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Results for "

intestinal FXR

" in MedChemExpress (MCE) Product Catalog:

20

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4

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8

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4

Isotope-Labeled Compounds

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-13771
    Ursodeoxycholic acid
    Maximum Cited Publications
    26 Publications Verification

    Ursodeoxycholate; Ursodiol; UDCA

    		 G protein-coupled Bile Acid Receptor 1 FXR Angiotensin-converting Enzyme (ACE) Endogenous Metabolite Infection Metabolic Disease Cancer
    Ursodeoxycholic acid (Ursodeoxycholate) is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid can be used for the research of a variety of hepatic and gastrointestinal diseases. Ursodeoxycholic acid also reduces ACE2 expression and is beneficial for reducing SARS-CoV-2 infection. Orally active .
    Ursodeoxycholic acid
  • HY-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-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-13771A
    Ursodeoxycholic acid sodium
    Maximum Cited Publications
    26 Publications Verification

    Ursodeoxycholate sodium; Ursodiol sodium; UCDA sodium

    		 G protein-coupled Bile Acid Receptor 1 FXR Endogenous Metabolite Metabolic Disease Inflammation/Immunology Cancer
    Ursodeoxycholic acid (Ursodeoxycholate) sodium is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid sodium acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid sodium can be used for the research of a variety of hepatic and gastrointestinal diseases. Orally active .
    Ursodeoxycholic acid sodium
  • HY-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-113478S
    Ursodeoxycholic acid-d4

    Ursodeoxycholate-d4; Ursodiol-d4; UDCA-d4

    		 Isotope-Labeled Compounds Infection Metabolic Disease
    Ursodeoxycholic acid-2,2,4,4-d4 is the deuterium labeled Ursodeoxycholic acid (HY-13771). Ursodeoxycholic acid is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid can be used for the research of a variety of hepatic and gastrointestinal diseases. Ursodeoxycholic acid also reduces ACE2 expression and is beneficial for reducing SARS-CoV-2 infection .
    Ursodeoxycholic acid-d4
  • HY-151481
    FXR antagonist 1

    		FXR Metabolic Disease
    FXR antagonist 1 (compound F6) is an orally active and selective intestinal FXR antagonist (IC50=2.1 μM). FXR antagonist 1 selectively inhibits intestinal FXR signalling through antagonism of intestinal FXR and feedback activation of hepatic FXR to improve hepatic steatosis, inflammation and fibrosis in NASH (nonalcoholic steatohepatitis) models. FXR antagonist 1 can be used in NASH studies .
    FXR antagonist 1
  • HY-13771R
    Ursodeoxycholic acid (Standard)

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

    		 Reference Standards G protein-coupled Bile Acid Receptor 1 FXR Angiotensin-converting Enzyme (ACE) Endogenous Metabolite Infection Metabolic Disease Cancer
    Ursodeoxycholic acid (Standard) is the analytical standard of Ursodeoxycholic acid. This product is intended for research and analytical applications. Ursodeoxycholic acid (Ursodeoxycholate) is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid can be used for the research of a variety of hepatic and gastrointestinal diseases. Ursodeoxycholic acid also reduces ACE2 expression and is beneficial for reducing SARS-CoV-2 infection. Orally active .
    Ursodeoxycholic acid (Standard)
  • HY-149831
    ZLY28

    		FXR Metabolic Disease
    ZLY28 is the first-in-class intestinal restricted and orally active FXR and FABP1 dual modulator. ZLY28 also is a novel anti-NASH agent. ZLY28 can be used for the research of nonalcoholic steatohepatitis (NASH) .
    ZLY28
  • 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-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-13771S1
    Ursodeoxycholic acid-13C

    Ursodeoxycholate-13C; Ursodiol-13C; UDCA-13C

    		 Isotope-Labeled Compounds G protein-coupled Bile Acid Receptor 1 FXR Endogenous Metabolite Cancer
    Ursodeoxycholic acid- 13C is the 13C labeled Ursodeoxycholic acid. Ursodeoxycholic acid (Ursodeoxycholate) is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. Ursodeoxycholic acid acts as signaling molecule, exerting its effects by interacting with bile acid activated receptors, including G-protein coupled bile acid receptor 5 (TGR5, GPCR19) and the farnesoid X receptor (FXR). Ursodeoxycholic acid can be used for the research of a variety of hepatic and gastrointestinal diseases. Orally active .
    Ursodeoxycholic acid-13C
  • 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-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-163466
    FXR agonist 7

    		FXR Inflammation/Immunology
    FXR agonist 7 (compound 33) is a potent agonist of FXR, with EC50 of 0.1 nM. FXR agonist 7 shows high intestinal distribution, good anti-inflammatory activity .
    FXR agonist 7
  • HY-168516
    FXR/CES2 modulator 1

    		FXR Others
    FXR/CES2 modulator 1 (compound LE-77) is a doul modulator that activates FXR and inhibits CES2. FXR/CES2 modulator 1 effectively mitigates the intestinal toxicity of irinotecan .
    FXR/CES2 modulator 1
  • HY-N13218
    Pueraria Extract

    		Others Cardiovascular Disease
    Pueraria Extract is a kudzu extract, and its components include: Isoflavones. Pueraria Extract (ethanol extract) can significantly improve cardiac damage in rats with acute myocardial infarction. Pueraria Extract improves bile acid levels by increasing the expression of CYP7A1 and restoring the diversity of intestinal microbiota. Pueraria Extract can also inhibit the FXR-FGF15 signaling pathway and increase the expression of OST-α to increase bile acid reabsorption and fecal excretion. .
    Pueraria Extract
  • 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-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-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

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