hepatic dysfunction

By Targets:	Apoptosis (2) Drug Metabolite (1) Endogenous Metabolite (2) Endothelin Receptor (1) FXR (2) Keap1-Nrf2 (1) Mitochondrial Metabolism (2) Nuclear Hormone Receptor 4A/NR4A (2)
By Research Areas:	Cancer (2) Cardiovascular Disease (3) Inflammation/Immunology (7) Metabolic Disease (1)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-42682

D(+)-Galactosamine hydrochloride 1 Publications Verification D-Galactosamine HCl	Others	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 .

HY-B1334A

Perhexiline maleate 2 Publications Verification	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 .

HY-P1624

Teduglutide 1 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 .

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 .

HY-42682R

D(+)-Galactosamine hydrochloride (Standard)	Others	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 .

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 .

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 .

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 .

HY-B1334

Perhexiline	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 .

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 .

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 .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	1,434 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 1,434 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

1,434 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 1,434 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	Target	Research Area