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hepatic fat accumulation

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18

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2

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1

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-10585
    Valproic acid
    Maximum Cited Publications
    65 Publications Verification

    VPA; 2-Propylpentanoic acid; Dipropylacetic acid

    		 Organoid HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Valproic acid (VPA) is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM. Valproic acid inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid is used in the epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches .
    Valproic acid
  • HY-10585A
    Valproic acid sodium
    Maximum Cited Publications
    65 Publications Verification

    Sodium Valproate; VPA sodium; 2-Propylpentanoic acid sodium

    		 Organoid HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite Infection Neurological Disease Metabolic Disease Cancer
    Valproic acid (Sodium Valproate) sodium is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid sodium activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches .
    Valproic acid sodium
  • 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-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-W018791
    Bifendate
    2 Publications Verification

    DDB

    		 HBV Autophagy Cytochrome P450 Atg8/LC3 p62 P-glycoprotein Infection Cardiovascular Disease Cancer
    Bifendate (DDB), extracted from Schisandrae chinensis, is an orally active anti-HBV agent against chronic hepatitis B. Bifendate inhibits ATG5-dependent autophagy and attenuates oleic acid-induced lipid accumulation with anti-oxidant properties in vitro. Bifendate can decrease alanine transaminase (ALT) level in mice. Bifendate attenuates hepatic steatosis in cholesterol/bile salt- and high-fat diet-induced hypercholesterolemia in mice. Bifendate potently increases the activity of cytochrome proteins (CYPs) and reverse P-gp-mediated multi-drug resistance (MDR) .
    Bifendate
  • 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-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-10585AR
    Valproic acid sodium (Standard)

    Sodium Valproate (Standard); VPA sodium (Standard); 2-Propylpentanoic acid sodium (Standard)

    		 Organoid Reference Standards HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite Infection Neurological Disease Metabolic Disease Cancer
    Valproic acid (sodium) (Standard) is the analytical standard of Valproic acid (sodium). This product is intended for research and analytical applications. Valproic acid (Sodium Valproate) sodium is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid sodium activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches .
    Valproic acid sodium (Standard)
  • HY-10585B
    Valproic acid sodium (2:1)

    Sodium Valproate (2:1); VPA sodium (2:1); 2-Propylpentanoic acid sodium (2:1)

    		 HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite Infection Neurological Disease Metabolic Disease Cancer
    Valproic acid (VPA) sodium (2:1) is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid sodium (2:1) activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium (2:1) is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches .
    Valproic acid sodium (2:1)
  • 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-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-W018791R
    Bifendate (Standard)

    DDB (Standard)

    		 Reference Standards HBV Autophagy Cytochrome P450 Atg8/LC3 p62 P-glycoprotein Infection Cardiovascular Disease Cancer
    Bifendate (DDB), extracted from Schisandrae chinensis, is an orally active anti-HBV agent against chronic hepatitis B. Bifendate inhibits ATG5-dependent autophagy and attenuates oleic acid-induced lipid accumulation with anti-oxidant properties in vitro. Bifendate can decrease alanine transaminase (ALT) level in mice. Bifendate attenuates hepatic steatosis in cholesterol/bile salt- and high-fat diet-induced hypercholesterolemia in mice. Bifendate potently increases the activity of cytochrome proteins (CYPs) and reverse P-gp-mediated multi-drug resistance (MDR) .
    Bifendate (Standard)
  • HY-W794759
    Valproic acid magnesium

    Magnesium valproate; VPA magnesium; 2-Propylpentanoic acid magnesium

    		 Organoid HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite Infection Neurological Disease Cancer
    Valproic acid magnesium (Magnesium valproate) is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM. Valproic acid magnesium inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid magnesium activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid magnesium is used in the epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches .
    Valproic acid magnesium
  • HY-10585AG
    Valproic acid sodium

    Sodium Valproate; VPA sodium; 2-Propylpentanoic acid sodium

    		 Organoid HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite Infection Neurological Disease Metabolic Disease Cancer
    Valproic acid (Sodium Valproate) sodium is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid sodium activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches .
    Valproic acid sodium
  • HY-W009417R
    Cedryl acetate (Standard)

    		Reference Standards Glycosidase Environmental Pollutants Metabolic Disease
    Cedryl acetate (Standard) is the analytical standard of Cedryl acetate. This product is intended for research and analytical applications. 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 (Standard)
  • HY-133180
    YW1128

    		Wnt β-catenin Metabolic Disease
    YW1128 (compound 3a) is a potent Wnt/β-Catenin inhibitor. YW1128 induces the proteasome degradation of β-catenin and subsequent inhibits the Wnt/β-catenin signaling in cells. YW1128 significantly decreases hepatic lipid accumulation. YW1128 improves glucose tolerance of high fat diet-fed mice without noticeable toxicity. YW1128 down regulates the genes involved in the glucose and fatty acid anabolism .
    YW1128
  • HY-186096
    LP-856866

    		ACSL Family GLP Receptor Metabolic Disease
    LP-856866 is an orally active ACSL5 inhibitor, with IC50 values of 8 nM and 4 nM against mouse and human ACSL5, respectively, and IC50 values of 6 nM and 17 nM against mouse and human ACSL1, respectively. LP-856866 induces delayed gastric emptying, promotes GLP-1 release, reduces food intake, decreases body weight and body fat mass, preserves lean body mass, improves glucose homeostasis, enhances insulin sensitivity, reduces hepatic lipid accumulation, and lowers serum triglyceride and total cholesterol levels. LP-856866 is applicable to research on diet-induced obesity .
    LP-856866
  • HY-184158
    HATC

    		AUTACs HIF/HIF Prolyl-Hydroxylase Metabolic Disease Inflammation/Immunology
    HATC is a HIF-1α AUTAC degrader. HATC links HIF-1α to LC3 to form a ternary complex that undergoes degradation via the autophagy-lysosome fusion pathway. HATC induces dose-dependent HIF-1α degradation in multiple cell types. HATC reduces visceral fat accumulation, hepatic lipid deposition, senescent cell aggregation, and bone loss; alleviates age-related intervertebral disc degeneration, liver dysfunction, kyphosis, and alveolar dilation; decreases circulating lactic acid levels; improves physical performance; and reverses age-related changes in granulocyte proportions. HATC extends median and maximum lifespan, reduces transcriptomic age, and causes no obvious persistent toxicity. HATC can be used in the research of age-related diseases (pink: LC3 ligand (HY-50759); blue: HIF-1α ligand (HY-P10426); Linker: (HY-W008264)) .
    HATC

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