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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 "
mitochondrial hepatotoxicity
" in MedChemExpress (MCE) Product Catalog:
Products (14)
14 Results for "mitochondrial hepatotoxicity" in MCE Product Catalog:
6
Target:
Environmental Pollutants FXR Calcium Channel Toll-like Receptor (TLR) SOD Reactive Oxygen Species (ROS) DNA/RNA Synthesis Interleukin Related NF-κB TNF Receptor Apoptosis
Research Areas:
Tris(2-chloroethyl) phosphate (TCEP) is a widely used organic phosphorus flame retardant, mainly used as a plasticizer. Tris(2-chloroethyl) phosphate has orally active hepatotoxicity, inducing an increase in reactive oxygen species (ROS) and calcium ions (Ca 2+) influx, a decrease in mitochondrial membrane potential (△Ψm), and causing DNA damage and cell apoptosis. Tris(2-chloroethyl) phosphate directly binds to FXR, inducing obesity and the formation of fatty liver in mice. Chloroethyl) phosphate activates the TLR4/NF-κB pathway, triggering liver inflammation .
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Cat. No.: HY-139838
CAS No.: 353292-31-6
Epyrifenacil is a protoporphyrinogen oxidase (PPO) inhibiting herbicide, potently targeting the PPO2 isoform from weeds such as Amaranthus palmeri with an IC50 of 0.637 nM. Epyrifenacil also inhibits liver mitochondrial PPO across species, with IC50 values of 2.2 nM (mouse), 2.6 nM (rat), 12.1 nM (rabbit), 7.6 nM (dog), and 10.2 nM (human). Epyrifenacil induces liver tumor development in mice. Epyrifenacil can be used for weed control, and also used as a tool compound in toxicological research to study the mechanism of PPO inhibition, chemical-induced hepatotoxicity, and the mode of action of non-genotoxic carcinogens in rodents [3].
Cat. No.: HY-B2004
CAS No.: 130000-40-7
Research Areas:
Thifluzamide is a fungicide that inhibits fungal respiration by blocking the ubiquinone-binding site in mitochondrial complex II. Thifluzamide exhibits significant activity against Basidiomycota pathogens (such as Rhizoctonia cerealis, Ustilago and Puccinia genera) and is commonly used in studies on wheat sharp eyespot. Thifluzamide displays a dual mechanism in regulating lipid metabolism: it reduces fatty acid synthase activity to inhibit endogenous fatty acid synthesis, and increases carnitine palmitoyltransferase-I activity to accelerate fatty acid β-oxidation, thereby reducing total cholesterol and triglyceride levels in the liver. Thifluzamide also induces hepatotoxicity in zebrafish models and carries a risk of developmental toxicity. Thifluzamide inhibition of Rhizoctonia cerealis may result in low to moderate levels of drug resistance, leading to the generation of stable drug-resistant mutants .
Category:
Cat. No.: HY-W275295
CAS No.: 307-55-1
Synonyms: PFDoA
Research Areas:
Perfluorododecanoic acid (PFDoA) is an orally active, blood-brain barrier-permeable perfluorinated compound. Perfluorododecanoic acid increases Caspase 3 activity, disrupts mitochondrial membrane potential, and elevates ROS levels. Perfluorododecanoic acid induces cognitive deficits. Perfluorododecanoic acid exhibits hepatotoxicity .
Synonyms: JAU-6476
Target:
Fungal Cytochrome P450 Microtubule/Tubulin Mitochondrial Metabolism DNA/RNA Synthesis Apoptosis Fatty Acid Synthase (FASN)
Research Areas:
Prothioconazole is an orally active broad-spectrum fungicide. Prothioconazole weakly inhibits CaCYP51 activity in Candida albicans, with an apparent IC50 of approximately 120 μM. Prothioconazole disrupts Microtubule stability by reducing the acetylation level of α-tubulin. Prothioconazole induces Mitochondrial dysfunction, oxidative stress, DNA damage, and Apoptosis. Prothioconazole accumulates 14-methylated sterols and depletes ergosterol in cells, culture media, plants, and animals. Prothioconazole interferes with pyruvate metabolism and glycolysis/gluconeogenesis processes in mouse liver, downregulates Fasn mRNA expression, and induces hepatotoxicity and renal metabolic disorders. Prothioconazole reduces the fertility of female mice. Prothioconazole inhibits body weight gain and increases liver/kidney indices in mice. Prothioconazole can be used in studies related to candidiasis .
Cat. No.: HY-N9279
CAS No.: 23291-96-5
Synonyms: Monocrotaline pyrrole; MCTP; 3,8-Didehydromonocrotaline
Target:
Synonyms: TCEP-d12
Target:
Isotope-Labeled Compounds Environmental Pollutants FXR Calcium Channel Toll-like Receptor (TLR) SOD Reactive Oxygen Species (ROS) DNA/RNA Synthesis Interleukin Related NF-κB TNF Receptor Apoptosis
Research Areas:
Tris(2-chloroethyl)phosphate-d12 is the deuterium labeled Tris(β-chloroethyl) phosphate. Tris(2-chloroethyl) phosphate is a widely used organic phosphorus flame retardant, mainly used as a plasticizer. Tris(2-chloroethyl) phosphate has orally active hepatotoxicity, inducing an increase in reactive oxygen species (ROS) and calcium ions (Ca²⁺) influx, a decrease in mitochondrial membrane potential (△Ψm), and causing DNA damage and cell apoptosis. Tris(2-chloroethyl) phosphate directly binds to FXR, inducing obesity and the formation of fatty liver in mice. Chloroethyl) phosphate activates the TLR4/NF-κB pathway, triggering liver inflammation.
Cat. No.: HY-108385
CAS No.: 1448049-50-0
Target:
Isotope-Labeled Compounds Endogenous Metabolite DNA/RNA Synthesis PPAR Reactive Oxygen Species (ROS) Apoptosis Fungal
Research Areas:
Ochratoxin A-D4 (Phe-OTA-D4) is the deuterium labeled Ochratoxin A. Ochratoxin A is an orally active food-borne mycotoxin that can cross the blood-brain barrier. Ochratoxin A is a secondary metabolite of fungi belonging to the genera Aspergillus and Penicillium, and is classified as a Group 2B carcinogen. Ochratoxin A exerts its effects through multiple pathways, including inducing oxidative stress, inhibiting mitochondrial respiration, causing oxidative DNA damage, disrupting the PPAR-γ-CD36 axis, inducing immunosuppression, generating ROS, mediating mitochondria-dependent apoptosis, inhibiting glutamate uptake, triggering demyelination and neuroinflammation, inducing DNA hypomethylation, and inhibiting cell proliferation. Ochratoxin A can induce nephrotoxicity, hepatotoxicity, immunotoxicity, and neurotoxicity, and also exhibits mutagenicity, teratogenicity, and carcinogenicity.
Cat. No.: HY-14922
CAS No.: 763903-67-9
Target:
Research Areas:
Fosalvudine tidoxil is an orally active nucleoside reverse transcriptase inhibitor (NRTI). Fosalvudine tidoxil is a prodrug derived from Alovudine (HY-B1516). Fosalvudine tidoxil is less toxic than Alovudine and can be used for the research of HIV-1 infection .
Cat. No.: HY-B2004R
CAS No.: 130000-40-7
Research Areas:
Thifluzamide (Standard) is the analytical standard of Thifluzamide. This product is intended for research and analytical applications. Thifluzamide is a fungicide that inhibits fungal respiration by blocking the ubiquinone-binding site in mitochondrial complex II. Thifluzamide exhibits significant activity against Basidiomycota pathogens (such as Rhizoctonia cerealis, Ustilago and Puccinia genera) and is commonly used in studies on wheat sharp eyespot. Thifluzamide displays a dual mechanism in regulating lipid metabolism: it reduces fatty acid synthase activity to inhibit endogenous fatty acid synthesis, and increases carnitine palmitoyltransferase-I activity to accelerate fatty acid β-oxidation, thereby reducing total cholesterol and triglyceride levels in the liver. Thifluzamide also induces hepatotoxicity in zebrafish models and carries a risk of developmental toxicity. Thifluzamide inhibition of Rhizoctonia cerealis may result in low to moderate levels of drug resistance, leading to the generation of stable drug-resistant mutants .
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.
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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
