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mitochondrial homeostasis

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-112879
    Mito-TEMPO
    Maximum Cited Publications
    164 Publications Verification

    		 Calcium Channel PINK1/Parkin Mitochondrial Metabolism Apoptosis Autophagy NOD-like Receptor (NLR) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca 2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. Mito-TEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. Mito-TEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke .
    Mito-TEMPO
  • HY-N9933
    Tauro-β-muricholic acid
    4 Publications Verification

    TβMCA

    		 FXR Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC50=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .
    Tauro-β-muricholic acid
  • HY-17355A
    Dexpramipexole dihydrochloride
    2 Publications Verification

    (R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride

    		 ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
    Dexpramipexole dihydrochloride
  • HY-W040307
    Saccharopine
    1 Publications Verification

    L-Saccharopine

    		 Endogenous Metabolite Metabolic Disease
    Saccharopine (L-Saccharopine), a lysine degradation intermediate, is a mitochondrial toxin. Lysine and α-ketoglutarate are converted into Saccharopine by the lysine-ketoglutarate reductase. Saccharopine is then oxidized to α-aminoapidate semialdehyde and glutamate by the saccharopine dehydrogenase. Saccharopine impairs development by disrupting mitochondrial homeostasis .
    Saccharopine
  • HY-W018587
    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 .
    TBPH
  • HY-125944
    MitoTEMPO hydrate
    Maximum Cited Publications
    164 Publications Verification

    		 Mitochondrial Metabolism PINK1/Parkin NOD-like Receptor (NLR) Autophagy Calcium Channel Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology
    MitoTEMPO hydrate is a mitochondria-targeted antioxidant . MitoTEMPO hydrate induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. MitoTEMPO hydrate regulates Ca 2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. MitoTEMPO hydrate reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. MitoTEMPO hydrate can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke .
    MitoTEMPO hydrate
  • HY-138207
    N-Oleoyl-L-phenylalanine

    		Mitochondrial Metabolism Drug Metabolite Inflammation/Immunology
    N-Oleoyl-L-phenylalanine is a long-chain N-acyl-L-phenylalanine and also a mitochondrial uncoupler. N-Oleoyl-L-phenylalanine uncouples UCP1-independent respiration in mitochondria, thereby helping to regulate glucose homeostasis. As an endogenous metabolite, the level of N-Oleoyl-L-phenylalanine increases in patients with ulcerative colitis after a high-fat diet. N-Oleoyl-L-phenylalanine can be used in studies related to ulcerative colitis .
    N-Oleoyl-L-phenylalanine
  • HY-P2914
    Carnitine acetyltransferase

    		Biochemical Assay Reagents Metabolic Disease Inflammation/Immunology
    Carnitine acetyltransferase is a mitochondrial matrix enzyme that catalyzes the interconversion of Acetyl-CoA and Acetylcarnitine (HY-126358). Carnitine acetyltransferase functions as a positive regulator of total body glucose tolerance and muscle activity of pyruvate dehydrogenase. Carnitine acetyltransferase is responsible for mitochondrial acetyl-CoA balance and regulation of fatty acid oxidation by utilizing short- and medium- chain fatty acids and their corresponding acylcarnitines as substrates. Carnitine acetyltransferase plays a crucial role in regulating glucose homeostasis. Carnitine acetyltransferase can be utilized in the research of aging, obesity, and diabetes .
    Carnitine acetyltransferase
  • HY-N0237
    Atractyloside A
    3 Publications Verification

    		 Toll-like Receptor (TLR) MyD88 NF-κB Mitochondrial Metabolism Interleukin Related Aquaporin Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Atractyloside A is an orally active inhibitor of the TLR4/MyD88/NF-κB signaling pathway and also an opener of the mitochondrial permeability transition pore (MPTP). Atractyloside A interferes with the activation of the TLR4/MyD88/NF-κB pathway, thereby inhibiting intestinal inflammatory responses. Atractyloside A reverses mucin synthesis impairment, improves intestinal barrier integrity, and restores homeostasis by altering the composition of the gut microbiota. Atractyloside A can be used in studies related to spleen deficiency diarrhea and myocardial injury .
    Atractyloside A
  • HY-W002199
    6:2 Fluorotelomer alcohol

    6:2 FTOH; 1H,1H,2H,2H-Perfluoro-1-octanol; 2-(Perfluorohexyl)ethanol

    		 Bacterial Apoptosis ERK TNF Receptor Infection Neurological Disease
    6:2 Fluorotelomer alcohol (6:2 FTOH) is an orally active, blood-brain barrier-permeable modulator of cyclin D1 and ETS1. 6:2 Fluorotelomer alcohol downregulates cyclin D1 expression, upregulates ETS1 via the TNF-α/ERK 1/2 pathway, impairs mitochondrial membrane potential and respiratory function, increases reactive oxygen species levels, disrupts calcium homeostasis and activates endoplasmic reticulum stress markers, and induces cell proliferation inhibition and endothelial-mesenchymal transition. Furthermore, 6:2 Fluorotelomer alcohol induces morphological abnormalities in zebrafish embryos and liver developmental damage, while disrupting the brain immune microenvironment in mice, causing systemic toxicity and delayed pup maturation in CD-1 mice. 6:2 Fluorotelomer alcohol also induces cortical neuron apoptosis, glial cell activation, synaptic abnormalities, colonic barrier damage, intestinal dysbiosis and autism spectrum disorder-like symptoms in mice. 6:2 Fluorotelomer alcohol shows no mutagenic, clastogenic, primary skin/eye irritation or skin sensitizing effects, exhibits no selective reproductive toxicity in CD-1 mice, and is classified as GHS Category 4 for acute oral toxicity. 6:2 Fluorotelomer alcohol can be used in studies of neurodevelopmental disorders and autism spectrum disorders .
    6:2 Fluorotelomer alcohol
  • HY-P10409
    SHLP2

    Small humanin-like peptide 2

    		 Apoptosis Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease
    SHLP2 (Small humanin-like peptide 2) is a small molecule peptide encoded by mitochondrial DNA, belonging to mitochondria derived peptide. SHLP2 has the activity of regulating apoptosis and inhibits cell death. SHLP2 binds to mitochondrial complex 1. SHLP2 improves mitochondrial metabolism by increasing respiration and biogenesis, reducing ROS, and decreasing mtDNA oxidation. SHLP2 also regulated energy homeostasis through the activation of hypothalamic neurons. SHLP2 can be used in the study of diseases related to mitochondrial dysfunction and anti-aging diseases, such as age-related macular degeneration and Parkinson’s disease .
    SHLP2
  • HY-121006
    Biguanide

    		Mitochondrial Metabolism AMPK Insulin Receptor Metabolic Disease Cancer
    Biguanide is an orally active antihyperglycemic agent. Biguanide inhibits mitochondrial ATP production, activates the LKB1-AMPK signaling pathway, and damages the energy homeostasis. Biguanide enhances insulin-receptor activation and downstream signaling. Biguanide exhibits potential in ameliorating the type 2 diabetes and the insulin-associated cancers.
    Biguanide
  • HY-17355B
    Dexpramipexole
    2 Publications Verification

    (R)-Pramipexole; R-(+)-Pramipexole; KNS-760704

    		 PINK1/Parkin Glutathione Peroxidase Sodium Channel ATP Synthase NOD-like Receptor (NLR) Mitophagy Ferroptosis Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
    Dexpramipexole
  • HY-139577
    Ninerafaxstat

    IMB-1018972; IMB-101

    		 Mitochondrial Metabolism Cardiovascular Disease Metabolic Disease
    Ninerafaxstat (IMB-1018972) is a novel orally active cardiac mitochondrial drug that restores myocardial energy homeostasis. Ninerafaxstat competitively inhibits 3-ketoacyl-CoA thiolase (3-KAT) to partially suppress fatty acid oxidation, and shifts cardiac energy metabolism from free fatty acid oxidation to glucose oxidation, regulating myocardial substrate utilization and thereby improving cardiac efficiency. Ninerafaxstat can be used for research on cardiovascular diseases .
    Ninerafaxstat
  • HY-17522
    Meptyldinocap

    2,4-DNOPC

    		 Fungal ERK JNK p38 MAPK Apoptosis Mitochondrial Metabolism Infection Endocrinology
    Meptyldinocap (2,4-DNOPC) is a fungicide and cytotoxic agent that acts against powdery mildew. Meptyldinocap upregulates the phosphorylation levels of ERK1/2, JNK and p38. Meptyldinocap induces apoptosis and endoplasmic reticulum stress, disrupts calcium homeostasis, inhibits cell proliferation and migration, downregulates the expression of proliferation- and pregnancy-related genes, and triggers mitochondrial dysfunction. Meptyldinocap can be used in studies related to powdery mildew and implantation failure .
    Meptyldinocap
  • HY-P2989
    Pyruvate carboxylase

    		Endogenous Metabolite Metabolic Disease Cancer
    Pyruvate carboxylase is a key mitochondrial anaplerotic enzyme that catalyzes the conversion of pyruvate to oxaloacetate. Pyruvate carboxylase not only maintains tricarboxylic acid cycle activity and redox homeostasis, but also drives hepatic gluconeogenesis and fatty acid synthesis. The activity of Pyruvate carboxylase is upregulated in insulin-resistant states, exacerbating hepatic glucose production. Pyruvate carboxylase also shows significantly enhanced expression in early-stage non-small cell lung cancer (NSCLC). Pyruvate carboxylase promotes tumor proliferation by supporting nucleotide and lipid synthesis, and its functional deficiency cannot be compensated by glutaminolysis. Pyruvate carboxylase can be used in the research of prediabetes type 2 and NSCLC .
    Pyruvate carboxylase
  • HY-W040307B
    Saccharopine hydrochloride
    1 Publications Verification

    L-Saccharopine hydrochloride

    		 Endogenous Metabolite Metabolic Disease
    Saccharopine (L-Saccharopine) hydrochloride, a lysine degradation intermediate, is a mitochondrial toxin. Lysine and α-ketoglutarate are converted into Saccharopine hydrochloride by the lysine-ketoglutarate reductase. Saccharopine hydrochloride is then oxidized to α-aminoapidate semialdehyde and glutamate by the saccharopine dehydrogenase. Saccharopine hydrochloride impairs development by disrupting mitochondrial homeostasis .
    Saccharopine hydrochloride
  • HY-171030
    Pro-GA

    		Reactive Oxygen Species (ROS) Cancer
    Pro-GA is a γ-glutamyl cyclotransferase (GGCT) inhibitor. Pro-GA inhibits the enzymatic activity of GGCT, disrupts glutathione homeostasis, induces the production of mitochondrial ROS, and upregulates the expression of p21, p27 and p16 in cells. Pro-GA inhibits the growth of cancer cells, induces cell cycle arrest and cellular senescence. Pro-GA exerts anti-tumor effects in breast cancer xenograft mouse models. Pro-GA can be used in research related to bladder cancer and breast cancer .
    Pro-GA
  • HY-139577A
    Ninerafaxstat trihydrochloride

    MB-1018972 trihydrochloride; IMB-101 trihydrochloride

    		 Mitochondrial Metabolism Cardiovascular Disease Metabolic Disease
    Ninerafaxstat trihydrochloride (IMB-1018972 trihydrochloride) is the trihydrochloride salt form of Ninerafaxstat (HY-139577). Ninerafaxstat trihydrochloride is a novel orally active cardiac mitochondrial drug that restores myocardial energy homeostasis. Ninerafaxstat trihydrochloride competitively inhibits 3-ketoacyl-CoA thiolase (3-KAT) to partially suppress fatty acid oxidation, and shifts cardiac energy metabolism from free fatty acid oxidation to glucose oxidation, regulating myocardial substrate utilization and thereby improving cardiac efficiency. Ninerafaxstat trihydrochloride can be used for research on cardiovascular diseases .
    Ninerafaxstat trihydrochloride
  • HY-114383
    ST-539

    		Deubiquitinase Autophagy Neurological Disease
    ST-539 is the inhibitor for deubiquitinase USP30 with IC50 of 0.37 μM. ST-539 promotes the ubiquitination of mitochondrial proteins, and induces mitochondrial autophagy, thereby regulating mitochondrial homeostasis. ST-539 can be used in research of neurodegenerative diseases .
    ST-539
  • HY-17355BS
    Dexpramipexole-d3 dihydrochloride

    (R)-Pramipexole-d3 dihydrochloride; R-(+)-Pramipexole-d3 dihydrochloride; KNS-760704-d3 dihydrochloride

    		 Isotope-Labeled Compounds ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole-d3 ((R)-Pramipexole-d3) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
    Dexpramipexole-d3 dihydrochloride
  • HY-126718
    Methylenecyclopropylpyruvate

    Ketohypoglycin

    		 Mitochondrial Metabolism Metabolic Disease
    Methylenecyclopropylpyruvate (Ketohypoglycin) is an inhibitor for gluconeogenesis. Methylenecyclopropylpyruvate inhibits ketogenesis and affects the fatty acids metabolism. Methylenecyclopropylpyruvate may interfere with the mitochondrial β-oxidation pathway, affects the contents and composition of coenzyme A, and affects the glucose homeostasis .
    Methylenecyclopropylpyruvate
  • HY-144361
    Antitumor agent-44

    		Apoptosis Cancer
    Antitumor agent-44 (Compound 5n) disrupts the mitochondrial homeostasis, induces cell cycle arrest and apoptosis in human adenocarcinoma cells. Antitumor agent-44 (Compound 5n) possesses good anti-tumor activity in a lung-cancer-cell xenograft mice model .
    Antitumor agent-44
  • HY-112749B
    (3S,4R)-ME-344

    		Heme Oxygenase (HO) Reactive Oxygen Species (ROS) Mitochondrial Metabolism Cancer
    (3S,4R)-ME-344 is the (3S,4R)-enantiomer of ME-344 (HY-112749). ME-344 is a mitochondrial Heme oxygenase 1 (HO-1) inhibitor. ME-344 specifically binds and alters HO-1 structure, and increases HO-1 translocation from the rough endoplasmic reticulum to mitochondria, but only in drug-sensitive cells (such as H460 and SHP-77 cells). ME-344 decreases mitochondrial ATP production and induces ROS, with subsequent disruption of redox homeostasis and mitochondrial function. ME-344 has significant antitumor activity, and can be used for cancers like breast cancer research .
    (3S,4R)-ME-344
  • HY-173128
    TZOA

    		Apoptosis Infection
    TZOA is an antiviral agent that inhibits the replication of infectious hematopoietic necrosis virus (IHNV) in a dose-dependent manner and significantly reduces viral titers. TZOA can effectively counteract IHNV-induced apoptosis, maintain mitochondrial membrane potential and homeostasis, and restore MAVS-mediated interferon expression. TZOA has antiviral activity .
    TZOA
  • HY-17355AR
    Dexpramipexole dihydrochloride (Standard)

    (R)-Pramipexole dihydrochloride (Standard); R-(+)-Pramipexole dihydrochloride (Standard); KNS-760704 dihydrochloride (Standard)

    		 Reference Standards ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) dihydrochloride (Standard) is the analytical standard of Dexpramipexole (dihydrochloride). This product is intended for research and analytical applications. Dexpramipexole dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
    Dexpramipexole dihydrochloride (Standard)
  • HY-155784
    SPC-180002

    		Sirtuin Reactive Oxygen Species (ROS) Keap1-Nrf2 Cancer
    SPC-180002 is a SIRT1/3 dual inhibitor, with IC50 values of 1.13 and 5.41 μM, respectively. SPC-180002 disturbs redox homeostasis via ROS generation, which leads to an increase in both p21 protein stability and mitochondrial dysfunction. SPC-180002 strongly inhibits cell cycle progression and cancer cell growth. SPC-180002 activates the Nrf2 signaling pathway .
    SPC-180002
  • HY-17522R
    Meptyldinocap (Standard)

    2,4-DNOPC (Standard)

    		 Reference Standards Bacterial Infection Endocrinology
    Meptyldinocap (2,4-DNOPC) (Standard) is the analytical standard of Meptyldinocap. This product is intended for research and analytical applications. Meptyldinocap is a fungicide and cytotoxic agent that acts against powdery mildew. Meptyldinocap upregulates the phosphorylation levels of ERK1/2, JNK and p38. Meptyldinocap induces apoptosis and endoplasmic reticulum stress, disrupts calcium homeostasis, inhibits cell proliferation and migration, downregulates the expression of proliferation- and pregnancy-related genes, and triggers mitochondrial dysfunction. Meptyldinocap can be used in studies related to powdery mildew and implantation failure .
    Meptyldinocap (Standard)
  • HY-175221
    WHN-11

    		Apoptosis Autophagy Cancer
    WHN-11 is an amino-Artemisinin (HY-B0094) derivative with anti-cancer activity against various cancer cell lines. WHN-11 deprives the cell of ATP, activates autophagy, and causes subsequent cell death by apoptosis. WHN-11 alters cellular protein homeostasis pathways to induce mitochondrial fission and dysfunction. WHN-11's anti-cancer activity is independent of substantive ROS production. WHN-11 can be used for the study of triple-negative breast cancer (TNBC) .
    WHN-11
  • HY-180786
    DdBIC

    		Nuclear Hormone Receptor 4A/NR4A Pyroptosis Reactive Oxygen Species (ROS) PERK Caspase Cancer
    DdBIC is a pyroptosis inducer. DdBIC binds to Nur77 and triggers its translocation to mitochondria, activates SDHA to deplete succinyl-CoA, disrupts heme homeostasis, induces electron leakage, and elicits mitochondrial ROS production. DdBIC induces mitochondrial ROS that oxidatively activates OMA1, promotes OPA1 cleavage and its release into the cytoplasm, activates the integrated stress response via PERK, and ultimately activates granzyme B to cleave GSDMC. DdBIC can be used for the study of melanoma .
    DdBIC
  • HY-182917
    MMB-DTCs-1,3-diaminopropane-DTCs-MMB

    		Cancer
    MMB-DTCs-1,3-diaminopropane-DTCs-MMB is a Cuproptosis/Ferroptosis/Apoptosis inducer, and serves as the active metabolite of DMAPT-DTCs-1,3-diaminopropane-DTCs-DMAPT dimethanesulfonate (HY-182918). MMB-DTCs-1,3-diaminopropane-DTCs-MMB induces mitochondrial dysfunction, promotes reactive oxygen species (ROS) production, disrupts redox homeostasis, and triggers apoptosis, ferroptosis and cuproptosis in lung cancer cells. MMB-DTCs-1,3-diaminopropane-DTCs-MMB can be used in the research of lung cancer .
    MMB-DTCs-1,3-diaminopropane-DTCs-MMB
  • HY-131453
    Mitochondrial respiration-IN-1

    		Mitochondrial Metabolism Cardiovascular Disease Inflammation/Immunology
    Mitochondrial respiration-IN-1 is a mitochondrial respiratory inhibitor. Mitochondrial respiration-IN-1 reduces platelet aggregation, adhesion, and platelet-induced coagulation responses. Mitochondrial respiration-IN-1 induces adaptive glycolysis, decreases mitochondrial membrane potential, selectively reduces ATP production derived from oxidative phosphorylation, and exerts bidirectional regulatory effects on cell proliferation. Mitochondrial respiration-IN-1 activates UPRmt and upregulates the expression of SDHA-1 and MT-CO1. Mitochondrial respiration-IN-1 restores metabolic homeostasis in type 2 diabetic mice. Mitochondrial respiration-IN-1 can be used to investigate diseases mediated by inappropriate platelet activation/aggregation and type 2 diabetes .
    Mitochondrial respiration-IN-1
  • HY-182284
    Anticancer agent 310

    		Reactive Oxygen Species (ROS) Apoptosis Bcl-2 Family Caspase SHMT Methylenetetrahydrofolate Dehydrogenase (MTHFD) Cytochrome P450 Cancer
    Anticancer agent 310 is an antitumor agent. Anticancer agent 310 releases nitric oxide to induce mitochondrial ROS burst, triggers mitochondrial dysfunction and activates the Bax/Bcl-2-Cyt c-Caspase-9/Caspase-3 apoptotic pathway. Anticancer agent 310 also reduces the levels of SHMT2 and MTHFD2, decreases the ratios of NADPH/NADP + and GSH/GSSG, thereby disrupting redox homeostasis and exacerbating intracellular ROS accumulation. Anticancer agent 310 can be used in research related to gastric cancer .
    Anticancer agent 310
  • HY-182683
    MMV085203

    		Parasite TrxR Reactive Oxygen Species (ROS) Infection
    MMV085203 is a potent Plasmodium falciparum inhibitor, with a PfTrxR EC50 of 900 nM. MMV085203 exerts potent antimalarial activity against both blood‑stage and sexual‑stage Plasmodium falciparum parasites, with superior efficacy toward clinical isolates of high clonal diversity. MMV085203 modulates parasite redox homeostasis, induces ROS production, and elevates mitochondrial TCA cycle intermediates. MMV085203 can be used for the research of malaria .
    MMV085203
  • HY-183538
    Necroptosis inducer 2

    		Necroptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism Mixed Lineage Kinase RIP kinase Cancer
    Necroptosis inducer 2 is a necroptosis inducer and copper chelator. Necroptosis inducer 2 chelates intracellular free copper ions, disrupts redox homeostasis, elevates ROS levels, disrupts mitochondrial membrane potential, and induces cancer cell necroptosis. Necroptosis inducer 2 upregulates the necroptosis markers p-MLKL and p-RIP3 expression. Necroptosis inducer 2 exhibits anti-tumor activity in mice. Necroptosis inducer 2 can be used for the research of cancer, such as triple-negative breast cancer .
    Necroptosis inducer 2
  • HY-W011086R
    Tri-O-tolyl phosphate (Standard)

    Tri-O-cresyl phosphate (Standard); TOTP (Standard)

    		 Biochemical Assay Reagents Reference Standards Apoptosis Neurological Disease Metabolic Disease
    Tri-O-tolyl phosphate (Tri-O-cresyl phosphate; TOTP) (Standard) is an analytical standard of Tri-O-tolyl phosphate (HY-W011086). This product is intended for research and analytical applications. Tri-O-tolyl phosphate is an aryl phosphate compounds commonly utilized as flame retardants and lubricant additives across various industrie. Tri-O-tolyl phosphate has neurotoxicity and reproductive toxicity, decreasing cell viability, inhibiting cell proliferation, triggering cell cycle arrest, induceing apoptosis, causing mitochondrial dysfunction, disrupts calcium homeostasis .
    Tri-O-tolyl phosphate (Standard)
  • HY-183549
    Ferroptosis/apoptosis inducer-4

    		Apoptosis Ferroptosis Cancer
    Ferroptosis/apoptosis inducer-4 is a pyridine-hydrazone-derived Cu (II) complex and a synergistic inducer of ferroptosis and apoptosis. Ferroptosis/apoptosis inducer-4 exerts anti-tumor proliferation and anti-metastasis effects with extremely low systemic toxicity. Ferroptosis/apoptosis inducer-4 disrupts cellular redox homeostasis by depleting glutathione and generating hydroxyl radicals through the Cu 2+/Cu + redox cycle. Ferroptosis/apoptosis inducer-4 also triggers mitochondrial dysfunction and endoplasmic reticulum stress, which in turn lead to Ca 2+ release, mitochondrial Ca 2+ overload, and the formation of a ROS−Ca 2+ self-amplifying feedback loop. Ferroptosis/apoptosis inducer-4 can be used in studies related to cervical cancer .
    Ferroptosis/apoptosis inducer-4
  • HY-160475
    AD-9308

    		Aldehyde Dehydrogenase (ALDH) Apoptosis Autophagy Cardiovascular Disease Metabolic Disease
    AD-9308 is a highly selective and orally active ALDH2 activator. AD-9308 activates ALDH2 to promote the clearance of 4-HNE, inhibiting myocardial fibrosis, inflammation and cell apoptosis. AD-9308 improves mitochondrial function, sarcoplasmic reticulum/ endoplasmic reticulum calcium transport and regulates autophagy, restoring intracellular homeostasis. AD-9308 improves the diastolic and systolic function of the heart in diabetic mice and reverses ventricular mal-reconstruction. AD-9308 can be used for the study of diabetic cardiomyopathy .
    AD-9308
  • HY-182052
    anti-NSCLC agent-2

    		Glutathione Peroxidase Reactive Oxygen Species (ROS) NO Synthase Ferroptosis Apoptosis Cancer
    anti-NSCLC agent-2 exhibits nanomolar anti-proliferative activity and acts on wild-type and drug-resistant non-small cell lung cancer (NSCLC) cells. anti-NSCLC agent-2 downregulates ferroptosis-related factors SLC7A11 and GPX4, disrupts cellular redox homeostasis, depletes glutathione, accumulates lipid peroxides, and simultaneously elevates mitochondrial nitric oxide and ROS levels to induce ferroptosis in tumor cells. anti-NSCLC agent-2 is applicable to research related to non-small cell lung cancer .
    anti-NSCLC agent-2
  • HY-183257
    ATI-1

    		Autophagy Beclin1 Reactive Oxygen Species (ROS) p97 Cancer
    ATI-1 is an autophagy initiation inhibitor. ATI-1 targets valosin-containing protein (VCP/p97, disrupts its interaction with UFL1, impairs UFMylation homeostasis associated with VCP, promotes polyubiquitination and degradation of Beclin1, and blocks the formation of early autophagosomes. ATI-1 induces synergistic death of autophagy-dependent malignant tumor cells under nutrient deprivation conditions, accompanied by decreased mitochondrial membrane potential, reduced ROS levels and lysosomal stress. ATI-1 exhibits anti-tumor efficacy in a pancreatic adenocarcinoma xenograft mouse model. ATI-1 can be used for the research of pancreatic adenocarcinoma and lung cancer .
    ATI-1
  • HY-182046
    HD202A

    		MNK PPAR Eukaryotic Initiation Factor (eIF) Stearoyl-CoA Desaturase (SCD) Metabolic Disease
    HD202A is an orally active, selective dual inhibitor of MNK1/MNK2 (with IC50 values of 6.09 nM and 8.06 nM, and Kd values of 1.913 μM and 5.244 μM, respectively) that inhibits the MNK-eIF4E signaling pathway. By downregulating perilipin 2 and SCD1, while upregulating adipose triglyceride lipase and PPARγ coactivator 1α, HD202A enhances mitochondrial fatty acid oxidation and redox homeostasis. HD202A effectively suppresses body weight gain, hepatic lipid accumulation and elevation of serum lipids, significantly improves glucose tolerance and insulin sensitivity of the organism, and ameliorates inflammatory features. With these comprehensive pharmacological activities, HD202A exhibits great application potential in studies of metabolic dysfunction-associated steatotic liver disease .
    HD202A

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