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Results for "

cholestasis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	5-HT Receptor (1) Apical Sodium-Dependent Bile Acid Transporter (2) Apoptosis (6) Autophagy (5) BCL6 (3) Caspase (3) Endogenous Metabolite (12) FOXO (1) FXR (7) Interleukin Related (3) Microtubule/Tubulin (1) NF-κB (1) STAT (5) TNF Receptor (1)
By Research Areas:	Cancer (7) Endocrinology (2) Inflammation/Immunology (5) Metabolic Disease (16) Neurological Disease (1)

Inhibitors & Agonists

Screening Libraries

Natural
Products

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-129987

Estradiol 17-(β-D-Glucuronide) (sodium)	Endogenous Metabolite	Metabolic Disease Endocrinology
Estradiol 17-(β-D-Glucuronide) sodium, a metabolite of estrogen, is well known to cause intrahepatic cholestasis in humans .

HY-W353102

Estradiol 17-(β-D-Glucuronide)	Endogenous Metabolite	Metabolic Disease Endocrinology
Estradiol 17-(β-D-Glucuronide), a metabolite of estrogen, is well known to cause intrahepatic cholestasis in humans. Estradiol 17-(β-D-Glucuronide) is a high-affinity substrate for oatp organic anion transporter .

HY-121238

Hyocholic Acid	Others	Metabolic Disease
Hyocholic Acid is a bile acid found in pig. Hyocholic Acid can also be found in urine samples from patients with cholestasis. Hyocholic Acid promotes GLP-1 secretion via activating TGR5 and inhibiting FXR in enteroendocrine cells. Hyocholic Acid is known for its exceptional resistance to type 2 diabetes .

HY-N2334

Glycochenodeoxycholic acid 3 Publications Verification Chenodeoxycholylglycine	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase	Metabolic Disease Cancer
Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .

HY-N2334A

Glycochenodeoxycholic acid sodium salt 3 Publications Verification Chenodeoxycholylglycine sodium salt; Sodium glycochenodeoxycholate	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase	Metabolic Disease Cancer
Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .

HY-168331

FXR agonist 10	FXR	Others
FXR agonist 10 (Compound 27) is an agonist for FXR with an EC₅₀ of 14.26 μM. FXR agonist 10 upregulates the expression of SHP and BSEP proteins, downregulates the expression of NTCP and CYP7A1 proteins. FXR agonist 10 ameliorates the ANIT-induced cholestasis in mouse model .

HY-120396

LY 293284	5-HT Receptor	Neurological Disease
LY 293284 is a potent and selective 5-HT1A receptor agonist. LY 293284 results in a significant drop in core temperature and consumes more food in cholestasis rat induced by bile duct resection .

HY-N10640

Alismanol M	FXR	Inflammation/Immunology
Alismanol M is a farnesoid X receptor (FXR) agonist with an EC₅₀ value of 50.25 μM. Alismanol M is a protostane-type triterpenoid that can be isolated from the rhizome of Alisma orientale. Alismanol M can be used for the research of cholestasis and nonalcoholic steatohepatitis .

HY-N2334AR

Glycochenodeoxycholic acid sodium salt (Standard)	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase	Metabolic Disease Cancer
Glycochenodeoxycholic acid sodium salt (Standard) is the analytical standard of Glycochenodeoxycholic acid sodium salt. This product is intended for research and analytical applications. Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .

HY-168523

S1647	Apical Sodium-Dependent Bile Acid Transporter	Metabolic Disease
S1647 is a ASBT and SOAT dual inhibitor. S1647 can be used in the study of intrahepatic cholestasis, cholestatic pruritus, and obstipation .

HY-125731

Glycodeoxycholic Acid 1 Publications Verification	Endogenous Metabolite STAT Autophagy	Inflammation/Immunology Cancer
Glycodeoxycholic Acid is a natural product found in Streptomyces nigricans, Trypanosoma brucei and C. elegans. Glycodeoxycholic Acid induces hepatocyte necrosis and autophagy in patients with obstructive cholestasis .

HY-B0172

Lithocholic acid Maximum Cited Publications 13 Publications Verification	Autophagy Endogenous Metabolite Apoptosis FXR	Metabolic Disease Cancer
Lithocholic acid is a toxic secondary bile acid that can promote intrahepatic cholestasis and promote tumorigenesis. Lithocholic acid is also a FXR antagonist and a PXR/SXR agonist .

HY-136066

Tauro-ω-muricholic acid sodium 1 Publications Verification TωMCA sodium	Others	Metabolic Disease
Tauro-ω-muricholic acid sodium (TωMCA sodium) is a bile acid released by the liver and an analog of tauro-α-muricholic acid. Tauro-ω-muricholic acid sodium is investigated as a potential marker in plasma for early-onset neonatal sepsis (EOS) and cholestasis studies

HY-16747

Maralixibat chloride SHP625 chloride; LUM001 chloride; Lopixibat chloride	Apical Sodium-Dependent Bile Acid Transporter	Metabolic Disease
Maralixibat (SHP625) chloride is an orally active ileal bile acid transporter (IBAT) inhibitor. Maralixibat chloride can be used for the research of rare cholestatic liver diseases including Alagille syndrome (ALGS), progressive familial intrahepatic cholestasis (PFIC) and biliary atresia .

HY-125731R

Glycodeoxycholic Acid (Standard)	Endogenous Metabolite STAT Autophagy	Inflammation/Immunology Cancer
Glycodeoxycholic Acid (Standard) is the analytical standard of Glycodeoxycholic Acid. This product is intended for research and analytical applications. Glycodeoxycholic Acid is a natural product found in Streptomyces nigricans, Trypanosoma brucei and C. elegans. Glycodeoxycholic Acid induces hepatocyte necrosis and autophagy in patients with obstructive cholestasis .

HY-B0172R

Lithocholic acid (Standard) 3α-Hydroxy-5β-cholanic acid (Standard)	Autophagy Endogenous Metabolite Apoptosis FXR	Metabolic Disease Cancer
Lithocholic acid (Standard) is the analytical standard of Lithocholic acid. This product is intended for research and analytical applications. Lithocholic acid is a toxic secondary bile acid that can promote intrahepatic cholestasis and promote tumorigenesis. Lithocholic acid is also a FXR antagonist and a PXR/SXR agonist .

HY-W399297

Isodeoxycholic acid 7α,12α-Dihydroxycholanoic acid	Endogenous Metabolite	Metabolic Disease
Isodeoxycholic acid (7α,12α-Dihydroxycholanoic acid) is the 3β-epimer of ursodeoxycholic acid. Isodeoxycholic acid has the effect on choleresis and liver biochemistry .

HY-168327

LH10	FXR	Inflammation/Immunology
LH10 is a fexaramine-based agonist for FXR with an EC₅₀ of 0.14 μM. LH10 exhibits liver protection efficacy, ameliorates the alpha naphthylisothiocyanate (ANIT)-induced cholestasis, APAP (HY-66005)-induced acute liver injury and non-alcoholic steatohepatitis (NASH) in mouse models .

HY-113212

Ursocholic acid 1 Publications Verification	Endogenous Metabolite Apoptosis	Metabolic Disease Inflammation/Immunology
Ursocholic acid, a bile acid present in mammalian bile, is converted to deoxycholic acid (UDC) by the mouse intestinal flora. Ursocholic acid acts as a gallstone dissolving agent in the liver through anti-apoptosis, anti-inflammatory, immunomodulatory, bile regulation, and coordinated changes in mitochondrial integrity and cell signaling, Ursocholic acid also has favorable effects on bones in patients with chronic cholestasis .

HY-109083A

Cilofexor tromethamine GS-9674 tromethamine	Autophagy FXR	Metabolic Disease
Cilofexor tromethamine (GS-9674 tromethamine) is a nonsteroidal farnesene oxide receptor agonist with activity in improving markers of cholestasis and liver injury. Cilofexor tromethamine was shown to be well tolerated in patients without cirrhosis and resulted in significant improvements in liver biochemical parameters and cholestatic markers. Cilofexor tromethamine offers a potential inhibitory option for the management of primary sclerosing cholangitis .

HY-139562

BMS-986318	FXR	Metabolic Disease
BMS-986318 is a potent nonbile acid FXR agonist with EC₅₀s of 53 and 350 nM in the FXR Gal4 and SRC-1 recruitment assays, respectively. BMS-986318 has a suitable ADME profile, and demonstrates efficacy in the mouse bile duct ligation model of liver cholestasis and fibrosis.BMS-986318 can be used for the research of nonalcoholic steatohepatitis .

HY-N3021

D-chiro-Inositol	Endogenous Metabolite NF-κB TNF Receptor FOXO Microtubule/Tubulin	Metabolic Disease
D-chiro-Inositol is a stereoisomer of inositol that exhibits activities such as improving glucose metabolism, anti-tumor effects, anti-inflammatory properties, and antioxidant activity. D-chiro-Inositol effectively alleviates cholestasis by enhancing bile acid secretion and reducing oxidative stress. D-chiro-Inositol improves insulin resistance, lowers hyperglycemia and circulating insulin levels, reduces serum androgen levels, and ameliorates some metabolic abnormalities associated with X syndrome by mimicking the action of insulin. Additionally, D-chiro-Inositol can induce a reduction in pro-inflammatory factors (such as Nf-κB) and cytokines (such as TNF-α), thereby exerting anti-inflammatory effects. D-chiro-Inositol may be used in the study of liver cirrhosis, breast cancer, type 2 diabetes, and polycystic ovary syndrome .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	1,453 compounds
Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug. DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver. MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 1,453 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

Drug-Induced Liver Injury (DILI) Compound Library

1,453 compounds

Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug.

DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver.

MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 1,453 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

Estradiol 17-(β-D-Glucuronide) (sodium)	Structural Classification Classification of Application Fields Source classification Metabolic Disease Endogenous metabolite Disease Research Fields Endocrinology Steroids	Endogenous Metabolite
Estradiol 17-(β-D-Glucuronide) sodium, a metabolite of estrogen, is well known to cause intrahepatic cholestasis in humans .

Estradiol 17-(β-D-Glucuronide)	Structural Classification Monophenols Classification of Application Fields Source classification Phenols Metabolic Disease Endogenous metabolite Disease Research Fields Endocrinology Steroids	Endogenous Metabolite
Estradiol 17-(β-D-Glucuronide), a metabolite of estrogen, is well known to cause intrahepatic cholestasis in humans. Estradiol 17-(β-D-Glucuronide) is a high-affinity substrate for oatp organic anion transporter .

Glycochenodeoxycholic acid 3 Publications Verification Chenodeoxycholylglycine	Structural Classification Microorganisms Classification of Application Fields Source classification Endogenous metabolite Disease Research Fields Steroids Cancer	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase
Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .

Glycochenodeoxycholic acid sodium salt 3 Publications Verification Chenodeoxycholylglycine sodium salt; Sodium glycochenodeoxycholate	Structural Classification Classification of Application Fields Source classification Endogenous metabolite Disease Research Fields Steroids Cancer	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase
Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .

Glycodeoxycholic Acid 1 Publications Verification	Structural Classification Microorganisms Classification of Application Fields Source classification Metabolic Disease Endogenous metabolite Disease Research Fields Steroids	Endogenous Metabolite STAT Autophagy
Glycodeoxycholic Acid is a natural product found in Streptomyces nigricans, Trypanosoma brucei and C. elegans. Glycodeoxycholic Acid induces hepatocyte necrosis and autophagy in patients with obstructive cholestasis .

Lithocholic acid Maximum Cited Publications 13 Publications Verification	Structural Classification Human Gut Microbiota Metabolites Microorganisms Classification of Application Fields Anti-aging Source classification Metabolic Disease Endogenous metabolite Disease Research Fields Steroids	Autophagy Endogenous Metabolite Apoptosis FXR
Lithocholic acid is a toxic secondary bile acid that can promote intrahepatic cholestasis and promote tumorigenesis. Lithocholic acid is also a FXR antagonist and a PXR/SXR agonist .

Alismanol M	Triterpenes Terpenoids Alisma orinentale (Samuel.) Juz. Plants Alismataceae	FXR
Alismanol M is a farnesoid X receptor (FXR) agonist with an EC₅₀ value of 50.25 μM. Alismanol M is a protostane-type triterpenoid that can be isolated from the rhizome of Alisma orientale. Alismanol M can be used for the research of cholestasis and nonalcoholic steatohepatitis .

Glycochenodeoxycholic acid sodium salt (Standard)	Structural Classification Source classification Endogenous metabolite Steroids	Endogenous Metabolite Apoptosis STAT BCL6 Interleukin Related Caspase
Glycochenodeoxycholic acid sodium salt (Standard) is the analytical standard of Glycochenodeoxycholic acid sodium salt. This product is intended for research and analytical applications. Glycochenodeoxycholic acid sodium salt (Sodium glycochenodeoxycholate) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid sodium salt inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid sodium salt induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid sodium salt is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC) .

Glycodeoxycholic Acid (Standard)	Structural Classification Microorganisms Source classification Endogenous metabolite Steroids	Endogenous Metabolite STAT Autophagy
Glycodeoxycholic Acid (Standard) is the analytical standard of Glycodeoxycholic Acid. This product is intended for research and analytical applications. Glycodeoxycholic Acid is a natural product found in Streptomyces nigricans, Trypanosoma brucei and C. elegans. Glycodeoxycholic Acid induces hepatocyte necrosis and autophagy in patients with obstructive cholestasis .

Lithocholic acid (Standard) 3α-Hydroxy-5β-cholanic acid (Standard)	Structural Classification Human Gut Microbiota Metabolites Microorganisms Classification of Application Fields Anti-aging Source classification Metabolic Disease Endogenous metabolite Disease Research Fields Steroids	Autophagy Endogenous Metabolite Apoptosis FXR
Lithocholic acid (Standard) is the analytical standard of Lithocholic acid. This product is intended for research and analytical applications. Lithocholic acid is a toxic secondary bile acid that can promote intrahepatic cholestasis and promote tumorigenesis. Lithocholic acid is also a FXR antagonist and a PXR/SXR agonist .

Isodeoxycholic acid 7α,12α-Dihydroxycholanoic acid	Structural Classification Classification of Application Fields Source classification Metabolic Disease Endogenous metabolite Disease Research Fields Steroids	Endogenous Metabolite
Isodeoxycholic acid (7α,12α-Dihydroxycholanoic acid) is the 3β-epimer of ursodeoxycholic acid. Isodeoxycholic acid has the effect on choleresis and liver biochemistry .

Ursocholic acid 1 Publications Verification	Structural Classification Microorganisms Classification of Application Fields Source classification Metabolic Disease Endogenous metabolite Disease Research Fields Steroids	Endogenous Metabolite Apoptosis
Ursocholic acid, a bile acid present in mammalian bile, is converted to deoxycholic acid (UDC) by the mouse intestinal flora. Ursocholic acid acts as a gallstone dissolving agent in the liver through anti-apoptosis, anti-inflammatory, immunomodulatory, bile regulation, and coordinated changes in mitochondrial integrity and cell signaling, Ursocholic acid also has favorable effects on bones in patients with chronic cholestasis .

D-chiro-Inositol	Structural Classification Natural Products Classification of Application Fields Source classification Metabolic Disease Endogenous metabolite Disease Research Fields	Endogenous Metabolite NF-κB TNF Receptor FOXO Microtubule/Tubulin
D-chiro-Inositol is a stereoisomer of inositol that exhibits activities such as improving glucose metabolism, anti-tumor effects, anti-inflammatory properties, and antioxidant activity. D-chiro-Inositol effectively alleviates cholestasis by enhancing bile acid secretion and reducing oxidative stress. D-chiro-Inositol improves insulin resistance, lowers hyperglycemia and circulating insulin levels, reduces serum androgen levels, and ameliorates some metabolic abnormalities associated with X syndrome by mimicking the action of insulin. Additionally, D-chiro-Inositol can induce a reduction in pro-inflammatory factors (such as Nf-κB) and cytokines (such as TNF-α), thereby exerting anti-inflammatory effects. D-chiro-Inositol may be used in the study of liver cirrhosis, breast cancer, type 2 diabetes, and polycystic ovary syndrome .

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