotoxicity-related studies .
    Roridin E
  • 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-P1141A
    GLP-1(9-36)amide TFA

    		GCGR Metabolic Disease
    GLP-1(9-36)amide TFA is a major metabolite of glucagon-like peptide-1-(7-36) amide formed by the enzyme dipeptidyl peptidase-4 (DPP-4). GLP-1(9-36)amide TFA acts as an antagonist to the human pancreatic GLP-1 receptor .
    GLP-1(9-36)amide TFA
  • 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-Y1269D
    Ammonium chloride, for molecular biology

    Salmiac, for molecular biology

    		 TGF-beta/Smad Apoptosis Chloride Channel Neurological Disease Cancer
    Ammonium chloride (Salmiac), for molecular biology is an inhibitor of Slc26a4 and SMAD2. Ammonium chloride, for molecular biology reduces the protein expression level of Slc26a4 in lung tissue, and attenuates ozone-induced increases in proinflammatory cytokines, inflammatory cells, pulmonary resistance, goblet cell hyperplasia, peribronchial inflammation and thiocyanate levels in mouse tissues and bronchoalveolar lavage fluid. Ammonium chloride, for molecular biology decreases the level of phosphorylated SMAD2, inhibits autophagy by reducing autophagy-related proteins, and enhances Cisplatin (HY-17394)-induced cancer cell apoptosis and DNA double-strand breaks. Ammonium chloride, for molecular biology also inhibits the TCA cycle, reduces ATP production, increases glucose utilization, regulates the levels of lactic acid, glutamic acid and ATP, and induces morphological degeneration of neuroblastoma cells. Ammonium chloride, for molecular biology can be used in studies related to ozone-induced airway injury, hepatocellular carcinoma, human cervical cancer, hepatic encephalopathy, Reye syndrome, epilepsy and neurodegenerative diseases .
    Ammonium chloride, for molecular biology
  • HY-B2099
    Buformin

    1-Butylbiguanide

    		 AMPK Metabolic Disease Cancer
    Buformin (1-Butylbiguanide), a potent AMPK activator, acts as an orally active biguanide antidiabetic agent. Buformin decreases hepatic gluconeogenesis and lowers blood glucose production in vivo. Buformin also has anti-cancer activities and is applied in cancer study (such as, cervical cancer and breast cancer, et al) .
    Buformin
  • 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-144035
    GLP-1R agonist 4

    		GCGR Metabolic Disease Inflammation/Immunology
    GLP-1R agonist 4 is a glucagon-like peptide-1 (GLP-1) receptor agonist. GLP-1 is an intestinal hypoglycemic hormone secreted by L-cells in the lower gastrointestinal tract. GLP-1R agonist 4 can be used for the research of type 2 diabetes mellitus, obesity, non-alcoholic steatohepatitis, insulin resistance and etc .
    GLP-1R agonist 4
  • HY-113402R
    Gamma-glutamylcysteine (Standard)

    γ-Glu-Cys (Standard)

    		 Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Inflammation/Immunology
    Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine (Standard)
  • HY-B0399A
    (±)-Carnitine

    DL-Carnitine; DL-Levocarnitine

    		 Mitochondrial Metabolism Metabolic Disease
    (±)-Carnitine (DL-Carnitine) is an orally effective racemic mixture of L-Carnitine (HY-B0399) and D-Carnitine. (±)-Carnitine elevates the mitochondrial NAD +/NADH ratio in the presence of 1,3-butanediol (HY-77490A). (±)-Carnitine does not increase glucose and urea production from L-glutamine, but stimulates propionate gluconeogenesis in rat renal cortical slices, and significantly reduces hepatic ketone body levels in rats fed a diet containing 30% high fat plus 20% 1,3-butanediol .
    (±)-Carnitine
  • HY-123115
    Leucrose

    5-O-α-D-Glucopyranosyl-D-fructose

    		 JAK STAT TNF Receptor Interleukin Related Metabolic Disease Inflammation/Immunology
    Leucrose (5-O-α-D-Glucopyranosyl-D-fructose) is an orally active Sucrose (HY-B1779) isomer naturally found in pollen and honey. Leucrose promotes phosphorylation of JAK1 and STAT6, reduces pro-inflammatory mediators and cytokinesas (TNFα, and IL-1β), increases M2 macrophage polarization and suppresses DSS (HY-116282C)-induced colitis. Leucrose suppresses hepatic triglyceride accumulation, improves fasting blood glucose levels, and regulates hepatic lipogenesis and fatty acid β-oxidation in high-fat diet-induced obese mice. Leucrose is slowly hydrolyzed into glucose and fructose by α-glucosidase and acts as as a sugar substitute in diet .
    Leucrose
  • HY-N0887
    Isoastragaloside I
    2 Publications Verification

    Isoastragaloside-I

    		 Akt NF-κB p38 MAPK PI3K FXR Keap1-Nrf2 NO Synthase COX Interleukin Related Integrin TGF-β Receptor Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Inflammation/Immunology
    Isoastragaloside I is a natural compound found in Astragalus membranaceus, with oral activity and multiple biological activities such as anti-inflammatory and antioxidant properties. Isoastragaloside I inhibits Akt, NF-κB, MAPKs and PI3K, enhances the activity of hepatic FXR, regulates the TGF-β/Smads signaling pathway, and upregulates antioxidant molecules downstream of Nrf2. Isoastragaloside I inhibits the expression of NO, TNF-α, iNOS, COX-2, IL-1β and VCAM-1, and reduces intracellular ROS levels. Isoastragaloside I attenuates blood-brain barrier disruption, restores intestinal barrier function, increases β-cell mass, improves glucose homeostasis, and elevates circulating adiponectin levels. Isoastragaloside I can be used for the study of neuroinflammation-related neurodegenerative diseases, cholestatic liver disease, and diabetes .
    Isoastragaloside I
  • HY-P10337
    OXM-7

    		GCGR GLP Receptor Metabolic Disease Endocrinology
    OXM-7 is a dual agonist of GLP-1R (EC50=0.024 nM) and GCGR (EC50=0.082 nM). OXM-7 can enhance glucose-stimulated insulin secretion and hepatic glucose output. OXM-7 lowers blood glucose levels. OXM-7 improves lipid metabolism .
    OXM-7
  • HY-177297
    LCZ960

    NVP-LCZ960

    		 Glucokinase Metabolic Disease
    LCZ960 is an orally active glucokinase (GK) activator. LCZ960 stimulates GK activity in hepatocytes in vitro and stimulates glucose uptake in vivo through hepatic GK activation. LCZ960 lowers blood glucose in mice with diet-induced obesity (DIO). LCZ960 maintains normoglycemia and improves glucose tolerance in DIO mice and rats. LCZ960 stimulates glycogen synthase flux and increases hepatic glycogen turnover in rats. LCZ960 induces increased hepatic glycogen recycling. LCZ960 can be used to study high-fat diet-induced obesity and type 2 diabetes .
    LCZ960
  • HY-136855
    MitoPBN

    		Sirtuin AMPK PGC-1α Apoptosis Reactive Oxygen Species (ROS) Metabolic Disease
    MitoPBN is a AMPK/SIRT3/PGC-1α axis modulator, reactive oxygen species scavenger and mitochondrial function enhancer. MitoPBN increases the phosphorylation level of AMPK, restores SIRT3 expression and reverses the down-regulation of PGC-1α, thereby promoting mitochondrial biogenesis. MitoPBN regulates glucose metabolism, reduces blood glucose by inhibiting hepatic gluconeogenesis and increasing hepatic glucose uptake, while scavenging mitochondrial superoxide anion/hydrogen peroxide, maintaining membrane potential and increasing ATP production. MitoPBN also reduces cell apoptosis, improves sperm motility, survival rate and membrane integrity, but may induce reductive stress in cryopreserved sperm at high concentrations. MitoPBN is widely applicable to research related to diabetes and type 2 diabetes .
    MitoPBN
  • HY-107129
    MK-3577

    		GCGR Metabolic Disease
    MK-3577 is an orally effective glucagon receptor (GCGR) antagonist that reduces hepatic glucose production and lowers blood glucose levels by blocking glucagon receptors on target organs, primarily the liver. Pharmacokinetic analysis in domestic cats indicates that MK-3577 reaches peak levels 3 to 4 hours after oral administration, with a half-life of approximately 15 hours. MK-3577 can be used in diabetes research .
    MK-3577
  • HY-N0468R
    Rebaudioside D (Standard)

    		Reference Standards Acetyl-CoA Carboxylase FXR Metabolic Disease
    Rebaudioside D (Standard) is the analytical standard of Rebaudioside D. This product is intended for research and analytical applications. 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 (Standard)
  • HY-N16527
    7-O-Galloyl-D-sedoheptulose

    		TNF Receptor Interleukin Related NADPH Oxidase Reactive Oxygen Species (ROS) NF-κB COX NO Synthase JNK AP-1 TGF-β Receptor Metabolic Disease
    7-O-Galloyl-D-sedoheptulose is an orally effective polyphenolic compound. 7-O-Galloyl-D-sedoheptulose lowers the serum levels of glucose, leptin, insulin, C-peptide, resistin, TNF-α, IL-6, and increases the serum level of adiponectin. 7-O-Galloyl-D-sedoheptulose significantly reduces the levels of ROS and lipid peroxidation products (TBARS) by down-regulating the protein expression of NADPH oxidase subunit Nox-4 and p22phox. 7-O-Galloyl-D-sedoheptulose down-regulates NF-κB and related pro-inflammatory factors (COX-2, iNOS), inhibits the phosphorylation of JNK and the activity of its downstream AP-1. 7-O-Galloyl-D-sedoheptulose reduces the expression of TGF-β1 and fibronectin, indicating its potential in anti-tissue fibrosis. 7-O-Galloyl-D-sedoheptulose can be used for the study of type 2 diabetes and its hepatic and pancreatic complications .
    7-O-Galloyl-D-sedoheptulose
  • HY-113402AR
    Gamma-glutamylcysteine TFA (Standard)

    γ-Glu-Cys TFA (Standard)

    		 Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine TFA (Standard)
  • HY-A0231
    Glymidine sodium

    Gondafon; Glycodiazine

    		 Insulin Receptor Metabolic Disease
    Glymidine sodium is an oral active antidiabetic. Glymidine sodium is the inhibitor of hepatic lipolysis. Glymidine sodium inhibits the glucose formation and supresses the elevated pyruvate oxidation which results from the inhibition of endogenous lipid mobilization .
    Glymidine sodium
  • HY-123765
    JTT-553

    		Acyltransferase Metabolic Disease
    JTT-553 is a DGAT1 inhibitor (IC50: 2.38 nM). JTT-553 reduces plasma concentrations of glucose, insulin, non-esterified fatty acids (NEFA), total cholesterol (TC), and hepatic triglycerides (TG). JTT-553 improves insulin-dependent glucose uptake and glucose intolerance in adipose tissue of DIO mice. JTT-553 reduces TNF-α mRNA levels and increases GLUT4 mRNA levels in adipose tissue of KK-Ay mice. JTT-553 improves adipose tissue insulin resistance and systemic glucose metabolism by reducing body weight. JTT-553 can be used in the study of obesity and type 2 diabetes mellitus (T2DM) .
    JTT-553
  • HY-161892
    FABP4-IN-4

    		FABP Metabolic Disease Inflammation/Immunology
    FABP4-IN-4 (Compound 30) is an orally active inhibitor for FABP, with IC50 of 1.18 μM for FABP 1. FABP4-IN-4 improves the glucose tolerance, reduces the level of blood glucose, plasma lipids and hepatic inflammatory factors, attenuates hepatic steatosis, and exhibits anti-inflammatory effects in mouse diet-induced obesity models .
    FABP4-IN-4
  • HY-159696
    ISIS 449884

    		GCGR Metabolic Disease
    ISIS 449884 is a 2'-O-methoxyethyl antisense oligonucleotide that targets GCGR. ISIS 449884 has an ability to reduce hepatic glucose output and lower the blood glucose level. ISIS 449884 can be used for the study of type 2 diabetes mellitus (T2DM) .
    ISIS 449884
  • HY-159696A
    ISIS 449884 sodium

    		GCGR Metabolic Disease
    ISIS 449884 sodium is a 2'-O-methoxyethyl antisense oligonucleotide that targets GCGR. ISIS 449884 sodium has an ability to reduce hepatic glucose output and lower the blood glucose level. ISIS 449884 sodium can be used for the study of type 2 diabetes mellitus (T2DM) .
    ISIS 449884 sodium
  • HY-12735
    SCH 900822

    		GCGR Metabolic Disease Endocrinology
    SCH 900822 is a potent and selective glucagon receptor (hGCGR) antagonist that blocks the binding of glucagon to its receptor, thereby reducing hepatic glycogenolysis and gluconeogenesis, thereby lowering blood glucose production. SCH 900822 can be used in the study of type 2 diabetes .
    SCH 900822
  • HY-19176
    S-15261

    		Insulin Receptor Metabolic Disease
    S-15261 is an orally active and potent anti-hyperglycemic agent. S-15261 reduces hepatic glucose production through direct and insulin-sensitizing effects. S-15261 can be used for the research of insulin resistance syndrome .
    S-15261

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