2. Search Result
Search Result
Results for "

mitophagy mitochondrial

" in MedChemExpress (MCE) Product Catalog:

42

Inhibitors & Agonists

4

Screening Libraries

3

Peptides

8

Natural
Products

2

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-112879
    Mito-TEMPO
    160+ Cited Publications

    		 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-15886
    Mdivi-1
    Maximum Cited Publications
    315 Publications Verification

    mitochondrial division inhibitor 1

    		 Dynamin Mitophagy Autophagy Apoptosis Cancer
    Mdivi-1 is a selective dynamin-related protein 1 (Drp1) inhibitor. Mdivi-1 is a mitochondrial division/mitophagy inhibitor.
    Mdivi-1
  • HY-15597
    Salinomycin
    45+ Cited Publications

    Procoxacin

    		 Bacterial Wnt β-catenin Mitophagy Autophagy Apoptosis Antibiotic Parasite Cancer
    Salinomycin (Procoxacin), a polyether potassium ionophore antibiotic, selectively inhibits the growth of gram-positive bacteria. Salinomycin is a potent inhibitor of Wnt/β-catenin signaling, blocks Wnt-induced LRP6 phosphorylation. Salinomycin shows selective activity against human cancer stem cells .
    Salinomycin
  • HY-152943
    MTK458
    4 Publications Verification

    EP-0035985

    		 PINK1/Parkin Mitophagy Mitochondrial Metabolism Neurological Disease Cancer
    MTK458 is an orally active brain penetrant PINK1 activator. MTK458 binds to PINK1 and stabilizes an active heterocomplex, thereby increasing mitophagy. MTK458 can be used for research on Parkinson's disease .
    MTK458
  • HY-160019
    MTX115325

    		Deubiquitinase Mitophagy Neurological Disease
    MTX115325 (Example 1) is an orally active, brain-penetrating USP30 inhibitor (IC50=12 nM) with neuroprotective activity. MTX115325 increases ubiquitination (EC50=32 nM) of the mitochondrial outer membrane protein TOM20 (a USP30 substrate), increasing mitophagy. MTX115325 prevents dopaminergic neuron loss and preserves striatal dopamine .
    MTX115325
  • HY-115576
    P62-mediated mitophagy inducer
    5 Publications Verification

    		 p62 Mitophagy Autophagy Mitosis Neurological Disease Cancer
    P62-mediated mitophagy inducer (PMI) is a P62-mediated mitophagy activator. P62-mediated mitophagy inducer activates mitochondrial autophagy without recruitment of Parkin or collapse of the mitochondrial membrane potential and remains active in cells lacking a fully functional PINK1/Parkin pathway. P62-mediated mitophagy inducer serves as a pharmacological tool to study the molecular mechanisms of mitosis, avoiding toxicity and some of the non-specific effects associated with the sudden dissipation of mitochondria lacking membrane potential .
    P62-mediated mitophagy inducer
  • 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-N10470
    Bleomycin A5
    1 Publications Verification

    Pingyangmycin

    		 Antibiotic DNA/RNA Synthesis Apoptosis Dynamin PINK1/Parkin Mitophagy Infection Cancer
    Bleomycin A5 (Pingyangmycin) is a glycopeptide antibiotic with multiple biological activities, which can be isolated from Streptomyces. Bleomycin A5 exerts cytotoxic effects by binding to Fe 2+ to form a complex, inducing single-strand and double-strand DNA breaks, and inhibiting DNA replication. Bleomycin A5 inhibits Drp1-mediated mitochondrial fission and suppresses PINK1/Parkin pathway-mediated mitophagy, ultimately triggering mitochondria-mediated cellular apoptosis. Bleomycin A5 can be used in cancer research .
    Bleomycin A5
  • HY-N0559
    Kirenol
    1 Publications Verification

    		 Casein Kinase Apoptosis AMPK Akt NF-κB TGF-beta/Smad Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a Kd value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis .
    Kirenol
  • HY-141659
    CMPD-39
    3 Publications Verification

    		 Mitophagy Deubiquitinase Neurological Disease
    CMPD-39 is a selective non-covalent inhibitor of the ubiquitin-specific protease USP30 (IC50=~20 nM), with high selectivity over other DUB family members (1-100 μM). CMPD-39 inhibits the deubiquitinating activity of USP30, enhances the ubiquitination of mitochondrial proteins TOMM20 and SYNJ2BP; thus, CMPD-39 promotes phosphoubuitin accumulation, thereby accelerating mitochondrial autophagy (mitophagy) and peroxisomal autophagy (pexophagy). CMPD-39 significantly restores impaired mitochondrial function in dopaminergic neurons derived from Parkinson's disease patients .
    CMPD-39
  • HY-125944
    MitoTEMPO hydrate
    160+ Cited Publications

    		 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-145337
    FT3967385

    FT385

    		 Deubiquitinase PINK1/Parkin Neurological Disease Cancer
    FT3967385 (FT385) is a selective covalent inhibitor that targets the outer mitochondrial membrane deubiquitinase (Deubiquitinase) USP30 (IC50 = 1.5 nM, Ki = 0.014 μM). By inhibiting the enzymatic activity of USP30, FT3967385 relieves its negative regulation of the PINK1-Parkin mediated mitochondrial ubiquitination cascade, thereby enhancing mitophagy. FT3967385 can be used for mechanistic studies of neurodegenerative diseases associated with mitochondrial dysfunction, such as Parkinson's disease .
    FT3967385
  • HY-N0392
    Polygalasaponin F

    		Toll-like Receptor (TLR) PI3K Akt NF-κB MDM-2/p53 Caspase MEK Bcl-2 Family p38 MAPK Mitophagy Reactive Oxygen Species (ROS) Apoptosis Calcium Channel Cardiovascular Disease Infection Neurological Disease
    Polygalasaponin F is an orally active triterpenoid saponin monomer. Polygalasaponin F downregulates the expression of Bax, p53, caspase-3, NF-κB p65 and MEK1; restores and upregulates the expression of Bcl-2; activates the PI3K/Akt signaling pathway; inhibits the phosphorylation of p38 MAPK, nuclear translocation of NF-κB, TLR4-mediated signaling pathway, mitophagy (Mitophagy) and ROS production; enhances cell viability and suppresses apoptosis (Apoptosis). Polygalasaponin F maintains mitochondrial function, alleviates Ca 2+ overload, upregulates pCREB and BDNF, preserves cell viability and inhibits the release of inflammatory cytokines. Polygalasaponin F alleviates lung injury induced by influenza A H1N1 and cerebral ischemia-reperfusion injury. Polygalasaponin F is applicable to researches related to Parkinson's disease, cerebral ischemia, pneumonia induced by influenza A H1N1, stroke and Alzheimer's disease .
    Polygalasaponin F
  • HY-N4087
    Platycodin D2
    3 Publications Verification

    		 Mitophagy Autophagy Ferroptosis Interleukin Related IFNAR Reactive Oxygen Species (ROS) Inflammation/Immunology Cancer
    Platycodin D2 is an orally active triterpenoid saponin found in Platycodon grandiflorum. Platycodin D2 induces mitophagy in cancer cells through NIX, thereby activating the P21/CyclinA2 pathway and promoting cell senescence. Platycodin D2 induces mitochondrial dysfunction, enhances autophagy, inhibits hepatocellular carcinoma cell proliferation, and exhibits anti-tumor activity against multiple cancer cell types. Platycodin D2 promotes mRNA expression of T-bet, GATA-3, Th1 cytokines IL-2 and IFN-γ, and Th2 cytokines IL-4 and IL-10, enhances splenocyte proliferation, and acts as a vaccine adjuvant with low rabbit red blood cell hemolytic activity. Platycodin D2 induces mitochondrial ROS production, incomplete autophagy, and ferroptosis to inhibit breast cancer cell proliferation. Platycodin D2 can be used for the research of cancer, inflammation and immunology .
    Platycodin D2
  • HY-134640
    AUTAC4
    4 Publications Verification

    		 AUTACs Mitophagy Neurological Disease Cancer
    AUTAC4 is a mitochondria-targeting autophagy-targeting chimera (AUTAC). AUTAC4 downregulates cytosolic proteins and promotes targeted mitochondrial turnover via mitophagy .
    AUTAC4
  • 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-172199
    THX6

    		ClpP Cancer
    THX6 is an hClpP activator with an EC50 of 1.18 μM. THX6 improves off-target profile with no affinity for hD2R and only weak affinity for hD3R (Ki = 51.1 µM) in HEK293 cells. THX6 shows good cytotoxicity in ONC201-resistant cells with an IC50 of 0.13 μM. THX6 changes the levels of fatty acids (PUFAs, MUFAs, and SFAs) in DIPG cells. THX6 decreases the level of proteins involved in oxidative phosphorylation, biogenesis, and mitophagy proteins, thereby resulting in a global collapse of mitochondrial integrity and function. THX6 can be used for diffuse intrinsic pontine glioma research .
    THX6
  • HY-Y1322
    Triphenyl phosphate

    		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-125918
    Bleomycin A5 hydrochloride

    Pingyangmycin hydrochloride

    		 Antibiotic DNA/RNA Synthesis Apoptosis Dynamin PINK1/Parkin Mitophagy Infection Cancer
    Bleomycin A5 (Pingyangmycin) hydrochloride is a glycopeptide antibiotic with multiple biological activities, which can be isolated from Streptomyces. Bleomycin A5 hydrochloride exerts cytotoxic effects by binding to Fe 2+ to form a complex, inducing single-strand and double-strand DNA breaks, and inhibiting DNA replication. Bleomycin A5 hydrochloride inhibits Drp1-mediated mitochondrial fission and suppresses PINK1/Parkin pathway-mediated mitophagy, ultimately triggering mitochondria-mediated cellular apoptosis. Bleomycin A5 hydrochloride can be used in cancer research .
    Bleomycin A5 hydrochloride
  • HY-169380
    PARL-IN-2
    1 Publications Verification

    		 PINK1/Parkin Mitophagy Metabolic Disease
    PARL-IN-2 (Compound 14) is a covalent inhibitor of the mitochondrial intramembrane protease PARL with an EC50 value of 0.16 μM. PARL-IN-2 leads to a robust activation of the PINK1/Parkin pathway. PARL-IN-2 promotes PINK1/Parkin-dependent mitophagy .
    PARL-IN-2
  • HY-178154
    FB231

    		PINK1/Parkin Mitochondrial Metabolism Neurological Disease
    FB231 is a Parkin activator. FB231 can induce mild mitochondrial stress, resulting in impaired mitochondrial function and activation of the integrated stress response. FB231 can lower the threshold for mitochondrial toxins to induce PINK1/Parkin-mediated mitophagy. FB231 can cause activation of the integrated stress response (ISR) and perturbation to iron-dependent pathways. FB231 can be used for the research of neurological disease, such as Parkinson’s disease .
    FB231
  • HY-147225
    TSPO Ligand-Linker Conjugates 1

    		AUTACs Mitophagy Neurological Disease Metabolic Disease Cancer
    TSPO Ligand-Linker Conjugates 1 contains a ligand for translocator protein (TSPO) and a linker, which is used for the synthesis of mitochondria-targeting autophagy-targeting chimera (AUTAC). AUTAC can bind the TSPO on the outer mitochondrial membrane (OMM) of mitochondria and degrades impaired mitochondria and proteins via mitophagy, and improves mitochondrial activity. TSPO Ligand-Linker Conjugates 1 can be used in mitochondrial dysfunction related research, including neurodegenerative diseases, cancer, and diabetes .
    TSPO Ligand-Linker Conjugates 1
  • HY-176568
    LCL768

    		Mitophagy PINK1/Parkin Mitochondrial Metabolism Neurological Disease Cancer
    LCL768 is a ceramide analog. LCL768 attenuates PARKIN succination to promote PARKIN activation and mitophagy. LCL768 induces CerS1-mediated endogenous C18-ceramide accumulation in mitochondria to mediate mitophagy, which is dependent on DRP1 activation via nitrosylation at C644. LCL768 alters mitochondrial metabolism, resulting in fumarate depletion and leading to tumor suppression. LCL768 improves sensorimotor defects in neurodegenerative diseases like ALS .
    LCL768
  • HY-16461
    Solenopsin

    (-)-Solenopsin A

    		 Akt Ribosomal S6 Kinase (RSK) PI3K PDK-1 FOXO Mitophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism Cardiovascular Disease
    Solenopsin ((-)-Solenopsin A) is an ATP-competitive and selective Akt-1 inhibitor with an IC50 of 5-10 μM, and also acts as an RSK1 inhibitor. Solenopsin inhibits the activities of PDK1 in lipid rafts, downregulates PI3K, blocks PI3K-dependent generation of 3-phosphoinositides, and suppresses the phosphorylation of FOXO1a. Solenopsin induces Mitophagy and ROS production, reduces mitochondrial oxygen consumption, and exhibits antiproliferative and antiangiogenic activities. Solenopsin can be used in research related to hyperproliferative skin diseases and malignant diseases .
    Solenopsin
  • HY-141659A
    (R)-CMPD-39

    		Mitophagy Deubiquitinase Neurological Disease
    (R)-CMPD-39 is the R enantiomer of CMPD-39 ( HY-141659 ). CMPD-39 is a selective non-covalent inhibitor of the ubiquitin-specific protease USP30 (IC50 =~20 nM), with high selectivity over other DUB family members (1-100 μM). CMPD-39 inhibits the deubiquitinating activity of USP30, enhances the ubiquitination of mitochondrial proteins TOMM20 and SYNJ2BP; thus, CMPD-39 promotes phosphoubuitin accumulation, thereby accelerating mitochondrial autophagy (mitophagy) and peroxisomal autophagy (pexophagy). CMPD-39 significantly restores impaired mitochondrial function in dopaminergic neurons derived from Parkinson's disease patients .
    (R)-CMPD-39
  • 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-Y1322S
    Triphenyl phosphate-d15

    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-15886R
    Mdivi-1 (Standard)

    mitochondrial division inhibitor 1 (Standard)

    		 Dynamin Mitophagy Autophagy Apoptosis Reference Standards Cancer
    Mdivi-1 (Standard) is the analytical standard of Mdivi-1. This product is intended for research and analytical applications. Mdivi-1 is a selective dynamin-related protein 1 (Drp1) inhibitor. Mdivi-1 is a mitochondrial division/mitophagy inhibitor.
    Mdivi-1 (Standard)
  • HY-P10416
    Q14

    Q14 peptide

    		 Deubiquitinase Mitophagy Others Neurological Disease
    Q14 is a polypeptide derived from the USP30 (ubiquitin specific peptidase 30) transmembrane (TM) domain with the ability to inhibit the deubiquitination activity of USP30 (IC50=57.2 nM). Q14 reduces USP30 activity by inhibiting the interaction between the USP30 transmembrane domain and its catalytic domain. Q14 peptide contains the LC3 interaction region (LIR) motif, which enables it to bind to the LC3 and accelerate the formation of autophagosomes, thereby promoting mitophagy. Q14 can be used in the study of neurodegenerative diseases as well as mitochondrial quality control and cell metabolism .
    Q14
  • HY-170565
    CHD-1

    		Mitophagy Apoptosis Cancer
    CHD-1 is a a hypoxia-activated antitumor prodrug. CHD-1 impairs mitochondrial morphology and membrane potential in hypoxic tumor cells, further triggering excessive mitophagy and inducing apoptosis. CHD-1 inhibits the growth of hypoxic tumor cells in vitro and the growth of HeLa xenograft in vivo .
    CHD-1
  • HY-161388
    NSCLC-IN-1

    		Ferroptosis Mitophagy Cancer
    NSCLC-IN-1 (Compound A10-2) induces mitophagy and ferroptosis through targeting transmembrane BAX inhibitor motif containing 6 (TMBIM6). NSCLC-IN-1 induces mitochondrial Ca 2+ imbalance, leading to mitochondrial damage. NSCLC-IN-1 reduces intracellular glutathione (GSH), increases the accumulation of lipid peroxides (LPO) and malondialdehyde (MDA) content. NSCLC-IN-1 is a potent anti-NSCLC agent .
    NSCLC-IN-1
  • HY-P10247
    Amyloid precursor C-terminal peptide

    		Mitochondrial Metabolism Neurological Disease
    Amyloid precursor C-terminal peptide is cleaved from the C-terminus of Amyloid Precursor Protein (APP). Amyloid precursor C-terminal peptide accumulation causes mitochondrial morphology alteration and basal mitophagy failure, which indicates that amyloid precursor protein C-terminal peptide may correspond to an etiological trigger of Alzheimer’s disease (AD) pathology .
    Amyloid precursor C-terminal peptide
  • 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-15597R
    Salinomycin (Standard)

    Procoxacin (Standard)

    		 Reference Standards Bacterial Wnt β-catenin Mitophagy Autophagy Apoptosis Antibiotic Parasite Cancer
    Salinomycin (Standard) is the analytical standard of Salinomycin. This product is intended for research and analytical applications. Salinomycin (Procoxacin), a polyether potassium ionophore antibiotic, selectively inhibits the growth of gram-positive bacteria. Salinomycin is a potent inhibitor of Wnt/β-catenin signaling, blocks Wnt-induced LRP6 phosphorylation. Salinomycin shows selective activity against human cancer stem cells[1][2][3].
    Salinomycin (Standard)
  • HY-176485
    Antiproliferative agent-70

    		Ferroptosis Mitophagy Reactive Oxygen Species (ROS) Cancer
    Antiproliferative agent-70 (compound 23) is a potent antiproliferative agent. Antiproliferative agent-70 shows antiproliferative activities and induces MMP depolarization. Antiproliferative agent-70 induces mitochondrial dysfunction. Antiproliferative agent-70 induces mitophagy and ferroptosis. Antiproliferative agent-70 increases the protein expression of PINK1, p-Parkin, p53 and p21. Antiproliferative agent-70 increases intracellular ROS levels. Antiproliferative agent-70 shows anticancer activity .
    Antiproliferative agent-70
  • HY-N0392R
    Polygalasaponin F (Standard)

    		Reference Standards Toll-like Receptor (TLR) PI3K Akt NF-κB Inflammation/Immunology Cancer
    Polygalasaponin F (Standard) is the analytical standard of Polygalasaponin F. This product is intended for research and analytical applications. Polygalasaponin F is an orally active triterpenoid saponin monomer. Polygalasaponin F downregulates the expression of Bax, p53, caspase-3, NF-κB p65 and MEK1; restores and upregulates the expression of Bcl-2; activates the PI3K/Akt signaling pathway; inhibits the phosphorylation of p38 MAPK, nuclear translocation of NF-κB, TLR4-mediated signaling pathway, mitophagy (Mitophagy) and ROS production; enhances cell viability and suppresses apoptosis (Apoptosis). Polygalasaponin F maintains mitochondrial function, alleviates Ca 2+ overload, upregulates pCREB and BDNF, preserves cell viability and inhibits the release of inflammatory cytokines. Polygalasaponin F alleviates lung injury induced by influenza A H1N1 and cerebral ischemia-reperfusion injury. Polygalasaponin F is applicable to researches related to Parkinson's disease, cerebral ischemia, pneumonia induced by influenza A H1N1, stroke and Alzheimer's disease.
    Polygalasaponin F (Standard)
  • HY-N0559R
    Kirenol (Standard)

    		Reference Standards Casein Kinase Apoptosis AMPK Akt NF-κB TGF-beta/Smad Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Kirenol (Standard) is the analytical standard of Kirenol (HY-N0559). This product is intended for research and analytical applications. Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a Kd value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.
    Kirenol (Standard)
  • HY-N12531
    Molephantin

    		Reactive Oxygen Species (ROS) Mitochondrial Metabolism Mitophagy Apoptosis PI3K Akt mTOR Neurological Disease Cancer
    Molephantin is a blood-brain barrier permeable anti-glioblastoma compound. Molephantin induces ROS generation, leading to mitochondrial damage, Mitophagy flux blockage and Apoptosis induction. Molephantin can suppress the PI3K/Akt/mTOR signaling pathway. Molephantin demonstrates antitumor effects against glioblastoma .
    Molephantin
  • HY-182553
    USP30-IN-2

    		Deubiquitinase Mitophagy Neurological Disease
    USP30-IN-2, a fused pyrroline, is an USP30 inhibitor with an IC50 <0.1 μM. USP30-IN-2 is expected to promote mitophagy and restore mitochondrial health. USP30-IN-2 can be used for research on Parkinson's disease .
    USP30-IN-2
  • HY-179574
    AURKA-IN-4

    		Molecular Glues Aurora Kinase Mitochondrial Metabolism Cancer
    AURKA-IN-4 (compound 13), a capsaicin-derived prohibitin ligand, is an AURKA inhibitor. AURKA-IN-4 acts as a molecular glue within the AURKA/PHB2/LC3 complex. AURKA-IN-4 is specific to the mitochondrial pool of AURKA, and inhibits AURKA-dependent mitophagy. AURKA-IN-4 can be used for cancer research .
    AURKA-IN-4
  • HY-P11812
    MLS peptide

    		Mitochondrial Metabolism Cytochrome P450 Metabolic Disease
    MLS peptide is a Mitochondria-targeting peptide. MLS peptide participates in respiratory chain function via encoding Cytochrome C oxidase .
    MLS peptide
  • HY-W283930
    YHV98-4

    		Tau Protein ATP Synthase Mitophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism Neurological Disease Inflammation/Immunology
    YHV98-4 is a selective, blood-brain barrier permeable Hv1 channel inhibitor. YHV98-4 specifically inhibits Hv1 with a half-maximal inhibitory concentration of 1 µM without inhibiting other ion channels. YHV98-4 reduces the propagation of p-tau. YHV98-4 increases ATP production, and enhances microglial mitophagy. YHV98-4 attenuates inflammatory pain via inhibition of Hv1 and ROS production. YHV98-4 enhances microglia-to-neuron mitochondrial transfer, promoting the delivery of functional mitochondria to rescue neuronal damage and improve cognitive function. YHV98-4 reduces inflammation. YHV98-4 can be used in the research of Alzheimer's disease .
    YHV98-4

Inquiry Online

Your information is safe with us. * Required Fields.

Salutation

  

Country or Region *

Applicant Name *

 

Organization Name *

Department *

     

Email Address *

 

Product Name *

Cat. No.

  

Requested quantity *

Phone Number *

     

Remarks

Inquiry Online

Inquiry Information

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent: