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Results for "

hepatic lipid accumulation

" in MedChemExpress (MCE) Product Catalog:

42

Inhibitors & Agonists

2

Peptides

22

Natural
Products

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-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-N2118
    Bilobetin
    2 Publications Verification

    		 PPAR PKA Akt p38 MAPK ERK Metabolic Disease
    Bilobetin, an active component of Ginkgo biloba, can reduce blood lipids and improve the effects of insulin. Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in β-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPARα accompanied by elevated cAMP level and PKA activity .
    Bilobetin
  • 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-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-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-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-N1990
    Gypenoside XLIX
    2 Publications Verification

    		 PPAR Sirtuin Keap1-Nrf2 Toll-like Receptor (TLR) NF-κB Reactive Oxygen Species (ROS) NOD-like Receptor (NLR) Apoptosis Pyroptosis Autophagy Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Gypenoside XLIX is a multifunctional bioactive compound that can be isolated from Gynostemma pentaphyllum, with a Ka value of 1.58 μM for its binding to SIRT1. Gypenoside XLIX acts as a PPAR-α agonist. It inhibits the activation of TLR4-mediated NF-κB signaling pathway by activating the Sirt1/Nrf2 signaling pathway, reduces ROS accumulation, and alleviates hepatic inflammatory injury in mice with sepsis-induced liver disease. Gypenoside XLIX targets SIRT1 to block YAP-NLRP3 activation and improve sepsis-induced cardiomyopathy. Gypenoside XLIX inhibits apoptosis (Apoptosis), pyroptosis (Pyroptosis), autophagy (Autophagy), lipid peroxidation, pro-inflammatory cytokines and anti-inflammatory cytokines. Gypenoside XLIX alleviates sepsis-induced splenic injury by inhibiting inflammation and oxidative stress, and mitigates sepsis-associated encephalopathy by targeting PPAR-α. Gypenoside XLIX prevents acute kidney injury by inhibiting IGFBP7/IGF1R-mediated programmed cell death and inflammation. Gypenoside XLIX inhibits the expression and activity of vascular cell adhesion molecule-1 in cytokine-induced human endothelial cells. Gypenoside XLIX is applicable to research related to acute liver injury, lung injury, cardiomyopathy, acute splenic injury, sepsis-associated encephalopathy, acute kidney injury, atherosclerosis and chronic inflammation .
    Gypenoside XLIX
  • HY-N0261
    Aurantio-obtusin
    1 Publications Verification

    		 TNF Receptor COX Cardiovascular Disease Inflammation/Immunology
    Aurantio-obtusin is a anthraquinone compound that can be extracted from cassia seed. Aurantio-obtusin has the effects of decreasing blood pressure, decreasing blood lipids and anti-inflammatory.Aurantio-obtusin is an orally active vasodilator. Aurantio-obtusin ameliorates hepatic steatosis through AMPK/ autophagy- and AMPK/TFEB mediated inhibition of lipid accumulation .
    Aurantio-obtusin
  • 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-129143
    Delphinidin-3-sambubioside chloride
    1 Publications Verification

    Dp3‐Sam chloride

    		 Apoptosis Metabolic Disease Inflammation/Immunology
    Delphinidin-3-sambubioside (Dp3‐Sam) chloride is an anthocyanin that has orally active anti-inflammatory activity. Delphinidin-3-sambubioside chloride inhibits LPS-induced inflammatory factors release. Delphinidin-3-sambubioside chloride also alleviates hepatic lipid accumulation in HFD rats. Delphinidin-3-sambubioside chloride can be isolated from Hibiscus sabdariffa L. .
    Delphinidin-3-sambubioside chloride
  • 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-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-N0909
    Notoginsenoside R2
    1 Publications Verification

    20(S)-Notoginsenoside R2; Ginsenoside Ng-R2

    		 Apoptosis MEK ERK Reactive Oxygen Species (ROS) Caspase COX β-catenin Src MDM-2/p53 JAK STAT Neurological Disease Metabolic Disease Inflammation/Immunology
    Notoginsenoside R2 (20(S)-Notoginsenoside R2; Ginsenoside Ng-R2) is an orally active notoginsenoside . Notoginsenoside R2 activates P90RSK and Nrf2 via the MEK1/2-ERK1/2 pathway to inhibit 6-OHDA-induced apoptotic damage in nerve cells. Notoginsenoside R2 upregulates SOX8/β-catenin by reducing miR-27a, thereby suppressing Aβ25-35-induced neuronal apoptosis and inflammatory responses . Notoginsenoside R2 alleviates lipid accumulation and mitochondrial dysfunction in diabetic nephropathy by inhibiting c-Src. Notoginsenoside R2 alleviates hepatic fibrosis by inducing hepatic stellate cell senescence and inhibiting the inflammatory microenvironment via JAK/STAT3 suppression . Notoginsenoside R2 can be used in research related to Parkinson's disease, Alzheimer's disease, diabetic nephropathy and hepatic fibrosis .
    Notoginsenoside R2
  • 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-142026
    Vitisin A

    (+)-Vitisin A

    		 Caspase ERK NF-κB Influenza Virus PAK LDLR PPAR PCSK9 Androgen Receptor Keap1-Nrf2 Monoamine Oxidase Cholinesterase (ChE) IKK Wnt β-catenin Reactive Oxygen Species (ROS) Apoptosis Cuproptosis Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC50 values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases .
    Vitisin A
  • HY-N0853A
    Alisol A 24-acetate
    1 Publications Verification

    Alisol A 24-monoacetate; Alisol A monoacetate

    		 AMPK Carnitine Palmitoyltransferase (CPT) Acyltransferase Fatty Acid Synthase (FASN) Acetyl-CoA Carboxylase Bcl-2 Family PPAR Nuclear Factor of activated T Cells (NFAT) PI3K Akt PKA ERK Apoptosis Autophagy Cardiovascular Disease Infection Neurological Disease Metabolic Disease Endocrinology
    Alisol A 24-acetate (Alisol A monoacetate) is an orally active derivative of protostane-type tetracyclic triterpenoid. Alisol A 24-acetate upregulates the expression of adiponectin, AMPKα, CPT1, and ACOX1; downregulates the expression of SREBP-1c, ACC, FAS, Bcl-2, Bcl-xl, PPAR-γ, perilipin A, and NFATc1; inhibits the activity of PI3K/Akt/mTOR and HMGR; and activates the PKA and ERK signaling pathways. Alisol A 24-acetate regulates cell apoptosis (apoptosis), autophagy (Autophagy, hepatic lipid accumulation, inflammatory response, neuroprotection, MRSA membrane integrity, and osteoclast differentiation. Alisol A 24-acetate can be used in research related to non-alcoholic fatty liver disease, nephrotoxicity, obesity, global cerebral ischemia-reperfusion injury, bacterial infection, and osteoporosis .
    Alisol A 24-acetate
  • 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-139040
    2-(Tetradecylthio)acetic acid

    		PPAR Metabolic Disease
    2-Tetradecylthio acetic acid is a pan-peroxisome proliferator activated receptor (pan-PPAR) activator. 2-Tetradecylthio acetic acid induces hypolipidemia. 2-Tetradecylthio acetic acid reduces plasma lipids and enhances hepatic fatty acid oxidation in rodents. 2-Tetradecylthio acetic acid increases the expression of genes involved in fatty acid uptake, activation, accumulation, and oxidation .
    2-(Tetradecylthio)acetic acid
  • 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-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-141439
    TBE 31

    		Keap1-Nrf2 Quinone Reductase Glutathione S-transferase Apoptosis TNF Receptor Inflammation/Immunology Cancer
    TBE 31 is an orally active Keap1/Nrf2 pathway activator and NQO1 inducer with a Dm value of 1.1 nM for NQO1. TBE 31 binds to cysteine residues of Keap1, inhibits ubiquitination and degradation of Nrf2, thereby activating the expression of ARE-dependent genes. TBE 31 induces cytoprotective enzymes including NQO1 and GST isoforms, promotes Nrf2 accumulation, and upregulates Nrf2-regulated genes related to antioxidation and lipid metabolism. TBE 31 inhibits pro-inflammatory responses, formation of AFB1-DNA adducts, endoplasmic reticulum stress, cell apoptosis (apoptosis), hepatic fibrosis, oxidative stress, and the expression of ChREBP. TBE 31 reduces the number of tumors in a mouse model of ultraviolet-induced skin carcinogenesis. TBE 31 enhances nerve growth factor-induced neurite outgrowth. TBE 31 attenuates LPS-induced serum TNF-α levels and immobility time in mice. TBE 31 can be used in research related to liver cancer, skin cancer, inflammation-related depression, and non-alcoholic steatohepatitis .
    TBE 31
  • HY-N0261R
    Aurantio-obtusin (Standard)

    		Reference Standards TNF Receptor COX Cardiovascular Disease Inflammation/Immunology
    Aurantio-obtusin (Standard) is the analytical standard of Aurantio-obtusin. This product is intended for research and analytical applications. Aurantio-obtusin is a anthraquinone compound that can be extracted from cassia seed. Aurantio-obtusin has the effects of decreasing blood pressure, decreasing blood lipids and anti-inflammatory.Aurantio-obtusin is an orally active vasodilator. Aurantio-obtusin ameliorates hepatic steatosis through AMPK/ autophagy-and AMPK/TFEB mediated inhibition of lipid accumulation .
    Aurantio-obtusin (Standard)
  • 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-174133
    HSD17B13-IN-104

    		17β-HSD Metabolic Disease Inflammation/Immunology
    HSD17B13-IN-104 (Compound 32) is an orally active, highly potent and selective HSD17B13 inhibitor (IC50=2.5 nM). HSD17B13-IN-104 regulates hepatic lipid metabolism by inhibiting the SREBP-1c/FAS pathway. HSD17B13-IN-104 blocks HSD17B13 enzymatic activity to improve hepatic lipid accumulation. HSD17B13-IN-104 is promising for research of metabolic dysfunction-associated steatohepatitis .
    HSD17B13-IN-104
  • 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-N10063
    Penispidin A

    		Others Metabolic Disease
    Penispidin A inhibits hepatic lipid accumulation in HepG2 cells.
    Penispidin A
  • HY-139230
    OLHHA

    		Cannabinoid Receptor PPAR Metabolic Disease
    OLHHA is a dual CB1 receptor antagonist and PPARα agonist. OLHHA also is a alcohol intake inhibitor with an EC50 value of 0.2 mg/kg. OLHHA reduces both hepatic lipid accumulation and circulating triglyceride levels. OLHHA shows anti-steatotic activity and has the potential for the research of non-alcoholic fatty liver disease (NAFLD) .
    OLHHA
  • HY-N2118R
    Bilobetin (Standard)

    		Reference Standards PPAR PKA Akt p38 MAPK ERK Metabolic Disease
    Bilobetin (Standard) is the analytical standard of Bilobetin. This product is intended for research and analytical applications. Bilobetin, an active component of Ginkgo biloba, can reduce blood lipids and improve the effects of insulin. Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in β-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPARα accompanied by elevated cAMP level and PKA activity .
    Bilobetin (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-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-139040R
    2-(Tetradecylthio)acetic acid (Standard)

    Tetradecylthioacetic acid (Standard)

    		 PPAR Reference Standards Metabolic Disease
    2-(Tetradecylthio)acetic acid (Standard) is the analytical standard of 2-(Tetradecylthio)acetic acid. This product is intended for research and analytical applications. 2-Tetradecylthio acetic acid is a pan-peroxisome proliferator activated receptor (pan-PPAR) activator. 2-Tetradecylthio acetic acid induces hypolipidemia. 2-Tetradecylthio acetic acid reduces plasma lipids and enhances hepatic fatty acid oxidation in rodents. 2-Tetradecylthio acetic acid increases the expression of genes involved in fatty acid uptake, activation, accumulation, and oxidation .
    2-(Tetradecylthio)acetic acid (Standard)
  • HY-129143R
    Delphinidin-3-sambubioside chloride (Standard)

    Dp3‐Sam chloride (Standard)

    		 Reference Standards Others Metabolic Disease Inflammation/Immunology
    Delphinidin-3-sambubioside (chloride) (Standard) is the analytical standard of Delphinidin-3-sambubioside (chloride). This product is intended for research and analytical applications. Delphinidin-3-sambubioside (Dp3‐Sam) chloride is an anthocyanin that has orally active anti-inflammatory activity. Delphinidin-3-sambubioside chloride inhibits LPS-induced inflammatory factors release. Delphinidin-3-sambubioside chloride also alleviates hepatic lipid accumulation in HFD rats. Delphinidin-3-sambubioside chloride can be isolated from Hibiscus sabdariffa L. .
    Delphinidin-3-sambubioside chloride (Standard)
  • HY-113402B
    Gamma-glutamylcysteine ammonium

    γ-Glu-Cys ammonium

    		 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 ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium 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 ammonium 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 ammonium 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 ammonium
  • HY-181876
    F44-S101

    		FXR Metabolic Disease
    F44-S101 is an orally active, potent, and selective gut-restricted FXR antagonist with an IC50 of 0.48 μM and lipid-lowering activity. F44-S101 selectively antagonizes intestinal FXR, feedback-activates hepatic FXR, promotes cholesterol metabolism and reduces lipid accumulation. F44-S101 decreases total cholesterol, triglyceride and low-density lipoprotein cholesterol levels. F44-S101 can be used in studies related to hyperlipidemia .
    F44-S101
  • HY-P11614
    LCA-H10

    		Liposome Cancer
    LCA-H10 is a lithocholic acid-histidine decapeptide conjugate, a biocompatible lipid nanoparticle (LNP) additive that reduces ionizable lipid proportions, functions as an endosomal escape inducer, and enhances siRNA encapsulation. LCA-H10 increases hepatic accumulation of LNPs in mice after intravenous injection when incorporated into LiLNP-LH and reduces proinflammatory cytokines (IL-6, TNF, IL-1β) in mouse serum. LCA-H10 can be used for the research of prostate cancer .
    LCA-H10
  • HY-182014
    TLC-2716

    		LXR Cardiovascular Disease Metabolic Disease
    TLC-2716 is an orally available, gut- and liver-restricted inhibitor against LXRα and LXRβ, with EC50 values of 7 nM and 15 nM, respectively. TLC-2716 represses LXRα/β transcriptional activity, downregulates genes involved in lipogenesis, lipid absorption and lipoprotein metabolism, and preserves peripheral reverse cholesterol transport. TLC-2716 reduces lipid accumulation, suppresses inflammation and fibrotic gene expression, enhances triglyceride-rich lipoprotein clearance, and improves glucose homeostasis and insulin sensitivity. TLC-2716 lowers serum and hepatic triglycerides, plasma cholesterol and other atherogenic lipid profiles in experimental models and humanized liver mice. TLC-2716 can be used for the research of dyslipidemia and related cardiometabolic disorders .
    TLC-2716
  • HY-182046
    HD202A

    		MNK PPAR Eukaryotic Initiation Factor (eIF) Stearoyl-CoA Desaturase (SCD) Metabolic Disease
    HD202A is an orally active, selective dual inhibitor of MNK1/MNK2 (with IC50 values of 6.09 nM and 8.06 nM, and Kd values of 1.913 μM and 5.244 μM, respectively) that inhibits the MNK-eIF4E signaling pathway. By downregulating perilipin 2 and SCD1, while upregulating adipose triglyceride lipase and PPARγ coactivator 1α, HD202A enhances mitochondrial fatty acid oxidation and redox homeostasis. HD202A effectively suppresses body weight gain, hepatic lipid accumulation and elevation of serum lipids, significantly improves glucose tolerance and insulin sensitivity of the organism, and ameliorates inflammatory features. With these comprehensive pharmacological activities, HD202A exhibits great application potential in studies of metabolic dysfunction-associated steatotic liver disease .
    HD202A
  • 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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