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mitochondrial hepatotoxicity

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Mitochondrial Metabolism (5) Apoptosis (5) Bcl-2 Family (1) Biochemical Assay Reagents (1) Calcium Channel (2) Carnitine Palmitoyltransferase (CPT) (1) Caspase (1) Cytochrome P450 (2) DNA/RNA Synthesis (4) Endogenous Metabolite (3) Environmental Pollutants (2) Fatty Acid Synthase (FASN) (1) Fungal (4) FXR (2) Glutathione S-transferase (1) Herbicide (1) HIV (1) HSP (1) Interleukin Related (2) Isotope-Labeled Compounds (2) Methionine Adenosyltransferase (MAT) (1) Microtubule/Tubulin (1) NF-κB (2) PPAR (1) Reactive Oxygen Species (ROS) (5) Reference Standards (1) Reverse Transcriptase (1) SOD (2) TNF Receptor (2) Toll-like Receptor (TLR) (2)
By Research Areas:	Cancer (4) Cardiovascular Disease (1) Endocrinology (1) Infection (4) Inflammation/Immunology (2) Metabolic Disease (4) Neurological Disease (3)

By Targets:

Mitochondrial Metabolism (5)

Apoptosis (5)

Bcl-2 Family (1)

Biochemical Assay Reagents (1)

Calcium Channel (2)

Carnitine Palmitoyltransferase (CPT) (1)

Caspase (1)

Cytochrome P450 (2)

DNA/RNA Synthesis (4)

Endogenous Metabolite (3)

Environmental Pollutants (2)

Fatty Acid Synthase (FASN) (1)

Fungal (4)

FXR (2)

Glutathione S-transferase (1)

Herbicide (1)

HIV (1)

HSP (1)

Interleukin Related (2)

Isotope-Labeled Compounds (2)

Methionine Adenosyltransferase (MAT) (1)

Microtubule/Tubulin (1)

NF-κB (2)

PPAR (1)

Reactive Oxygen Species (ROS) (5)

Reference Standards (1)

Reverse Transcriptase (1)

SOD (2)

TNF Receptor (2)

Toll-like Receptor (TLR) (2)

By Research Areas:

Cancer (4)

Cardiovascular Disease (1)

Endocrinology (1)

Infection (4)

Inflammation/Immunology (2)

Metabolic Disease (4)

Neurological Disease (3)

Inhibitors & Agonists

Screening Libraries

Biochemical Assay Reagents

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: Mitochondrial Metabolism Mitophagy

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-107859

Tris(2-chloroethyl) phosphate 5+ Cited Publications TCEP	Environmental Pollutants Apoptosis FXR Calcium Channel Toll-like Receptor (TLR) SOD Reactive Oxygen Species (ROS) DNA/RNA Synthesis Interleukin Related NF-κB TNF Receptor	Others
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 (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 .

HY-W250122

Glutamic acid sodium salt 1 Publications Verification Monosodium glutamate	Biochemical Assay Reagents Reactive Oxygen Species (ROS) Mitochondrial Metabolism Apoptosis HSP Bcl-2 Family	Neurological Disease Metabolic Disease Inflammation/Immunology
Glutamic acid sodium salt (Monosodium glutamate) is an orally active food flavor enhancer. Glutamic acid sodium salt causes ROS generation, mitochondrial dysfunction, and Apoptosis. Glutamic acid sodium salt upregulates CHOP, Grp78, and Bcl-2. Glutamic acid sodium salt impairs cognition, induces depressive-like behavior, induces hyperalgesia, and induces obesity and insulin resistance. Glutamic acid sodium salt can be used to study neurotoxicity (e.g., brain damage, cognitive impairment), metabolic disorders (e.g., obesity, insulin resistance), hepatotoxicity, and renal toxicity, as well as pain-related disorders .

HY-139838

Epyrifenacil	Herbicide	Others Cancer
Epyrifenacil is a protoporphyrinogen oxidase (PPO) inhibiting herbicide, potently targeting the PPO₂isoform 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].

HY-B2004

Thifluzamide	Environmental Pollutants Fungal Mitochondrial Metabolism	Infection
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 .

HY-113256

Linoleyl carnitine	Carnitine Palmitoyltransferase (CPT) Endogenous Metabolite	Metabolic Disease
Linoleyl carnitine is an acylcarnitine and metabolite. Linoleyl carnitine in the liver is negatively correlated with pantothenic acid and citric acid in serum. Linoleyl carnitine accumulates in mitochondrial CPT II deficiency .

HY-W275295

Perfluorododecanoic acid PFDoA	Reactive Oxygen Species (ROS) Caspase Mitochondrial Metabolism	Neurological Disease Metabolic Disease
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 .

HY-N1282

Seneciphylline	Glutathione S-transferase Cytochrome P450	Cancer
Seneciphylline is an orally effective hepatotoxic inducer. Seneciphylline is metabolized by CYP450 enzymes into active intermediates, which covalently bind to intracellular biomacromolecules such as proteins and DNA to form adducts, which in turn trigger a series of toxic reactions, such as inducing cell apoptosis and damaging mitochondrial function. Seneciphylline can be used in hepatotoxicity research[1][2].

HY-116568

Prothioconazole JAU-6476	Fungal Cytochrome P450 Microtubule/Tubulin Mitochondrial Metabolism DNA/RNA Synthesis Apoptosis Fatty Acid Synthase (FASN)	Infection Metabolic Disease Endocrinology
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 .

HY-N9279

Dehydromonocrotaline Monocrotaline pyrrole; MCTP; 3,8-Didehydromonocrotaline	Endogenous Metabolite	Cardiovascular Disease Cancer
Dehydromonocrotaline is a mitochondrial respiratory chain complex I NADH oxidase inhibitor, with a IC₅₀ of 62.06 μM and a K_i of 8.1 μM in rats. Dehydromonocrotaline exerts non-competitive inhibitory effects by modifying cysteine thiol groups on complex I, and does not bind to the NADH-binding site. Dehydromonocrotaline dissipates mitochondrial membrane potential and reduces ATP levels. Dehydromonocrotaline can be used in studies related to hepatotoxicity, pulmonary hypertension and liver tumors .

HY-107859S

Tris(2-chloroethyl)phosphate-d12 TCEP-d₁₂	Isotope-Labeled Compounds Reactive Oxygen Species (ROS) Apoptosis DNA/RNA Synthesis Calcium Channel FXR Toll-like Receptor (TLR) NF-κB SOD Interleukin Related TNF Receptor	Others
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.

HY-108385

Ochratoxin A-D4	Isotope-Labeled Compounds Endogenous Metabolite DNA/RNA Synthesis PPAR Reactive Oxygen Species (ROS) Apoptosis Fungal	Inflammation/Immunology Cancer
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.

HY-14922

Fosalvudine tidoxil	Reverse Transcriptase HIV	Infection
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 .

HY-B2004R

Thifluzamide (Standard)	Reference Standards Fungal Mitochondrial Metabolism	Infection
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 .

HY-182303

Carboxyatractyloside CATR	Methionine Adenosyltransferase (MAT)	Neurological Disease
Carboxyatractyloside (CATR) is a tight-binding inhibitor of adenine nucleotide translocase, and represents the major toxic component of Xanthium sibiricum. Carboxyatractyloside competes with ADP for binding to the translocase, blocks the translocation of ADP/ATP across the inner mitochondrial membrane, and thereby inhibits ADP-stimulated respiration. In the presence of Cyclosporin A (HY-B0579), Carboxyatractyloside still induces permeability transition in liver mitochondria of aged rats, exhibiting significant hepatotoxicity and nephrotoxicity. Carboxyatractyloside is widely used in studies related to hepatotoxicity, nephrotoxicity and Alzheimer's disease .

Cat. No.	Product Name

HY-L076

Drug-Induced Liver Injury (DILI) Compound Library	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.

Drug-Induced Liver Injury (DILI) Compound Library

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.

Cat. No.	Product Name	Type

HY-W250122

Glutamic acid sodium salt 1 Publications Verification Monosodium glutamate	Biochemical Assay Reagents
Glutamic acid sodium salt (Monosodium glutamate) is an orally active food flavor enhancer. Glutamic acid sodium salt causes ROS generation, mitochondrial dysfunction, and Apoptosis. Glutamic acid sodium salt upregulates CHOP, Grp78, and Bcl-2. Glutamic acid sodium salt impairs cognition, induces depressive-like behavior, induces hyperalgesia, and induces obesity and insulin resistance. Glutamic acid sodium salt can be used to study neurotoxicity (e.g., brain damage, cognitive impairment), metabolic disorders (e.g., obesity, insulin resistance), hepatotoxicity, and renal toxicity, as well as pain-related disorders .

Glutamic acid sodium salt

1 Publications Verification

Monosodium glutamate

Biochemical Assay Reagents

Glutamic acid sodium salt (Monosodium glutamate) is an orally active food flavor enhancer. Glutamic acid sodium salt causes ROS generation, mitochondrial dysfunction, and Apoptosis. Glutamic acid sodium salt upregulates CHOP, Grp78, and Bcl-2. Glutamic acid sodium salt impairs cognition, induces depressive-like behavior, induces hyperalgesia, and induces obesity and insulin resistance. Glutamic acid sodium salt can be used to study neurotoxicity (e.g., brain damage, cognitive impairment), metabolic disorders (e.g., obesity, insulin resistance), hepatotoxicity, and renal toxicity, as well as pain-related disorders .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-113256

Linoleyl carnitine	Structural Classification Natural Products Endogenous metabolite Source Classification	Carnitine Palmitoyltransferase (CPT) Endogenous Metabolite
Linoleyl carnitine is an acylcarnitine and metabolite. Linoleyl carnitine in the liver is negatively correlated with pantothenic acid and citric acid in serum. Linoleyl carnitine accumulates in mitochondrial CPT II deficiency .

HY-N1282

Seneciphylline	Alkaloids other families Pyrrole Alkaloids Classification of Application Fields Plants Compositae Sophora yunnanensis C. Y. Ma Disease Research Fields Source Classification Cancer	Glutathione S-transferase Cytochrome P450
Seneciphylline is an orally effective hepatotoxic inducer. Seneciphylline is metabolized by CYP450 enzymes into active intermediates, which covalently bind to intracellular biomacromolecules such as proteins and DNA to form adducts, which in turn trigger a series of toxic reactions, such as inducing cell apoptosis and damaging mitochondrial function. Seneciphylline can be used in hepatotoxicity research[1][2].

HY-N9279

Dehydromonocrotaline Monocrotaline pyrrole; MCTP; 3,8-Didehydromonocrotaline	Pyrrolizidine Alkaloids Structural Classification Alkaloids Endogenous metabolite Source Classification	Endogenous Metabolite
Dehydromonocrotaline is a mitochondrial respiratory chain complex I NADH oxidase inhibitor, with a IC₅₀ of 62.06 μM and a K_i of 8.1 μM in rats. Dehydromonocrotaline exerts non-competitive inhibitory effects by modifying cysteine thiol groups on complex I, and does not bind to the NADH-binding site. Dehydromonocrotaline dissipates mitochondrial membrane potential and reduces ATP levels. Dehydromonocrotaline can be used in studies related to hepatotoxicity, pulmonary hypertension and liver tumors .

Cat. No.	Product Name	Chemical Structure

HY-107859S

Tris(2-chloroethyl)phosphate-d12
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.

Tris(2-chloroethyl)phosphate-d12

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.

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mitochondrial hepatotoxicity

Inhibitors & Agonists

Screening Libraries

Biochemical Assay Reagents

NaturalProducts

Isotope-Labeled Compounds

Natural
Products