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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
14 Results for "
hepatic impairment
" in MedChemExpress (MCE) Product Catalog:
Products (14)
14 Results for "hepatic impairment" in MCE Product Catalog:
3
Target:
Research Areas:
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 .
1
1 Cited Publications
Cat. No.: HY-N0468
CAS No.: 63279-13-0
Category:
other families Terpenoids Metabolic Disease Diterpenoids Plants Disease Research Fields Sweeteners Food Research
Target:
1
1 Cited Publications
Cat. No.: HY-N3121
CAS No.: 33708-72-4
Category:
Flavonols other families Flavonoids Phenols Polyphenols Plants Disease Research Fields Cancer
Target:
1
Cat. No.: HY-W018587
CAS No.: 26040-51-7
Target:
Mitochondrial Metabolism Cytochrome P450 TNF Receptor Interleukin Related HSP LDLR Eukaryotic Initiation Factor (eIF) ClpP
Research Areas:
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 .
Target:
Carboxylesterase (CES) Free Fatty Acid Receptor Reactive Oxygen Species (ROS) Mitochondrial Metabolism Ferroptosis Apoptosis
Research Areas:
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 .
Target:
Cat. No.: HY-W766140
Synonyms: 4-Hydroxy duloxetine glucuronide sodium; LY550408 sodium
Target:
Research Areas:
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 .
Category:
Infection Alkaloids Human Gut Microbiota Metabolites Microorganisms Endogenous metabolite Disease Research Fields Cancer Indole Alkaloids
Target:
Target:
Research Areas:
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 .
Cat. No.: HY-N0468R
CAS No.: 63279-13-0
Category:
Cat. No.: HY-172559
Target:
Research Areas:
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.: HY-L076
642 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 642 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.: HY-P991753
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
