5 Results for "

host hepatic

" in MedChemExpress (MCE) Product Catalog:
Products (5)

5 Results for "host hepatic" in MCE Product Catalog:

Actinine
Actinine
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Cat. No.: HY-113270
CAS No.: 407-64-7
Synonyms: γ-Butyrobetaine; Deoxycarnitine
Category:  

Natural Products Microorganisms Marine algae Marine natural products Endogenous metabolite

Target:  

Endogenous Metabolite

Actinine is a metabolic and pro-atherogenic intermediate with oral activity. Actinine acts as a substrate for the yeaW/X microbial enzyme complex to generate trimethylamine (TMA). Actinine accelerates atherosclerosis development in a gut microbe-dependent manner. Actinine can be used for the research of atherosclerosis .
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Methyl cholate
Methyl cholate
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Cat. No.: HY-107830
CAS No.: 1448-36-8
Purity:  99.81%
Category:  

Microorganisms Metabolic Disease Disease Research Fields Steroids

Target:  

Endogenous Metabolite Collagen

Methyl cholate is a bile acid analog and a specific inhibitor of TcdB toxin from Clostridioides difficile. Methyl cholate exerts a stronger selective inhibitory effect on TcdB than on TcdA. Methyl cholate induces conformational stabilization by binding to a unique site of TcdB, thereby blocking the binding of the toxin to host receptors and its self-processing process. Methyl cholate effectively protects human fibroblasts from TcdB-induced cytopathic effects. Methyl cholate exhibits dose-dependent anti-hepatic fibrosis activity in both cellular and zebrafish models, and significantly reduces the expression levels of α-SMA and COL-I. Methyl cholate is suitable for in-depth research in the fields of Clostridioides difficile infection and hepatic fibrosis .
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Methyl cholate (Standard)
Methyl cholate (Standard)
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Cat. No.: HY-107830R
CAS No.: 1448-36-8
Category:  

Microorganisms Steroids

Target:  

Reference Standards Endogenous Metabolite Collagen

Methyl cholate (Standard) is the analytical standard of Methyl cholate. This product is intended for research and analytical applications. Methyl cholate is a bile acid analog and a specific inhibitor of TcdB toxin from Clostridioides difficile. Methyl cholate exerts a stronger selective inhibitory effect on TcdB than on TcdA. Methyl cholate induces conformational stabilization by binding to a unique site of TcdB, thereby blocking the binding of the toxin to host receptors and its self-processing process. Methyl cholate effectively protects human fibroblasts from TcdB-induced cytopathic effects. Methyl cholate exhibits dose-dependent anti-hepatic fibrosis activity in both cellular and zebrafish models, and significantly reduces the expression levels of α-SMA and COL-I. Methyl cholate is suitable for in-depth research in the fields of Clostridioides difficile infection and hepatic fibrosis .
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Methyl cholate-d5
Methyl cholate-d5
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Cat. No.: HY-W746556
CAS No.: 52886-39-2
Methyl cholate-d5 is the deuterium labeled Methyl cholate. Methyl cholate is a bile acid analog and a specific inhibitor of TcdB toxin from Clostridioides difficile. Methyl cholate exerts a stronger selective inhibitory effect on TcdB than on TcdA. Methyl cholate induces conformational stabilization by binding to a unique site of TcdB, thereby blocking the binding of the toxin to host receptors and its self-processing process. Methyl cholate effectively protects human fibroblasts from TcdB-induced cytopathic effects. Methyl cholate exhibits dose-dependent anti-hepatic fibrosis activity in both cellular and zebrafish models, and significantly reduces the expression levels of α-SMA and COL-I. Methyl cholate is suitable for in-depth research in the fields of Clostridioides difficile infection and hepatic fibrosis .
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Drug-Induced Liver Injury (DILI) Compound Library
Drug-Induced Liver Injury (DILI) Compound Library
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Cat. No.: HY-L076
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.

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