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Results for "

hepatic impairment

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Acetyl-CoA Carboxylase (2) Adrenergic Receptor (1) Apoptosis (2) Carboxylesterase (CES) (1) ClpP (1) Cytochrome P450 (1) Dopamine Receptor (1) Drug Metabolite (2) Endogenous Metabolite (1) Eukaryotic Initiation Factor (eIF) (1) Ferroptosis (1) Free Fatty Acid Receptor (1) FXR (2) GCGR (1) HSP (1) iGluR (1) Interleukin Related (1) Keap1-Nrf2 (1) LDLR (1) Mitochondrial Metabolism (2) PERK (1) Reactive Oxygen Species (ROS) (1) Reference Standards (1) TNF Receptor (1)
By Research Areas:	Cancer (2) Cardiovascular Disease (2) Inflammation/Immunology (3) Metabolic Disease (8) Neurological Disease (3)

By Targets:

Acetyl-CoA Carboxylase (2)

Adrenergic Receptor (1)

Apoptosis (2)

Carboxylesterase (CES) (1)

ClpP (1)

Cytochrome P450 (1)

Dopamine Receptor (1)

Drug Metabolite (2)

Endogenous Metabolite (1)

Eukaryotic Initiation Factor (eIF) (1)

Ferroptosis (1)

Free Fatty Acid Receptor (1)

FXR (2)

GCGR (1)

HSP (1)

iGluR (1)

Interleukin Related (1)

Keap1-Nrf2 (1)

LDLR (1)

Mitochondrial Metabolism (2)

PERK (1)

Reactive Oxygen Species (ROS) (1)

Reference Standards (1)

TNF Receptor (1)

By Research Areas:

Cancer (2)

Cardiovascular Disease (2)

Inflammation/Immunology (3)

Metabolic Disease (8)

Neurological Disease (3)

Inhibitors & Agonists

Screening Libraries

Natural
Products

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

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 .

HY-17553

Coluracetam 3 Publications Verification MKC-231	iGluR	Neurological Disease
Coluracetam (MKC-231) is an orally taken choline uptake enhancer. Coluracetam can improve the reduced acetylcholine levels in the hippocampus of rats and mice, enhancing learning difficulties, memory deficits, and cognitive impairments. Coluracetam induces a lower degree of hepatic venous hyperglycemia .

HY-N3121

Pachypodol	PERK Keap1-Nrf2 Apoptosis	Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
Pachypodol is an orally active methoxyflavonoid compound. Pachypodol activates the ERK-dependent Nrf2 pathway and inhibits Apoptosis. Pachypodol exhibits activities such as antioxidant, cytoprotective, anti-inflammatory effects. Pachypodol improves cognition. Pachypodol exerts protective effects against cardiac and liver damage. Pachypodol has anticancer activity against colon cancer .

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 .

HY-110390

GR148672X	Carboxylesterase (CES) Free Fatty Acid Receptor Reactive Oxygen Species (ROS) Mitochondrial Metabolism Ferroptosis Apoptosis	Cardiovascular Disease Cancer
GR148672X is an inhibitor of carboxylesterase 1 (CES1) and hepatic microsomal triglyceride hydrolase (TGH). GR148672X blocks the catalytic activity of CES1, impairs the functions of triglyceride and cholesteryl ester lipase, reduces triglyceride mobilization and secretion, and decreases apolipoprotein B-100 secretion in primary rat hepatocytes. Under low-glucose conditions, GR148672X inhibits the survival of colorectal cancer cells by reducing free fatty acid availability, inducing toxic triglyceride accumulation, ROS production, mitochondrial damage, ferroptosis and apoptosis. GR148672X can be used in studies related to colorectal cancer and atherosclerosis .

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 .

HY-W766140

4-Hydroxy duloxetine β-D-glucuronide sodium 4-Hydroxy duloxetine glucuronide sodium; LY550408 sodium	Drug Metabolite	Metabolic Disease
4-Hydroxy duloxetine β-D-glucuronide (4-Hydroxy duloxetine glucuronide) sodium is a major metabolite of Duloxetine (HY-B0161). 4-Hydroxy duloxetine β-D-glucuronide sodium is promising for research of hepatic or renal impairment .

HY-135525

Agroclavine	Dopamine Receptor Adrenergic Receptor	Neurological Disease Inflammation/Immunology
Agroclavine acts as an agonist of the D1-dopamine receptor and α₁-adrenergic receptor. Agroclavine enhances the sensitivity of the brain to magnetic fields; it impairs spatial memory without affecting hippocampal long-term potentiation (LTP). Agroclavine exerts bidirectional regulatory effects on immune activity: it enhances NK cell activity with low toxicity under normal conditions, while it inhibits NK cell activity and exhibits significant cardiac and hepatic toxicity under stress conditions. Agroclavine can be used for research on neuroelectrophysiology, learning and memory, and immunoregulation .

HY-144035

GLP-1R agonist 4	GCGR	Metabolic Disease Inflammation/Immunology
GLP-1R agonist 4 is a glucagon-like peptide-1 (GLP-1) receptor agonist. GLP-1 is an intestinal hypoglycemic hormone secreted by L-cells in the lower gastrointestinal tract. GLP-1R agonist 4 can be used for the research of type 2 diabetes mellitus, obesity, non-alcoholic steatohepatitis, insulin resistance and etc .

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 .

HY-172559

Solifenacin N-glucuronide	Drug Metabolite	Metabolic Disease
Solifenacin N-glucuronide is a metabolite formed by direct glucuronidation of the muscarinic receptor antagonist Solifenacin (HY-A0034). The levels of Solifenacin N-glucuronide are associated with diseases such as hepatic impairment .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	641 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 641 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

641 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 641 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.

Cat. No.	Product Name	Category	Target	Chemical Structure