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Results for "

hepatic dysfunction

" in MedChemExpress (MCE) Product Catalog:

37

Inhibitors & Agonists

1

Screening Libraries

1

Biochemical Assay Reagents

5

Peptides

15

Natural
Products

2

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B1334A
    Perhexiline maleate
    Maximum Cited Publications
    6 Publications Verification

    		 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-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-42682
    D(+)-Galactosamine hydrochloride
    3 Publications Verification

    D-Galactosamine HCl

    		 Drug Derivative Inflammation/Immunology
    D(+)-Galactosamine (D-Galactosamine) hydrochloride, which is an established experimental toxin, primarily causes liver injury by the generation of free radicals and depletion of UTP nucleotides. D(+)-Galactosamine hydrochloride intoxication also induces renal dysfunction thus, renal failure is often associated with the end-stage of the liver damage. Lipopolysaccharide/D(+)-Galactosamine-induced acute liver injury is a known animal model of fulminant hepatic failure .
    D(+)-Galactosamine hydrochloride
  • HY-P1624
    Teduglutide
    2 Publications Verification

    ALX-0600

    		 Nuclear Hormone Receptor 4A/NR4A FXR Inflammation/Immunology
    Teduglutide (ALX-0600) is an analog of human glucagon like peptide-2 (GLP-2). Teduglutide can activate the expression of nuclear receptor subfamily 4 group a member 1 (NR4a1)/nur77 and intestinal FXR signaling in human hepatic stellate cells, thereby improving liver inflammation and fibrosis in mice with sclerosing cholangitis. Teduglutide can alleviate intestinal dysfunction in mice, improve lung injury, alleviate obesity related neuroinflammation and cell apoptosis .
    Teduglutide
  • HY-148013
    K284-6111
    1 Publications Verification

    		 Glycosidase Amyloid-β NF-κB COX ERK NO Synthase Interleukin Related Neurological Disease Inflammation/Immunology
    K284-6111 is a high-affinity and orally active CHI3L1 inhibitor, and inhibits CHI3L1 expression. K284-6111 inhibits ERK and NF-κB pathway. K284-6111 suppresses nuclear translocation of p50 and p65, and phosphorylation of IκB. K284-6111 improves memory dysfunction by alleviating amyloidogenesis and neuroinflammation, with the reduction of inflammatory proteins (eg: iNOS, COX-2, GFAP, and Iba-1). K284-6111 reduces atopic-like skin inflammation and inhibits LPS (HY-D1056) -induced liver injury. K284-6111 can be used for the study of Alzheimer's diseases and sepsis like hepatic injury .
    K284-6111
  • HY-B1334
    Perhexiline
    Maximum Cited Publications
    6 Publications Verification

    		 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-N0732
    Jolkinolide B
    1 Publications Verification

    		 IAP Akt Caspase NF-κB TGF-beta/Smad JAK Bacterial Apoptosis Infection Metabolic Disease Inflammation/Immunology Cancer
    Jolkinolide B is a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud with oral activity. Jolkinolide B downregulates XIAP, cIAP1, cIAP2, and phosphorylated Akt, upregulates Smac, activates caspase-3 and caspase-9, and inhibits NF-κB, TGFβ/smad3 and JAK/STAT3 pathways. Jolkinolide B exerts comprehensive biological effects including inducing cancer cell apoptosis, suppressing inflammatory responses, improving lung function, alleviating hepatic steatosis and eliminating intracellular Mycobacterium tuberculosis. Jolkinolide B can be used for the research of leukemia, histiocytic lymphoma, asthma, metabolic dysfunction-associated steatotic liver disease and tuberculosis .
    Jolkinolide B
  • 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-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-W779068
    Chenodeoxycholic acid 3-sulfate disodium

    		Endogenous Metabolite Inflammation/Immunology
    Chenodeoxycholic acid 3-sulfate disodium is a bile acid. Chenodeoxycholic acid 3-sulfate disodium level corresponds closely with the extent of hepatic dysfunction .
    Chenodeoxycholic acid 3-sulfate disodium
  • 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-N0046
    Notoginsenoside Fe

    Notoginseng triterpenes; Ginsenoside Mb

    		 Apoptosis Src Neurological Disease Metabolic Disease Cancer
    Notoginsenoside Fe (Notoginseng triterpenes; Ginsenoside Mb) is a saponin with anti-obesity and anti-neuroblastoma activities. Notoginsenoside Fe can be isolated from leaves of Panax notoginseng. Notoginsenoside Fe specifically activates paraventricular nucleus neurons in the hypothalamus, effectively reducing body weight, improving fasting blood glucose and protecting liver function by decreasing food intake, increasing resting metabolic rate and enhancing energy expenditure. Notoginsenoside Fe also inhibits the c-Src signaling pathway, blocks the proliferation and viability of human neuroblastoma cells, while improving mitochondrial dysfunction and alleviating apoptosis. Notoginsenoside Fe can be used in studies related to diet-induced obesity and neuroblastoma .
    Notoginsenoside Fe
  • 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-113360
    Chenodeoxycholic acid 3-sulfate

    		Endogenous Metabolite Inflammation/Immunology
    Chenodeoxycholic acid 3-sulfate is a bile acid. Chenodeoxycholic acid 3-sulfate level corresponds closely with the extent of hepatic dysfunction .
    Chenodeoxycholic acid 3-sulfate
  • 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-42682R
    D(+)-Galactosamine hydrochloride (Standard)

    D-Galactosamine HCl (Standard)

    		 Reference Standards Inflammation/Immunology
    D(+)-Galactosamine (hydrochloride) (Standard) is the analytical standard of D(+)-Galactosamine (hydrochloride). This product is intended for research and analytical applications. D(+)-Galactosamine (D-Galactosamine) hydrochloride, which is an established experimental toxin, primarily causes liver injury by the generation of free radicals and depletion of UTP nucleotides. D(+)-Galactosamine hydrochloride intoxication also induces renal dysfunction thus, renal failure is often associated with the end-stage of the liver damage. Lipopolysaccharide/D(+)-Galactosamine-induced acute liver injury is a known animal model of fulminant hepatic failure .
    D(+)-Galactosamine hydrochloride (Standard)
  • HY-W099331
    Monoethylglycinexylidide hydrochloride

    MEGX hydrochloride; Norlidocaine hydrochloride

    		 Drug Metabolite Metabolic Disease Inflammation/Immunology
    Monoethylglycinexylidide (MEGX) hydrochloride is a metabolite of Lidocain (HY-B0185) via oxidative N-deethylation of Lignocaine by liver cytochrome P-450 enzymes in the liver. Monoethylglycinexylidide has proven to be a highly sensitive indicator of hepatic dysfunction, especially in the field of liver transplantation .
    Monoethylglycinexylidide hydrochloride
  • HY-178015
    THR-β agonist 11

    		Thyroid Hormone Receptor Metabolic Disease Inflammation/Immunology
    THR-β agonist 11 is an orally active and selective thyroid hormone receptor (THR-β) agonist. THR-β agonist 11 shows potent cholesterol-lowering activity in cholesterol-fed rats. THR-β agonist 11 significantly reduces serum total TG, LDL-cholesterol, liver total TC and TG levels, and alleviates hepatic steatosis, inflammation and fibrosis in HFD-CCl4-induced Metabolic dysfunction-associated steatohepatitis (MASH) model mice. THR-β agonist 11 can be used for the study of metabolic dysfunction-associated steatohepatitis (MASH) and other fibrotic diseases .
    THR-β agonist 11
  • HY-P1624S1
    Teduglutide-Leu(13C6,15N) sodium

    ALX-0600-Leu(13C6,15N) sodium

    		 Isotope-Labeled Compounds Nuclear Hormone Receptor 4A/NR4A FXR Inflammation/Immunology
    Teduglutide-Leu( 13C6, 15N) (ALX-0600-Leu( 13C6, 15N)) sodium is the 13C- and 15N-labeled Teduglutide (HY-P1624). Teduglutide (ALX-0600) is an analog of human glucagon like peptide-2 (GLP-2). Teduglutide can activate the expression of nuclear receptor subfamily 4 group a member 1 (NR4a1)/nur77 and intestinal FXR signaling in human hepatic stellate cells, thereby improving liver inflammation and fibrosis in mice with sclerosing cholangitis. Teduglutide can alleviate intestinal dysfunction in mice, improve lung injury, alleviate obesity related neuroinflammation and cell apoptosis .
    Teduglutide-Leu(13C6,15N) sodium
  • HY-101410A
    SDMA (p-hydroxyazobenzene-p′-sulfonate)

    Symmetric dimethylarginine (p-hydroxyazobenzene-p′-sulfonate); NG,NG'-Dimethyl-L-arginine (p-hydroxyazobenzene-p′-sulfonate)

    		 Endogenous Metabolite NO Synthase NF-κB Inflammation/Immunology
    SDMA p-hydroxyazobenzene-p′-sulfonate is the p-hydroxyazobenzene-p′-sulfonate salt form of SDMA (HY-101410). SDMA p-hydroxyazobenzene-p′-sulfonate is an endogenous inhibitor of nitric oxide synthase (NO synthase) activity. SDMA p-hydroxyazobenzene-p′-sulfonate is an activator for NF-κB, and promotes the expression of IL-6 and TNF-α. SDMA p-hydroxyazobenzene-p′-sulfonate is stable in serum and plasma, and can be used as a kidney biomarker of hepatic and renal dysfunction .
    SDMA (p-hydroxyazobenzene-p′-sulfonate)
  • HY-P1624A
    Teduglutide TFA

    ALX-0600 TFA

    		 Nuclear Hormone Receptor 4A/NR4A FXR Inflammation/Immunology
    Teduglutide TFA is a dipeptidyl peptidase IV resistant glucagon-like peptide 2 (GLP-2) analogue. Teduglutide TFA can activate the expression of nuclear receptor subfamily 4 group a member 1 (NR4a1)/nur77 and intestinal FXR signaling in human hepatic stellate cells, thereby improving liver inflammation and fibrosis in mice with sclerosing cholangitis. Teduglutide TFA can alleviate intestinal dysfunction in mice, improve lung injury, alleviate obesity related neuroinflammation and cell apoptosis .
    Teduglutide TFA
  • HY-105168
    TAK 044

    		Endothelin Receptor Cardiovascular Disease
    TAK 044 is an antagonist of Endothelin Receptor. TAK 044 strongly inhibits ET-induced deterioration in various animal models. TAK 044 can be used in study ET-related diseases such as acute myocardial infarction,acute renal failure, acute hepatic malfunction, and subarachnoid hemorrhage .
    TAK 044
  • 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-125129
    Carlinoside

    		Keap1-Nrf2 Others
    Carlinoside is a flavone glycoside with hepatoprotective efficiency. Carlinoside reduces hepatic bilirubin accumulation by stimulating bilirubin-UGT activity through Nrf2 gene expression. Carlinoside has the potential to intervene hyperbilirubinemia due to liver dysfunction .
    Carlinoside
  • HY-159881
    SHS206

    		Mitophagy Metabolic Disease
    SHS206 (compound 6n) is an orally active mitochondrial uncoupler that reduces hepatic triglyceride levels. SHS206 exhibits in vivo efficacy in the GAN mouse model and shows inhibitory effects on metabolic dysfunction-associated steatohepatitis (MASH) .
    SHS206
  • HY-B1334AR
    Perhexiline maleate (Standard)

    		Carnitine Palmitoyltransferase (CPT) Mitochondrial Metabolism Apoptosis Reference Standards Cardiovascular Disease Cancer
    Perhexiline (maleate) (Standard) is the analytical standard of Perhexiline (maleate). This product is intended for research and analytical applications. 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 (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-P1624S
    Teduglutide-Ala(13C3,15N) sodium

    ALX-0600-Ala(13C3,15N) sodium

    		 Isotope-Labeled Compounds Nuclear Hormone Receptor 4A/NR4A FXR Inflammation/Immunology
    Teduglutide-Ala( 13C3, 15N) (ALX-0600-Ala( 13C3, 15N)) sodium is the 13C- and 15N-labeled Teduglutide (HY-P1624). Teduglutide (ALX-0600) is an analog of human glucagon like peptide-2 (GLP-2). Teduglutide can activate the expression of nuclear receptor subfamily 4 group a member 1 (NR4a1)/nur77 and intestinal FXR signaling in human hepatic stellate cells, thereby improving liver inflammation and fibrosis in mice with sclerosing cholangitis. Teduglutide can alleviate intestinal dysfunction in mice, improve lung injury, alleviate obesity related neuroinflammation and cell apoptosis .
    Teduglutide-Ala(13C3,15N) sodium
  • HY-N0732R
    Jolkinolide B (Standard)

    		Reference Standards IAP Akt Caspase NF-κB TGF-beta/Smad JAK Bacterial Apoptosis Infection Inflammation/Immunology Cancer
    Jolkinolide B (Standard) is the analytical standard of Jolkinolide B (HY-N0732). This product is intended for research and analytical applications. Jolkinolide B is a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud with oral activity. Jolkinolide B downregulates XIAP, cIAP1, cIAP2, and phosphorylated Akt, upregulates Smac, activates caspase-3 and caspase-9, and inhibits NF-κB, TGFβ/smad3 and JAK/STAT3 pathways. Jolkinolide B exerts comprehensive biological effects including inducing cancer cell apoptosis, suppressing inflammatory responses, improving lung function, alleviating hepatic steatosis and eliminating intracellular Mycobacterium tuberculosis. Jolkinolide B can be used for the research of leukemia, histiocytic lymphoma, asthma, metabolic dysfunction-associated steatotic liver disease and tuberculosis .
    Jolkinolide B (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-182751
    ACLY-IN-4

    		ATP Citrate Lyase Inflammation/Immunology
    ACLY-IN-4 is an ATP-citrate lyase (ACLY) inhibitor with an IC50 of 0.022 μM and a Kd of 0.19 μM. ACLY-IN-4 binds to the allosteric binding site of ACLY. ACLY-IN-4 exhibits hypolipidemic, anti-steatotic, insulin sensitivity-improving, anti-oxidative stress, anti-inflammatory and anti-fibrotic activities. ACLY-IN-4 alleviates hepatic steatosis, systemic insulin resistance, oxidative stress, hepatic inflammation and fibrosis. ACLY-IN-4 can be used for the research of metabolic dysfunction-associated steatohepatitis .
    ACLY-IN-4
  • HY-182750
    ACLY-IN-3

    		ATP Citrate Lyase Inflammation/Immunology
    ACLY-IN-3 is an ATP-citrate lyase (ACLY) inhibitor with an IC50 of 0.036 μM and a target Kd of 0.54 μM. ACLY-IN-3 interacts with the allosteric binding site of ACLY to inhibit its activity. ACLY-IN-3 exhibits excellent lipid-lowering effects and alleviates hepatic inflammation and liver fibrosis. ACLY-IN-3 can be used for the research of metabolic dysfunction-associated steatohepatitis .
    ACLY-IN-3
  • HY-N17383
    Ligusticum cycloprolactam

    		Toll-like Receptor (TLR) NF-κB Collagen Interleukin Related Cadherin NOD-like Receptor (NLR) TGF-β Receptor FXR Apoptosis Metabolic Disease Inflammation/Immunology
    Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease .
    Ligusticum cycloprolactam
  • HY-183279
    FXR antagonist 4

    		FXR AMPK Metabolic Disease
    FXR antagonist 4 (Compound 4l) is an orally active, selective FXR antagonist with an IC50 of 0.70 μM. FXR antagonist 4 binds to FXR, differentially regulates bile acid and lipid transporter genes, and exerts no effect on gluconeogenesis-related genes. FXR modulator 1 activates the AMPK signaling pathway to inhibit fatty acid synthesis. FXR modulator 1 alleviates hepatic steatosis, ballooning degeneration and fibrosis, and improves dyslipidemia. FXR modulator 1 can be used for research on metabolic dysfunction-associated steatohepatitis .
    FXR antagonist 4
  • HY-182294
    HYJ-2

    		URAT1 Metabolic Disease Inflammation/Immunology
    HYJ-2 is a URAT1 inhibitor and urate-lowering agent. HYJ-2 inhibits URAT1-mediated urate transport and interacts with key residues within the URAT1 binding pocket. HYJ-2 reduces serum urate levels in hyperuricemic mice without inducing liver or kidney injury. HYJ-2 shows low cytotoxicity to hepatocytes and renal cells. HYJ-2 does not significantly induce hepatocyte apoptosis or mitochondrial dysfunction. HYJ-2 can be used in studies related to hyperuricemia and gout .
    HYJ-2
  • 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-183309
    FXR/HSD17B13-modulator-2

    		FXR 17β-HSD Inflammation/Immunology
    FXR/HSD17B13-modulator-2 is a dual FXR activator and HSD17B13 inhibitor with human FXR EC50 of 128 nM, human HSD17B13 IC50 of 0.18 μM, high selectivity over related nuclear receptors and HSD17B isoforms, and oral effectiveness.FXR/HSD17B13-modulator-2 alleviates fatty liver, regulates lipid metabolism, reduces inflammation, and attenuates hepatic fibrosis.FXR/HSD17B13-modulator-2 is the first non-carboxylic acid dual FXR/HSD17B13 modulator.FXR/HSD17B13-modulator-2 can be used for the research of metabolic dysfunction-associated steatohepatitis .
    FXR/HSD17B13-modulator-2

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