PINK1/Parkin Activator

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 Na_v1.8 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.

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.

Ciliatoside A is a naturally bioactive compound that exhibits significant anti-inflammatory, antiviral, and neuroprotective activities. Ciliatoside A serves as a mitophagy inducer and NLRP3 inflammasome inhibitor, activating AMPK, SIRT1, and the PINK1/Parkin axis, and inhibiting pyroptosis and apoptosis. Ciliatoside A promotes autophagic flux, autophagosome-lysosome fusion, mTOR inhibition, and p62-dependent HBc degradation; reduces Aβ aggregation, plaque deposition, microglial/astrocyte activation, and bacterial load; and maintains neuronal integrity, mitochondrial membrane potential, and ATP production. Ciliatoside A is used in research on Alzheimer's disease, Klebsiella pneumoniae-induced pneumonia, hepatitis B virus infection, and inflammation.

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.

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 Na_v1.8 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.

Nivitol (UP302) is a natural phenolic compound discovered from Dianella ensifolia and also acts as a Tyrosinase inhibitor. Nivitol competitively and reversibly inhibits tyrosinase, suppressing melanin production. Nivitol inhibits homogentisate 1,2-dioxygenase (HGD). In human leukemia cells, Nivitol inhibits PI3K/AKT pathway phosphorylation, increases ROS, decreases mitochondrial membrane potential, and induces G2/M cell cycle arrest, apoptosis, and PINK1/Parkin-mediated mitophagy. Nivitol exhibits inhibition of tumor growth in the MV411 xenograft mouse model. Nivitol is used for research on exogenous ochronosis, hyperpigmentation, and leukemia.

Mito-TEMPO (Standard) is the analytical standard of Mito-TEMPO (HY-112879). This product is intended for research and analytical applications. Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/ParK_in pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca²⁺ 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 K_idney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke.

Cyflumetofen (Standard) is the analytical standard of Cyflumetofen (HY-W663938). This product is intended for research and analytical applications. Cyflumetofen is a non-systemic acylacetonitrile Acaricide. Cyflumetofen interferes with the Wnt/β-catenin signaling pathway, induces Apoptosis, and reduces the level of tight junction proteins. Cyflumetofen upregulates the expression of Pink1, Parkin and Lrrk2 genes associated with the pathogenesis of Parkinson's disease in zebrafish larvae. Cyflumetofen induces developmental toxicity and oxidative stress in zebrafish larvae, damages neurons, reduces motor activity, alters brain tissue structure, and disrupts blood-brain barrier structure. Cyflumetofen exhibits acaricidal activity against spider mites. Cyflumetofen can be used in studies related to Parkinson's disease and infestations by spider mites (Tetranychus urticae, Tetranychus kanzawai, Panonychus citri).