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mitochondrial disorder

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-153169
    6PPD-Q
    Maximum Cited Publications
    7 Publications Verification

    6PPD-Quinone

    		 α-synuclein Environmental Pollutants Others
    6PPD-Q (6PPD-Quinone) is an environmental pollutant that can be detected in human urine and is widely present in the environment. 6PPD-Q targets and binds to CNR2, CNR1, AA2AR, LCAT, and TRPA1, with CNR2 exhibiting the highest binding affinity, potentially acting as a CNR2 receptor agonist to activate cannabinoid receptors. 6PPD-Q induces intestinal inflammation and barrier damage by disrupting mitochondrial function, reducing neuronal glycolysis metabolites and TCA cycle intermediates, and exacerbating α-synuclein (α-syn) aggregation. 6PPD-Q is applicable in research on environmental toxicology, neurodegenerative diseases, and inflammation-related disorders .
    6PPD-Q
  • HY-N5034
    Phosphorylethanolamine
    4 Publications Verification

    Monoaminoethyl phosphate; NSC 254167; O-Phosphoethanolamine

    		 Endogenous Metabolite Neurological Disease Metabolic Disease Cancer
    Phosphorylethanolamine (Monoaminoethyl phosphate) is a membrane phospholipid and an important precursor of Phosphatidylcholine (HY-B2233B). It is found in most animal tissues and various human extracranial tumors, playing a critical role in membrane integrity, cell division, mitochondrial respiratory function, and more. Studies have shown that changes in the abundance of Phosphorylethanolamine are associated with Alzheimer's disease and Parkinson's disease. Lowering the ratio of Phosphorylethanolamine to Phosphatidylcholine in the liver can improve insulin signaling. Phosphorylethanolamine holds promise for research in the fields of cancer, neurodegenerative disorders, and metabolic diseases .
    Phosphorylethanolamine
  • HY-134539
    IMT1
    5+ Cited Publications

    		 Oxidative Phosphorylation Mitochondrial Metabolism DNA/RNA Synthesis Metabolic Disease Cancer
    IMT1 is a first-in-class specific and noncompetitive human mitochondrial RNA polymerase (POLRMT) inhibitor. IMT1 causes a conformational change of POLRMT, which blocks substrate binding and transcription in a dose-dependent way in vitro. IMT1 reduces deoxynucleoside triphosphate levels and citric acid cycle intermediates, resulting in a marked depletion of cellular amino acid levels. IMT1 has the potential for mitochondrial transcription disorders related diseases .
    IMT1
  • HY-N0157
    Orotic acid
    3 Publications Verification

    6-Carboxyuracil; Vitamin B13

    		 Nucleoside Antimetabolite/Analog Endogenous Metabolite Metabolic Disease
    Orotic acid (6-Carboxyuracil), a precursor in biosynthesis of pyrimidine nucleotides and RNA, is released from the mitochondrial dihydroorotate dehydrogenase (DHODH) for conversion to UMP by the cytoplasmic UMP synthase enzyme. Orotic acid is a marker for measurement in routine newborn screening for urea cycle disorders. Orotic acid can induce hepatic steatosis and hepatomegaly in rats .
    Orotic acid
  • HY-119976
    Boscalid
    1 Publications Verification

    		 Environmental Pollutants Apoptosis Fungal Mitochondrial Metabolism Succinate Dehydrogenase Infection
    Boscalid is a succinate dehydrogenase (SDHI) inhibitor with antifungal activity. Boscalid binds to the ubiquinone-binding site of fungal mitochondrial complex II, blocks ATP production and aerobic respiration, exhibits good control efficacy against a variety of plant fungal diseases including gray mold, sclerotinia rot and powdery mildew, and is widely used for disease control in agriculture. Boscalid induces apoptosis, altered lipid metabolism, mitochondrial dysfunction, respiratory impairment, oxidative stress, ROS accumulation and neurodevelopmental disorders in zebrafish. Boscalid reduces foraging ability, shortens median death time and causes chronic toxicity in exposed honeybees. Boscalid also possesses genotoxicity, cytotoxicity, elevated mitochondrial superoxide levels and early-stage apoptosis .
    Boscalid
  • 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-B0762
    Acetyl-L-carnitine hydrochloride
    2 Publications Verification

    O-Acetyl-L-carnitine hydrochloride; ALCAR hydrochloride

    		 Caspase Apoptosis Neurological Disease
    Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) hydrochloride is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine hydrochloride selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine hydrochloride can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine hydrochloride exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine hydrochloride is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression .
    Acetyl-L-carnitine hydrochloride
  • HY-P2048
    MOTS-c (human)
    1 Publications Verification

    		 Apoptosis GLUT AMPK Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    MOTS-c (human) is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders .
    MOTS-c (human)
  • HY-113218
    Acetyl-L-carnitine
    2 Publications Verification

    O-Acetyl-L-carnitine; ALCAR

    		 Caspase Apoptosis Neurological Disease
    Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression .
    Acetyl-L-carnitine
  • HY-B0863
    Glyphosate
    1 Publications Verification

    		 Environmental Pollutants Necroptosis Apoptosis Autophagy Neurological Disease
    Glyphosate, a non-selective systemic biocide with broad-spectrum activity, is an herbicidal derivative of the amino acid glycine. Glyphosate inhibits the enzymatic activity of the 5-endopyruvylshikimate 3-phosphate synthase (EPSPS) in the shikimic acid pathway, preventing the synthesis of the aromatic amino acids tyrosine, phenylalanine, and tryptophan. Glyphosate induces oxidative stress, neuroinflammation, and mitochondrial dysfunction, processes that lead to neuronal death by autophagia, necrosis, or apoptosis, as well as the appearance of behavioral and motor disorders .
    Glyphosate
  • HY-113166
    Dodecanoylcarnitine
    1 Publications Verification

    (-)-Lauroylcarnitine

    		 Endogenous Metabolite Metabolic Disease Inflammation/Immunology
    Dodecanoylcarnitine ((-)-Lauroylcarnitine) is a medium long-chain acylcarnitine, an intermediate product in key energy metabolic pathways of fatty acid β-oxidation and amino acids catabolism. The abnormal decrease in the Dodecanoylcarnitine levels indicats that mitochondrial fuel metabolism, including fatty acid oxidation is significantly disturbed. Changes in plasma concentrations of Dodecanoylcarnitine are not only associated with type II diabetes, but also with pre-diabetes status. Dodecanoylcarnitine is present in fatty acid oxidation disorders such as long-chain acyl CoA dehydrogenase deficiency, carnitine palmitoyltransferase I/II deficiency, and is also associated with celiac disease. Dodecanoylcarnitine deomonstrates high sensitivities and specificities in predicting asthma. Combined model of Decanoylcarnitine (HY-113069), Dodecanoylcarnitine, PC (16:0/0:0), and Asp Arg Pro can be used as a potential biomarker for the diagnosis of Yin-deficiency-heat syndrome .
    Dodecanoylcarnitine
  • HY-135885
    VBIT-12
    5+ Cited Publications

    		 VDAC Neurological Disease
    VBIT-12 is a potent VDAC1 inhibitor. VBIT-12 directly interacts with VDAC1 and prevents VDAC1 oligomerization, and thus inhibits apoptotic action of VDAC1 .
    VBIT-12
  • 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 .
    Glutamic acid sodium salt
  • HY-124410
    Mitoquinol
    3 Publications Verification

    		 Reactive Oxygen Species (ROS) HIF/HIF Prolyl-Hydroxylase Metabolic Disease Inflammation/Immunology
    Mitoquinol is an orally active mitochondria-targeted antioxidant. Mitoquinol can regulate mitochondrial respiration and oxidation. Mitoquinol inhibits ROS production, and improves phagocytosis and glycolysis in ethanol-exposed macrophages via the HIF-1α-PFKP axis. Additionally, Mitoquinol can partially alleviate heat stress-induced decreases in growth performance, inflammatory responses, and metabolic disorders in pigs .
    Mitoquinol
  • HY-W013150
    Alpidem

    		GABA Receptor Neurological Disease
    Alpidem, an anxiolytic agent, is an orally active and brain-penetrant GABAA receptor ligand, binds to α1β2γ2 subunit-containing GABAA receptors (IC50 of 17 nM) over α5β2γ2 subunit-containing GABAA receptors (IC50 of >10 μM). Alpidem modulates calcium-induced mitochondrial permeability transition, induces glutathione depletion and hepatocyte necrosis, potentiates TNF-α toxicity, inhibits marble-burying and locomotor activity, enhances stressed rodent feeding behavior, and exerts anticonvulsant effects. Alpidem can be used for the research of anxiety, anxiety disorders, and convulsions .
    Alpidem
  • HY-N0735
    Phellodendrine chloride
    2 Publications Verification

    		 Autophagy Apoptosis AMPK mTOR STAT Interleukin Related PKC p38 MAPK NF-κB COX Reactive Oxygen Species (ROS) PI3K Akt MMP Neurological Disease Inflammation/Immunology Cancer
    Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and glutamine metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway .
    Phellodendrine chloride
  • HY-B0762S
    Acetyl-L-carnitine-d3 hydrochloride

    O-Acetyl-L-carnitine-d3 hydrochloride

    		 Isotope-Labeled Compounds Caspase Apoptosis Neurological Disease
    Acetyl-L-carnitine-d3 (O-Acetyl-L-carnitine-d3) hydrochloride is the deuterium labeled Acetyl-L-carnitine hydrochloride (HY-B0762). Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) hydrochloride is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine hydrochloride selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine hydrochloride can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine hydrochloride exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine hydrochloride is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression .
    Acetyl-L-carnitine-d3 hydrochloride
  • HY-175739
    TFAM activator 1

    		Mitochondrial Metabolism CXCR Neurological Disease Metabolic Disease Inflammation/Immunology
    TFAM activator 1 is a TFAM activator. TFAM activator 1 increases TFAM protein levels, promotes mitochondrial DNA stability, increases mitochondrial DNA copy number, and prevents mitochondrial DNA from escaping into the cytoplasm. TFAM activator 1 improves cellular energy metabolism in cybrid cells. TFAM activator 1 reduces fibrosis markers in fibroblasts. TFAM activator 1 can be used in the research of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes syndrome, systemic sclerosis, and autoimmune diseases .
    TFAM activator 1
  • HY-142035
    N-Propargylglycine
    1 Publications Verification

    		 Mitochondrial Metabolism Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    N-Propargylglycine is a brain-penetrant and orally active PRODH inhibitor. N-Propargylglycine covalently modifies enzyme-bound FAD and active site lysine, causing enzyme structural distortion, protein decay, and irreversible inhibition of proline and 4-hydroxyproline catabolism. N-Propargylglycine induces UPRmt, upregulates mitochondrial chaperones and YME1L1, enhances mitochondrial proteostasis, blocks astrocytic L-proline consumption, and abolishes L-proline’s ATP-maintaining and viability-protective effects. N-Propargylglycine stimulates neural processes, increases brain proline, hydroxyproline, and sarcosine levels, partially normalizes Huntington’s disease whole brain transcriptomes. N-Propargylglycine reduces hyperoxaluria, prevents calcium oxalate stone formation, reduces kidney tubular damage, and restores weight and survival in Grhpr knockout mice. N-Propargylglycine can be used for the research of breast cancer, neurodegenerative disorders, Huntington’s disease, and primary hyperoxaluria type 2 .
    N-Propargylglycine
  • 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-P1723
    Spexin
    2 Publications Verification

    Neuropeptide Q

    		 Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Neurological Disease
    Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .
    Spexin
  • HY-N0430
    Coptisine

    Coptisin

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine
  • HY-N0430A
    Coptisine Sulfate
    5 Publications Verification

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine Sulfate
  • HY-120332
    Sonlicromanol hydrochloride

    KH176 hydrochloride

    		 Reactive Oxygen Species (ROS) Metabolic Disease
    Sonlicromanol (KH176) hydrochloride, a chemical entity derivative of Trolox, is a blood-brain barrier permeable ROS-redox modulator. Sonlicromanol (KH176) hydrochloride is used in the study for mitochondrial disorders .
    Sonlicromanol hydrochloride
  • HY-P5763
    Phoenixin-20

    PNX-20

    		 Epigenetic Reader Domain PGC-1α Neurological Disease
    Phoenixin-20 (PNX-20) is a bioactive peptide with hormone-like actions in vertebrates, and can stimulates hypothalamo-pituitary-gonadal hormones and regulate reproductive processes in mammals. Phoenixin-20 promotes neuronal mitochondrial biogenesis via CREB-PGC-1α pathway. Phoenixin-20 has anxiolytic effect .
    Phoenixin-20
  • HY-112597A
    Mavodelpar

    REN001; HPP593

    		 PPAR Inflammation/Immunology
    Mavodelpar (REN001) is a selective PPARδ agonist. Mavodelpar suppresses glomerular injury and renal fibrosis. Mavodelpar can be used for the research of primary mitochondrial myopathies (PMM) and long-chain fatty acid oxidation disorders (LC-FAOD) . Mavodelpar is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    Mavodelpar
  • HY-P2048A
    MOTS-c(human) acetate
    1 Publications Verification

    		 AMPK GLUT Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    MOTS-c (human) acetate is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) acetate inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) acetate has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders .
    MOTS-c(human) acetate
  • HY-N6711
    Equisetin

    		HIV Integrase Bacterial Antibiotic Reactive Oxygen Species (ROS) STAT AMPK 11β-HSD Infection Metabolic Disease
    Equisetin is an N-methylserine-derived acyl tetramic acid, quorum sensing inhibitor (QSI), herbicides and antibiotics. Equisetin specifically inhibits the anionic carriers of substrates in the inner mitochondrial membrane. Equisetin inhibits the activity of HIV-1 integrase, 11β-HSD1, and 2,4-dinitrophenol (Dnp)-stimulated ATPase (IC50 = ~8 nmol per mg of protein). Equisetin exhibits growth inhibition of bacteria, anti-inflammatory, amelioration of lipid-associated disorders, and cytotoxic effects .
    Equisetin
  • HY-128578
    KPLH1130
    2 Publications Verification

    		 PDHK NO Synthase Interleukin Related HIF/HIF Prolyl-Hydroxylase Metabolic Disease Inflammation/Immunology
    KPLH1130 is a pyruvate dehydrogenase kinase (PDK) inhibitor. KPLH1130 potently inhibits M1 macrophage polarization by reducing the expression of pro-inflammatory cytokines, decreasing the levels of M1 phenotype markers (HIF-1α, iNOS) and nitric oxide (NO) production. KPLH1130 prevents the reduction of mitochondrial oxygen consumption rate (OCR) induced by inflammatory stimuli (LPS ((HY-D1056) + IFN-γ) in various macrophage types. KPLH1130 improves glucose tolerance in HFD-fed mice. KPLH1130 can be used for the study of obesity-associated metabolic disorders and other inflammatory conditions .
    KPLH1130
  • HY-N0427
    Phellodendrine

    		Akt NF-κB AMPK mTOR PKC STAT Interleukin Related p38 MAPK COX Reactive Oxygen Species (ROS) Apoptosis Autophagy PI3K MMP Neurological Disease Inflammation/Immunology Cancer
    Phellodendrine is an orally active plant alkaloid. Phellodendrine inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and glutamine metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway .
    Phellodendrine
  • HY-139308
    T0467
    2 Publications Verification

    		 PINK1/Parkin Mitochondrial Metabolism Neurological Disease
    T0467 activates parkin mitochondrial translocation in a PINK1-dependent manner in vitro. T0467 do not induce mitochondrial accumulation of PINK1in dopaminergic neurons. T0467 is a potential compound for PINK1-Parkin signaling activation, and can be used for parkinson's disease and related disorders research .
    T0467
  • HY-114520
    TT01001

    		Monoamine Oxidase Mitochondrial Metabolism Apoptosis Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease
    TT01001 is a selective and orally active mitoNEET agonist and a monoamine oxidase B (MAO-B) inhibitor (IC50 = 8.84 μM). TT01001 does not activate PPARγ but interacts with MitoNEET. TT01001 attenuates oxidative stress and neuronal apoptosis by preventing mitoNEET-mediated mitochondrial dysfunction. TT01001 improves type II diabetes and ameliorates mitochondrial function of mice. TT01001 can used for the studies of type II diabetes and neurological disorders .
    TT01001
  • HY-N0157R
    Orotic acid (Standard)

    6-Carboxyuracil (Standard); Vitamin B13 (Standard)

    		 Reference Standards Nucleoside Antimetabolite/Analog Endogenous Metabolite Metabolic Disease
    Orotic acid (Standard) is the analytical standard of Orotic acid. This product is intended for research and analytical applications. Orotic acid (6-Carboxyuracil), a precursor in biosynthesis of pyrimidine nucleotides and RNA, is released from the mitochondrial dihydroorotate dehydrogenase (DHODH) for conversion to UMP by the cytoplasmic UMP synthase enzyme. Orotic acid is a marker for measurement in routine newborn screening for urea cycle disorders. Orotic acid can induce hepatic steatosis and hepatomegaly in rats .
    Orotic acid (Standard)
  • HY-W747676
    Glyphosate-13C

    		Isotope-Labeled Compounds Apoptosis Autophagy Necroptosis Neurological Disease
    Glyphosate- 13C is the 13C-labeled Glyphosate (HY-B0863). Glyphosate, a non-selective systemic biocide with broad-spectrum activity, is an herbicidal derivative of the amino acid glycine. Glyphosate inhibits the enzymatic activity of the 5-endopyruvylshikimate 3-phosphate synthase (EPSPS) in the shikimic acid pathway, preventing the synthesis of the aromatic amino acids tyrosine, phenylalanine, and tryptophan. Glyphosate induces oxidative stress, neuroinflammation, and mitochondrial dysfunction, processes that lead to neuronal death by autophagia, necrosis, or apoptosis, as well as the appearance of behavioral and motor disorders .
    Glyphosate-13C
  • HY-B0445B
    α-NAD

    α-Nicotinamide Adenine Dinucleotide

    		 Mitochondrial Metabolism Endogenous Metabolite Metabolic Disease
    α-NAD (α-Nicotinamide Adenine Dinucleotide) serves as a substrate for reninase, functions as an analog of β-NAD, affects the kinetics of NAD-dependent enzymes, and also plays a critical role as a cofactor in mitochondrial redox reactions .
    α-NAD
  • 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 .
    Prothioconazole
  • HY-E70121
    Succinyl-CoA synthetase

    		Endogenous Metabolite Mitochondrial Metabolism Neurological Disease Metabolic Disease Inflammation/Immunology
    Succinyl-CoA synthetase is a mitochondrial matrix enzyme and catalyst. Succinyl-CoA synthetase supports TCA, ketone and heme metabolism and is activated by mitochondrial phosphate. Succinyl-CoA synthetase distributes broadly across mammalian tissues with distinct substrate-related biochemical features. Succinyl-CoA synthetase gains structural stability after phosphorylation and relies on SUCLG1-encoded subunit for activity. Succinyl-CoA synthetase malfunction links to metabolic and neurological disorders. Succinyl-CoA synthetase serves as a research tool for mitochondrial hepatoencephalomyopathy .
    Succinyl-CoA synthetase
  • HY-W004850
    Aminoacetone hydrochloride

    		Endogenous Metabolite Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease
    Aminoacetone hydrochloride is an α-aminoketone and also a catabolite of threonine and glycine. When accumulated under pathological conditions, Aminoacetone hydrochloride participates in oxidative damage and protein dysfunction via the production of reactive oxygen species (ROS) and methylglyoxal, and it is associated with phenotypes such as diabetes, mitochondrial damage and sleep disorders .
    Aminoacetone hydrochloride
  • HY-117433S
    4-Hydroperoxy Cyclophosphamide-d4

    		DNA Alkylator/Crosslinker Apoptosis Reactive Oxygen Species (ROS) Drug Metabolite Inflammation/Immunology
    4-Hydroperoxy Cyclophosphamide-d4 is the deuterium labeled 4-Hydroperoxy cyclophosphamide. 4-Hydroperoxy cyclophosphamide is the active metabolite form of the proagent Cyclophosphamide. 4-Hydroperoxy cyclophosphamide crosslinks DNA and induces T cell apoptosis independent of death receptor activation, but activates mitochondrial death pathways through production of reactive oxygen species (ROS). 4-Hydroperoxy cyclophosphamide has the potential for lymphomas and autoimmune disorders .
    4-Hydroperoxy Cyclophosphamide-d4
  • HY-144604
    FPR2 agonist 2

    		Formyl Peptide Receptor (FPR) Infection Neurological Disease
    FPR2 agonist 2 is a potent and CNS-penetrant FPR2 agonist with an EC50 of 0.13 μM, 1.1 μM for FPR2 and FPR1, respectively. FPR2 agonist 2 inhibits the production of pro-inflammatory cytokines, counterbalances the changes in mitochondrial function, and inhibits caspase-3 activity .
    FPR2 agonist 2
  • HY-B0762S1
    Acetyl-L-carnitine-d3-1 hydrochloride

    O-Acetyl-L-carnitine-d3-1 hydrochloride

    		 Isotope-Labeled Compounds Caspase Apoptosis Neurological Disease
    Acetyl-L-carnitine-d3-1 (O-Acetyl-L-carnitine-d3-1) hydrochloride is the deuterium labeled Acetyl-L-carnitine hydrochloride (HY-B0762). Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) hydrochloride is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine hydrochloride selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine hydrochloride can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine hydrochloride exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine hydrochloride is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression .
    Acetyl-L-carnitine-d3-1 hydrochloride
  • HY-169728
    SID 24785302

    		Hexokinase Parasite Infection
    SID 24785302 is a hexokinase inhibitor with antiparasitic activity. SID 24785302 exhibits activity against T. brucei and Leishmania. SID 24785302 can be used for the research of mitochondrial DNA disorders and parasitic infection .
    SID 24785302
  • HY-N0157A
    Orotic acid zinc
    3 Publications Verification

    6-Carboxyuracil zinc; Vitamin B13 zinc

    		 Nucleoside Antimetabolite/Analog Endogenous Metabolite Metabolic Disease
    Orotic acid (zinc), a precursor in biosynthesis of pyrimidine nucleotides and RNA, is released from the mitochondrial dihydroorotate dehydrogenase (DHODH) for conversion to UMP by the cytoplasmic UMP synthase enzyme. Orotic acid (zinc) is a marker for measurement in routine newborn screening for urea cycle disorders. Orotic acid (zinc) can induce hepatic steatosis and hepatomegaly in rats .
    Orotic acid zinc
  • HY-N0157S1
    Orotic acid-13C,15N2 monohydrate

    6-Carboxyuracil-13C,15N2 monohydrate; Vitamin B13-13C,15N2 monohydrate

    		 Nucleoside Antimetabolite/Analog Endogenous Metabolite Metabolic Disease
    Orotic acid- 13C, 15N2 (monohydrate) is the 13C and 15N labeled Orotic acid . Orotic acid (6-Carboxyuracil), a precursor in biosynthesis of pyrimidine nucleotides and RNA, is released from the mitochondrial dihydroorotate dehydrogenase (DHODH) for conversion to UMP by the cytoplasmic UMP synthase enzyme. Orotic acid is a marker for measurement in routine newborn screening for urea cycle disorders. Orotic acid can induce hepatic steatosis and hepatomegaly in rats .
    Orotic acid-13C,15N2 monohydrate
  • HY-135808
    BIZ 114

    		NF-κB Inflammation/Immunology
    BIZ 114 (Example 11) is a fatty acid derivative and potent inhibits the TNF-α activated NF-κΒ pathway. BIZ 114 has the potential to prevent and / or treat ophthalmic disorders such as retinal degenerative disorders and ocular inflammatory diseases .
    BIZ 114
  • HY-148322
    Sirtuin modulator 5

    		Sirtuin Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Sirtuin modulator 5 is a sirtuin modulating agent. Sirtuin modulator 5 can activate SIRT1 with a DC50 value of <50 μM. Sirtuin modulator 5 can be used for increasing the lifespan of a cell and used for the research of variety of diseases including, for example, diseases or disorders related to aging or stress, diabetes, obesity, neurodegenerative diseases, cardiovascular disease, blood clotting disorders, inflammation, cancer, and/or flushing as well as diseases or disorders that would benfit from increased mitochondrial activity .
    Sirtuin modulator 5
  • HY-176975
    DRP1 Allosteric-IN-3

    		Dynamin Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
    DRP1 Allosteric-IN-3 (Compound 2b) is an allosteric inhibitor of DRP1. Its IC50 value for the DRP1:MiD49 protein-protein interaction is 11 μM. DRP1 Allosteric-IN-3 can be used to study various diseases related to mitochondrial division disorders .
    DRP1 Allosteric-IN-3
  • HY-B0863B
    Glyphosate isopropylammonium

    		Apoptosis Autophagy Necroptosis Neurological Disease
    Glyphosate isopropylammonium, a non-selective systemic biocide with broad-spectrum activity, is an herbicidal derivative of the amino acid glycine. Glyphosate isopropylammonium inhibits the enzymatic activity of the 5-endopyruvylshikimate 3-phosphate synthase (EPSPS) in the shikimic acid pathway, preventing the synthesis of the aromatic amino acids tyrosine, phenylalanine, and tryptophan. Glyphosate isopropylammonium induces oxidative stress, neuroinflammation, and mitochondrial dysfunction, processes that lead to neuronal death by autophagia, necrosis, or apoptosis, as well as the appearance of behavioral and motor disorders .
    Glyphosate isopropylammonium
  • HY-P1723A
    Spexin TFA

    Neuropeptide Q TFA

    		 Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Metabolic Disease
    Spexin (Neuropeptide Q) TFA is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin TFA can function through both central and peripheral actions. Spexin TFA upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin TFA improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin TFA can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .
    Spexin TFA
  • HY-N0735R
    Phellodendrine chloride (Standard)

    		Reference Standards Autophagy mTOR AMPK Apoptosis STAT Interleukin Related PKC p38 MAPK NF-κB COX Reactive Oxygen Species (ROS) PI3K Akt MMP Neurological Disease Inflammation/Immunology Cancer
    Phellodendrine chloride (Standard) is the analytical standard of Phellodendrine chloride (HY-N0735). Phellodendrine chloride is an orally active plant alkaloid. Phellodendrine chloride inhibits the proliferation of KRAS-mutated pancreatic cancer cells by suppressing macropinocytosis and glutamine metabolism, inducing ROS accumulation and mitochondrial apoptosis. Phellodendrine chloride promotes autophagy by activating the AMPK/mTOR pathway, alleviating intestinal damage in ulcerative colitis. Phellodendrine chloride can alleviate gouty arthritis by inhibiting the IL-6/STAT3 signaling pathway. Phellodendrine chloride suppresses allergic reactions by altering the conformation of MRGPRB3/MRGPRX2 protein, thereby inhibiting the activation of PKC and subsequent downstream MAPK and NF-κB signaling. Phellodendrine chloride inhibits the AKT/NF-κB pathway and down-regulates the expression of COX-2, thereby protecting zebrafish embryos from oxidative stress. Phellodendrine chloride has an anti-major depressive disorder (MDD) effect by down-regulating CHRM1, HTR1A, and the PI3K/Akt signaling pathway.
    Phellodendrine chloride (Standard)

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