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disrupts mitochondrial metabolism

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19

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5

Natural
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3

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-W008151

    Mitochondrial Metabolism Carnitine Palmitoyltransferase (CPT) Metabolic Disease
    Diphenyl Phosphate inhibits growth and energy metabolism in zebrafish and mice in a sex-specific manner. Diphenyl Phosphate can inhibit the activity of SDH (respiratory complex II), reduce the expression of CPT1 and disrupts the integrity of the mitochondrial membrane. Diphenyl Phosphate may be used in research on metabolic diseases .
    Diphenyl Phosphate
  • HY-34740

    Mitochondrial Metabolism Neurological Disease Metabolic Disease
    Ethylmalonic acid is a short-chain organic dicarboxylic acid. Ethylmalonic acid synergistically induces mitochondrial permeability transition (MP) with Ca 2+, inhibits Mi-CK, and disrupts mitochondrial energy metabolism. Ethylmalonic acid can be used in the research of SCADD, EE and other genetic metabolic diseases characterized by EMA accumulation .
    Ethylmalonic acid
  • HY-Y1322

    Environmental Pollutants Mitophagy Apoptosis NF-κB p38 MAPK ERK JNK PI3K Akt Monoamine Oxidase Reactive Oxygen Species (ROS) PPAR Indoleamine 2,3-Dioxygenase (IDO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring .
    Triphenyl phosphate
  • HY-135700

    Calcineurin Ras HMG-CoA Reductase (HMGCR) Metabolic Disease Inflammation/Immunology
    Mevalonolactone is an intermediate metabolite in the eukaryotic mevalonate pathway, serving as the stable δ-lactone form of mevalonate with oral activity. Mevalonolactone exhibits binding affinity for ZNF384 (Ka = 12.6 μM) and inhibitory activity against aconitase (aconitase). Mevalonolactone promotes the nuclear localization of ZNF384 and enhances its binding to the GGPPS promoter. Mevalonolactone induces insulin resistance, disrupts glucose and lipid metabolism, enhances the isoprenylation of K-Ras, and inhibits the activation of the insulin signaling pathway. Mevalonolactone inhibits polypeptide synthesis of HMG-CoA reductase in isolated rat hepatocytes, promotes its degradation, and reduces its enzymatic activity. Mevalonolactone impairs mitochondrial function in rat brains. Mevalonolactone promotes the development of metabolically unhealthy obesity. Mevalonolactone can be used in research related to metabolically abnormal obesity, mevalonic aciduria, HMGCR-related limb-girdle myopathy, and statin-induced myopathy .
    Mevalonolactone
  • HY-155063

    HSP Mitochondrial Metabolism Cancer
    TRAP1-IN-1 (compound 35) is a potent and selective inhibitor of TRAP1,a mitochondrial isoform of Hsp90. TRAP1-IN-1 has >250-fold TRAP1 selectivity over Grp94,and disrupts TRAP1 tetramer stability,induces TRAP1 client protein degradation. TRAP1-IN-1 also inhibits mitochondrial complex I of oxidative phosphorylation OXPHOS,disrupts the mitochondrial membrane potential,and enhances glycolysis metabolism .
    TRAP1-IN-1
  • HY-34740S

    Mitochondrial Metabolism Isotope-Labeled Compounds Neurological Disease Metabolic Disease
    Ethylmalonic acid-d3 is the deuterium labeled Ethylmalonic acid (HY-34740). Ethylmalonic acid is a short-chain organic dicarboxylic acid. Ethylmalonic acid synergistically induces mitochondrial permeability transition (MP) with Ca 2+, inhibits Mi-CK, and disrupts mitochondrial energy metabolism. Ethylmalonic acid can be used in the research of SCADD, EE and other genetic metabolic diseases characterized by EMA accumulation .
    Ethylmalonic acid-d3
  • HY-116568

    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 .
    Prothioconazole
  • HY-Y1322S

    Celluflex TPP-d15; DHPF 005-d15; Disflamol TP-d15; Disflamoll TP-d15; NSC 57868-d15; Phenyl phosphate ((PhO)3PO)-d15; Phoscon FR 903N-d15

    Isotope-Labeled Compounds Environmental Pollutants ERK Indoleamine 2,3-Dioxygenase (IDO) p38 MAPK NF-κB Akt Monoamine Oxidase Mitophagy Reactive Oxygen Species (ROS) JNK PI3K PPAR Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate-d15 is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.
    Triphenyl phosphate-d15
  • HY-179557

    Glutathione Peroxidase Reactive Oxygen Species (ROS) Apoptosis Ferroptosis PD-1/PD-L1 Cancer
    iMQT_020 is a selective allosteric SLC1A5_var inhibitor. iMQT_020 disrupts the trimeric assembly of SLC1A5_var, causing metabolic crisis in cancer cells and selectively suppressing their growth. iMQT_020 reduces glutamine anaplerosis and oxidative phosphorylation, resulting in a broad disruption of cancer metabolism. iMQT_020 reduces GSH levels and increases cellular ROS and mitochondrial ROS. iMQT_020 induces apoptosis and ferroptosis. iMQT_020 can epigenetically upregulate PD-L1 expression. iMQT_020 can be used for the study of pancreatic cancer, lung cancer, and colon cancer .
    iMQT_020
  • HY-W134163

    trans-2-Octenal

    Fungal Reactive Oxygen Species (ROS) Mitochondrial Metabolism Phosphatase Pyruvate Kinase Infection
    (E)-2-Octenal is an Antifungal agent. (E)-2-Octenal disrupts cell membrane integrity and causes ROS accumulation. (E)-2-Octenal decreases the activities of phosphofructokinase and pyruvate kinase. (E)-2-Octenal inhibits Neofusicoccum parvum growth by disrupting mitochondrial energy metabolism. (E)-2-Octenal suppresses the growth of a Prochloraz (HY-B0845)-resistant Penicillium italicum strain. (E)-2-octenal exerts a broad-spectrum and potent inhibitory effect on various fungi, including Sclerotium rolfsii, Metarhizium anisopliae sensu lato, and Aspergillus flavus, etc. (E)-2-Octenal can be used for the research of citrus blue mold and mango stem-end rot .
    (E)-2-Octenal
  • HY-W008151R

    Mitochondrial Metabolism Reference Standards Metabolic Disease
    Diphenyl Phosphate inhibits growth and energy metabolism in zebrafish and mice in a sex-specific manner. Diphenyl Phosphate can inhibit the activity of SDH (respiratory complex II), reduce the expression of CPT1 and disrupts the integrity of the mitochondrial membrane. Diphenyl Phosphate may be used in research on metabolic diseases .
    Diphenyl Phosphate (Standard)
  • HY-34740S1

    Mitochondrial Metabolism Isotope-Labeled Compounds Neurological Disease Metabolic Disease
    Ethylmalonic acid-d5 is the deuterium labeled Ethylmalonic acid (HY-34740). Ethylmalonic acid is a short-chain organic dicarboxylic acid. Ethylmalonic acid synergistically induces mitochondrial permeability transition (MP) with Ca 2+, inhibits Mi-CK, and disrupts mitochondrial energy metabolism. Ethylmalonic acid can be used in the research of SCADD, EE and other genetic metabolic diseases characterized by EMA accumulation .
    Ethylmalonic acid-d5
  • HY-34740R

    Reference Standards Mitochondrial Metabolism Neurological Disease Metabolic Disease
    Ethylmalonic acid (Standard) is the analytical standard of Ethylmalonic acid (HY-34740). This product is intended for research and analytical applications. Ethylmalonic acid is a short-chain organic dicarboxylic acid. Ethylmalonic acid synergistically induces mitochondrial permeability transition (MP) with Ca 2+, inhibits Mi-CK, and disrupts mitochondrial energy metabolism. Ethylmalonic acid can be used in the research of SCADD, EE and other genetic metabolic diseases characterized by EMA accumulation .
    Ethylmalonic acid (Standard)
  • HY-155064

    HSP Metabolic Disease
    TRAP1-IN-2 (compound 36) is a selective degrader of TRAP1 downstream proteins without affecting Hsp90's cytoplasmic downstream proteins. TRAP1-IN-2 also inhibits OXPHOS and alters cellular glycolysis metabolism. TRAP1-IN-2 destabilizes TRAP1 tetramers and disrupts mitochondrial membrane potential.
    TRAP1-IN-2
  • HY-W331198

    Insecticide Ferroptosis Infection
    Tralopyril is an orally active, blood-brain barrier-penetrating antifouling insecticide and endocrine disruptor. By interfering with the thyroid hormone system and mitochondrial oxidative phosphorylation, Tralopyril downregulates the transcription of genes such as TRHR, Nkx2.1, TRα and induces ferroptosis. Tralopyril disrupts amino acid, energy and lipid metabolism, exhibits significant skeletal and reproductive toxicity, and causes developmental damage. Tralopyril has a long half-life in vivo and wide tissue distribution, posing potential risks to aquatic organisms and human health. Tralopyril shows species specificity in in vitro liver microsomal metabolism, exerts lethal effects on target insects and laboratory animals, and is commonly used in studies of chlorfenapyr poisoning and related toxic mechanisms .
    Tralopyril
  • HY-162688

    Telomerase G-quadruplex Apoptosis Ferroptosis Others
    Anticancer agent 239 (Compound 5) is a ligand of hTERT promoter G-quadruplex DNA structures (hTERT G4) (Kd = 1.1 μM), and downregulates hTERT expression. Anticancer agent 239 decreases telomerase activity, shortens telomere length, and induces DNA damage, acute cellular senescence, and apoptosis. Anticancer agent 239 causes mitochondrial dysfunction, disrupts iron metabolism and activates ferroptosis in cancer cells. Anticancer agent 239 inhibits tumor growth in MDA-MB-231 xenograft mouse model .
    Anticancer agent 239
  • HY-181720

    Caspase PARP Apoptosis Cancer
    Antitumor agent-214 is a chalcone analogue with anti-tumor activity. Antitumor agent-214 induces cell cycle arrest and apoptosis in tumor cells, disrupts mitochondrial metabolism, and upregulates the expression of caspase 3, caspase 7 and caspase 9, downregulates PARP1. Antitumor agent-214 can be used for anti-tumor research related to colorectal cancer, breast cancer, lung cancer, and cervical cancer .
    Antitumor agent-214
  • HY-183858

    Lactate Dehydrogenase Cancer
    NCATS-SM1440 is a glycolysis inhibitor and metabolic regulator that targets LDHA and LDHB (IC50=0.06 μM and 0.03 μM, respectively). Upon binding to LDHA, NCATS-SM1440 blocks the glycolysis pathway and reduces lactate production. NCATS-SM1440 drives the shift of pyruvate metabolism toward mitochondrial metabolism, effectively disrupting the dependence of cancer cells on aerobic glycolysis. NCATS-SM1440 can be widely used in research related to cancer, Ewing's sarcoma, and other related conditions .
    NCATS-SM1440

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