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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
197 Results for "
PINK
" in MedChemExpress (MCE) Product Catalog:
Products (197)
197 Results for "PINK" in MCE Product Catalog:
189
189 Publications Verification
Synonyms: Carbonyl cyanide 3-chlorophenylhydrazone; Carbonyl Cyanide m-Chlorophenylhydrazone
Target:
Oxidative Phosphorylation PINK1/Parkin STING IFNAR Mitochondrial Metabolism Bacterial Apoptosis
Research Areas:
CCCP is an oxidative phosphorylation (OXPHOS) uncoupler. CCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation .
179
179 Cited Publications
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 .
179
179 Cited Publications
Target:
Mitochondrial Metabolism PINK1/Parkin NOD-like Receptor (NLR) Autophagy Calcium Channel Apoptosis
Research Areas:
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 .
120
120 Cited Publications
Synonyms: Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone
Research Areas:
FCCP is an uncoupler of oxidative phosphorylation (OXPHOS) in mitochondria. FCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation .
46
24
14
14 Cited Publications
Synonyms: Tip60 HAT inhibitor
Research Areas:
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 .
13
8
8 Cited Publications
Synonyms: Diazoresorcinol sodium
8
Target:
Research Areas:
Bavdegalutamide (ARV-110) is an orally active, specific androgen receptor (AR) PROTAC degrader. Bavdegalutamide promotes ubiquitination and degradation of AR. Bavdegalutamide can be used for the research of prostate cancer (Pink: AR ligand (HY-168299); Blue: E3 ligase ligand (HY-W093272); Black: linker (HY-W091986)) .
6
Research Areas:
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 .
6
6 Cited Publications
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 .
5
5 Cited Publications
MT-802 is a BTK PROTAC degrader. MT-802 degrades wild-type BTK (DC50 = 14.6 nM) and BTK mutants including E41K, C481S (DC50 = 14.9 nM), C481R, C481Y, C481T, C481F, L528W, and inhibits their Y223 phosphorylation. BI-4732 can be used for the study of Ibrutinib (HY-10997)-resistant chronic lymphocytic leukemia (CLL). (Pink: BTK ligand (HY-150885), Blue: CRBN Ligand (HY-14658), Black: Linker (HY-141371), E3 ligase ligand-linker conjugate (HY-176340)) .
3
3 Cited Publications
Target:
Research Areas:
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 .
2
2 Cited Publications
Cat. No.: HY-160415A
WD6305 TFA is a potent and selective METTL3-METTL14 PROTAC degrader. WD6305 TFA has DC50 values of 140 nM and 194 nM for METTL3 and METTL14, respectively. WD6305 TFA inhibits m 6A modification and proliferation of AML cells, and induces apoptosis. WD6305 TFA has antitumor activity [1].(Pink: UZH2 (HY-115717); Black: Linker; Blue: VHL ligand (HY-150803))
2
2 Cited Publications
Cat. No.: HY-169380
CAS No.: 3099681-58-7
Target:
Research Areas:
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 .
2
2 Cited Publications
Cat. No.: HY-17355A
CAS No.: 104632-27-1
Synonyms: (R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride
Target:
ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS)
Research Areas:
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 .
2
2 Cited Publications
Cat. No.: HY-17355B
CAS No.: 104632-28-2
Synonyms: (R)-Pramipexole; R-(+)-Pramipexole; KNS-760704
Target:
PINK1/Parkin Glutathione Peroxidase Sodium Channel ATP Synthase NOD-like Receptor (NLR) Mitophagy Ferroptosis Autophagy Apoptosis Reactive Oxygen Species (ROS)
Research Areas:
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 .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
