hepatic impairment

By Targets:	Apoptosis (1) ClpP (1) Cytochrome P450 (1) Drug Metabolite (1) Endogenous Metabolite (1) Eukaryotic Initiation Factor (eIF) (1) HSP (1) iGluR (1) Interleukin Related (1) Keap1-Nrf2 (1) LDLR (1) Mitochondrial Metabolism (1) PERK (1) TNF Receptor (1)
By Research Areas:	Cancer (1) Cardiovascular Disease (1) Inflammation/Immunology (1) Metabolic Disease (4) Neurological Disease (2)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

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-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-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-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 .

HY-175082

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 .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	1,469 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 1,469 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

1,469 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 1,469 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

HY-129297

CMPF	Structural Classification Classification of Application Fields Ketones, Aldehydes, Acids Source classification Metabolic Disease Endogenous metabolite Disease Research Fields	Endogenous Metabolite
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-N3121

Pachypodol	Flavonols Structural Classification Flavonoids other families Classification of Application Fields Source classification Phenols Polyphenols Plants Disease Research Fields Cancer	PERK Keap1-Nrf2 Apoptosis
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 .

MCE Japan Authorized Agent ナミキ商事株式会社コスモ・バイオ株式会社重松貿易株式会社
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hepatic impairment

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