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Results for "

PINK1

" in MedChemExpress (MCE) Product Catalog:

40

Inhibitors & Agonists

7

Natural
Products

1

Isotope-Labeled Compounds

3

Antibodies

3

Oligonucleotides

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-100941
    CCCP
    Maximum Cited Publications
    176 Publications Verification

    Carbonyl cyanide 3-chlorophenylhydrazone; Carbonyl Cyanide m-Chlorophenylhydrazone

    		 Oxidative Phosphorylation PINK1/Parkin STING IFNAR Mitochondrial Metabolism Bacterial Apoptosis Inflammation/Immunology Cancer
    CCCP is an oxidative phosphorylation (OXPHOS) uncoupler. CCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation [1].
    CCCP
  • HY-100410
    FCCP
    105+ Cited Publications

    Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone

    		 Oxidative Phosphorylation PINK1/Parkin Mitochondrial Metabolism Cancer
    FCCP is an uncoupler of oxidative phosphorylation (OXPHOS) in mitochondria. FCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation [1].
    FCCP
  • 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 [1] .
    Mito-TEMPO
  • HY-N0109
    Salidroside
    Maximum Cited Publications
    44 Publications Verification

    Rhodioloside

    		 PINK1/Parkin mTOR Apoptosis Prolyl Endopeptidase (PREP) Cancer
    Salidroside (Rhodioloside) is a prolyl endopeptidase inhibitor. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling. Salidroside protects dopaminergic neurons by enhancing PINK1/Parkin-mediated mitophagy.
    Salidroside
  • 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 [1].
    MTK458
  • HY-15887
    MG 149
    10+ Cited Publications

    Tip60 HAT inhibitor

    		 Histone Acetyltransferase Epigenetic Reader Domain Apoptosis PINK1/Parkin Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    MG149 (Tip60 HAT inhibitor) is a selective and potent Tip60 inhibitor with IC50 of 74 uM, similar potentcy for MOF (IC50 = 47 uM); little potent for PCAF and p300 (IC50 >200 uM). MG 149 inhibits KAT8 and blocks PINK1 kinase activity. MG149 inhibits the phosphorylation of Parkin and ubiquitin, thereby suppressing the initiation of PINK1-dependent mitophagy. MG 149 can reverse chronic restraint stress (CRS) induced hypertension and related molecular changes. MG 149 commonly used in research on diseases such as hypertension and Parkinson's disease [1] .
    MG 149
  • HY-N0535
    (+)-Magnoflorine chloride
    1 Publications Verification

    Magnoflorine chloride; α-Magnoflorine chloride; Thalictrine chloride

    		 Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Infection Metabolic Disease
    (+)-Magnoflorine (α-Magnoflorine) chloride is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine chloride promotes Parkin/PINK1-mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine chloride inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine chloride upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine chloride also has significant antifungal activity [1] .
    (+)-Magnoflorine chloride
  • 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 [1].
    P62-mediated mitophagy inducer
  • 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 [1] .
    Bleomycin A5
  • 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 [1] .
    Dexpramipexole dihydrochloride
  • HY-N0334
    (+)-Magnoflorine

    Magnoflorine; α-Magnoflorine; Thalictrine

    		 Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Cardiovascular Disease Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    (+)-Magnoflorine (α-Magnoflorine) is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine also has significant antifungal activity [1] .
    (+)-Magnoflorine
  • 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 [1] .
    MitoTEMPO hydrate
  • HY-N0334A
    (+)-Magnoflorine iodide
    1 Publications Verification

    Magnoflorine iodide; α-Magnoflorine iodide; Thalictrine iodide

    		 Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Cardiovascular Disease Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    (+)-Magnoflorine (α-Magnoflorine) iodide is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine iodide promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine iodide inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine iodide also has significant antifungal activity [1] .
    (+)-Magnoflorine iodide
  • 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 [1] .
    FT3967385
  • HY-162567
    AP-4-139B

    		HSP Beclin1 Autophagy Cancer
    AP-4-139B is a blood-brain barrier-permeable HSP70 inhibitor with a IC50 of 180 nM against hHSP70. AP-4-139B binds directly to HSP70 and inhibits its ATPase activity. AP-4-139B promotes Autophagy by increasing the phosphorylation of Beclin-1. AP-4-139B exerts antitumor effects in preclinical models of colorectal cancer and pancreatic ductal adenocarcinoma [1] .
    AP-4-139B
  • HY-174806
    Y040-7904

    7-(β-D-Galactopyranosyloxy)-4-phenylchromen-2-one

    		 Mitophagy PINK1/Parkin Amyloid-β Neurological Disease
    Y040-7904 is a mitophagy activator. Y040-7904 enhances mitophagy by promoting mitochondria transport to autophagosomes and the fusion of autophagosomes with autolysosomes. Y040-7904 induces mitophagy through the SIRT1/FoxO3 pathway. Y040-7904 upregulates the levels of Parkin, PINK1, and LC3II/I. Y040-7904 reduces amyloid-β (Aβ) accumulation in both in vitro and in vivo models of Alzheimer’s disease.
    Y040-7904
  • HY-136065
    bpV(phen)
    3 Publications Verification

    		 PTEN Phosphatase Parasite Apoptosis Infection Metabolic Disease Inflammation/Immunology Cancer
    bpV(phen), a insulin-mimetic agent, is a potent protein tyrosine phosphatase (PTP) and PTEN inhibitor with IC50s of 38 nM, 343 nM and 920 nM for PTEN, PTP-β and PTP-1B, respectively. bpV(phen) inhibits proliferation of the protozoan parasite Leishmania in vitro. bpV(phen) strongly induces the secretion of a large number of chemokines and pro-inflammatory cytokines, and it activates a Th1-type pathway (IL-12, IFNγ). bpV(phen) can also induce cell apoptosis, and has anti-angiogenic and anti-tumor activity [1] .
    bpV(phen)
  • HY-152265
    PARL-IN-1

    		PINK1/Parkin Mitophagy Neurological Disease
    PARL-IN-1 is a potent PARL inhibitor with an IC50 value of 28 nM. PARL-IN-1 inhibits PARL and leads to a robust activation of the PINK1/Parkin pathway. PARL-IN-1 promotes PINK1/Parkin-dependent mitophagy [1].
    PARL-IN-1
  • 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 [1] .
    Dexpramipexole
  • 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 [1].
    T0467
  • HY-125036
    MitoBloCK-11

    		PINK1/Parkin Neurological Disease
    MitoBloCK-11 is a new small molecule with a protein-binding target, Seo1. MitoBloCK-11 plays an important role in the delivery of PINK1 pathway. MitoBloCK-11 can be used in the study of autosomal recessive Parkinson's disease [1].
    MitoBloCK-11
  • 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 [1] .
    Bleomycin A5 hydrochloride
  • HY-145816A
    JPS016 TFA
    1 Publications Verification

    		 HDAC PROTACs Apoptosis PINK1/Parkin Autophagy Reactive Oxygen Species (ROS) Cancer
    JPS016 TFA is a class I histone deacetylase (HDAC) PROTAC inhibitor. JPS016 TFA recruits the VHL E3 ligase (Ligands for E3 Ligase) to mediate the ubiquitination and proteasomal degradation of HDAC1, HDAC2 and HDAC3. JPS016 TFA reduces the viability of colon cancer cells and induces Apoptosis. JPS016 TFA activates the PINK1/Parkin mitochondrial Autophagy pathway, enhances cardiomyocyte viability, alleviates mitochondrial damage, and reduces mitochondrial ROS production in cells. JPS016 TFA is applicable to research related to colon cancer and sepsis cardiomyopathy [1] .
    JPS016 TFA
  • HY-RS10559
    PINK1 Human Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others

    PINK1 Human Pre-designed siRNA Set A contains three designed siRNAs for PINK1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.

    PINK1 Human Pre-designed siRNA Set A
    PINK1 Human Pre-designed siRNA Set A
  • 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 [1].
    PARL-IN-2
  • HY-100941R
    CCCP (Standard)

    Carbonyl cyanide 3-chlorophenylhydrazone (Standard); Carbonyl Cyanide m-Chlorophenylhydrazone (Standard)

    		 Oxidative Phosphorylation PINK1/Parkin Reference Standards STING IFNAR Mitochondrial Metabolism Bacterial Apoptosis Inflammation/Immunology Cancer
    CCCP (Standard) is the analytical standard of CCCP. This product is intended for research and analytical applications. CCCP is an oxidative phosphorylation (OXPHOS) uncoupler. CCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation [1].
    CCCP (Standard)
  • HY-N0109R
    Salidroside (Standard)
    Maximum Cited Publications
    44 Publications Verification

    Rhodioloside (Standard)

    		 Prolyl Endopeptidase (PREP) mTOR Apoptosis PINK1/Parkin Reference Standards Cancer
    Salidroside (Standard) is the analytical standard of Salidroside. This product is intended for research and analytical applications. Salidroside (Rhodioloside) is a prolyl endopeptidase inhibitor. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling. Salidroside protects dopaminergic neurons by enhancing PINK1/Parkin-mediated mitophagy.
    Salidroside (Standard)
  • HY-122818
    BpV(phen) trihydrate
    3 Publications Verification

    Bisperoxovanadium(phen) trihydrate

    		 PTEN Phosphatase Parasite Apoptosis Infection Metabolic Disease Inflammation/Immunology Cancer
    BpV(phen) trihydrate, a insulin-mimetic agent, is a potent protein tyrosine phosphatase (PTP) and PTEN inhibitor with IC50s of 38 nM, 343 nM and 920 nM for PTEN, PTP-β and PTP-1B, respectively. BpV(phen) trihydrate inhibits proliferation of the protozoan parasite Leishmania in vitro. bpV(phen) trihydrate strongly induces the secretion of a large number of chemokines and pro-inflammatory cytokines, and it activates a Th1-type pathway (IL-12, IFNγ). BpV(phen) trihydrate can also induce cell apoptosis, and has anti-angiogenic and anti-tumor activity [1] .
    BpV(phen) trihydrate
  • HY-164826
    Acetyl zingerone

    		Interleukin Related Reactive Oxygen Species (ROS) MMP Pyroptosis Ferroptosis Notch Keap1-Nrf2 PINK1/Parkin Mitophagy Caspase Apoptosis Inflammation/Immunology Cancer
    Acetyl zingerone is an analog of Zingerone (HY-14621). Acetyl zingerone downregulates the expression of ROS metabolism-related genes, fibroblast senescence-related genes, keratinocyte differentiation-related genes, and IL-17A target genes. Acetyl zingerone inhibits the activities of MMP-1, MMP-3, and MMP-12, as well as the activation of NLRP3 inflammasome, pyroptosis (pyroptosis), ferroptosis (ferroptosis), cartilage destruction, and UVA-induced cyclobutane pyrimidine dimer formation. Acetyl zingerone upregulates the expression of collagen, proteoglycan, extracellular matrix glycoprotein, Notch pathway, and GPX4 gene, activates Nrf2 and HO-1, induces extracellular matrix synthesis and PINK1/Parkin-mediated mitophagy (mitophagy), and promotes chondrocyte survival. Acetyl zingerone alleviates the progression of osteoarthritis in mice . Acetyl zingerone can be used in research related to skin aging, inflammatory skin diseases, osteoarthritis, melanoma, and non-melanoma skin cancer [1] .
    Acetyl zingerone
  • HY-162325
    WJ-39

    		Aldose Reductase Mitochondrial Metabolism Apoptosis Mitophagy Metabolic Disease
    WJ-39 is an orally active aldose reductase (AR) inhibitor. WJ-39 improves tubular damage in diabetic nephropathy rats by activating PINK1/Parkin signaling, promoting mitophagy, and attenuating apoptosis [1].
    WJ-39
  • HY-100410R
    FCCP (Standard)

    Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (Standard)

    		 Oxidative Phosphorylation PINK1/Parkin Reference Standards Mitochondrial Metabolism Cancer
    FCCP (Standard) is the analytical standard of FCCP. This product is intended for research and analytical applications. FCCP is an uncoupler of oxidative phosphorylation (OXPHOS) in mitochondria. FCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation [1].
    FCCP (Standard)
  • 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 [1].
    FB231
  • HY-152265A
    PARL-IN-1 TFA

    		PINK1/Parkin Mitophagy Neurological Disease
    PARL-IN-1 TFA is a potent PARL inhibitor with an IC50 value of 28 nM. PARL-IN-1 TFA inhibits PARL and leads to a robust activation of the PINK1/Parkin pathway. PARL-IN-1 TFA promotes PINK1/Parkin-dependent mitophagy [1].
    PARL-IN-1 TFA
  • HY-145816
    JPS016

    		PROTACs HDAC Apoptosis PINK1/Parkin Autophagy Reactive Oxygen Species (ROS) Cardiovascular Disease Cancer
    JPS016 is a class I histone deacetylase (HDAC) PROTAC inhibitor. JPS016 recruits the VHL E3 ligase (Ligands for E3 Ligase) to mediate the ubiquitination and proteasomal degradation of HDAC1, HDAC2 and HDAC3. JPS016 reduces the viability of colon cancer cells and induces Apoptosis. JPS016 activates the PINK1/Parkin mitochondrial Autophagy pathway, enhances cardiomyocyte viability, alleviates mitochondrial damage, and reduces mitochondrial ROS production in cells. JPS016 is applicable to research related to colon cancer and sepsis cardiomyopathy [1] .
    JPS016
  • HY-170992
    Autophagy agonist-1

    		Autophagy CDK Atg8/LC3 PINK1/Parkin Cancer
    Autophagy agonist-1 (compound 22) is an Autophagy agonist. Autophagy agonist-1 exhibits significant anticancer activity against HepG2 cells and normal cells with IC50s of 8.8 μM and > 50 μM. Autophagy agonist-1 induces G1/S phase cell cycle arrest and inhibits CDK4 and CyclinD1 expression while upregulating P21. Autophagy agonist-1 promotes the accumulation of autophagosomes and the proteins LC3 and PINK1, enhancing autophagy and mitophagy in HepG2 cells [1].
    Autophagy agonist-1
  • 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-RS23042
    Pink1 Rat Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others

    Pink1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Pink1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.

    Pink1 Rat Pre-designed siRNA Set A
    Pink1 Rat Pre-designed siRNA Set A
  • HY-RS16608
    Pink1 Mouse Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others

    Pink1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Pink1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.

    Pink1 Mouse Pre-designed siRNA Set A
    Pink1 Mouse Pre-designed siRNA Set A
  • 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 [1].
    Antiproliferative agent-70
  • 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)

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