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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
38 Results for "
mitochondrial membrane potential loss
" in MedChemExpress (MCE) Product Catalog:
Products (38)
38 Results for "mitochondrial membrane potential loss" in MCE Product Catalog:
186
186 Publications Verification
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 .
186
186 Publications Verification
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 .
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1 Cited Publications
Cat. No.: HY-N1983
CAS No.: 38395-02-7
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Research Areas:
Sodium metavanadate, 99% (Sodium vanadate (V), 99%) is an orally active phosphate structural analog and protein tyrosine phosphatase (PTPases) inhibitor. Sodium metavanadate, 99% mimics phosphate to interfere with phosphoprotein reactions, inhibits GAPDH, Na +/K +-ATPase and microbial membrane ATPase, and acts as a terminal electron acceptor for anaerobic respiration. Sodium metavanadate, 99% induces ROS production, G2/M phase arrest, mitochondrial membrane potential loss and apoptosis in breast cancer cells, and reduces tumor volume in tumor-bearing mice. Sodium metavanadate, 99% also exhibits oral insulin-sensitizing and metabolic regulatory activities, and reduces plasmodium parasitemia levels. Sodium metavanadate, 99% can be used in studies related to cadmium exposure-induced metabolic syndrome, plasmodium infection, breast cancer and type 1 diabetes .
Cat. No.: HY-156202
CAS No.: 35750-48-2
Target:
Research Areas:
Geranylgeranoic acid (Compound 5) is inhibits lysine-specific demethylase 1 (LSD1) with an IC50 value of 46.97 µM. Geranylgeranoic acid induces apoptosis via loss of the mitochondrial membrane potential and activation of interleukin-1β-converting enzyme (ICE) and cysteine protease precursor 32 (CPP32) in Huh7 and PLC/PRF/5 human hepatoma cells and MLE-10 transformed mouse hepatocytes. Geranylgeranoic acid an isoprenoid with anticancer activity, which is found in S. chinensis .
Research Areas:
Coenzyme Q2 is a benzoquinone electron carrier in the mitochondrial electron transport chain and a p53-dependent apoptosis inducer. Coenzyme Q2 induces p53 phosphorylation at Ser15, promoting p53 accumulation and functional activation. Coenzyme Q2 induces ROS generation, caspase-3 activation, DNA fragmentation, phosphatidylserine externalization, mitochondrial permeability transition pore opening, and oxidative phosphorylation uncoupling. Coenzyme Q2 inhibits Complex I, Complex III, and Complex IV activities, disrupting electron transport and membrane potential generation. Coenzyme Q2 induces excessive mitochondrial proton leak in forebrain mitochondria. Coenzyme Q2 causes loss of righting reflex in mice, accompanied by slow-wave delta EEG activity and reversible loss of wakefulness. Coenzyme Q2 inhibits lipid peroxidation and scavenges superoxide radicals. Coenzyme Q2 is used in research on leukemia, myocardial ischemia-reperfusion injury, and mitochondrial encephalomyopathy .
Cat. No.: HY-P990189
Cat. No.: HY-148365
Purity: 98.02%
Target:
Research Areas:
NecroIr1 is an iridium(III) complex, serves as necroptosis inducers in Cisplatin (HY-17394)-resistant lung cancer cells (A549R). NecroIr1 selectively accumulates in mitochondria, leading to oxidative stress and loss of mitochondrial membrane potential (MMP). NecroIr1 activates receptor-interacting serine-threonine kinase 3 (RIPK3) and Mixed Lineage Kinase (MLKL), and regulates CDK4 expression .
Cat. No.: HY-148366
Purity: 98.99%
Target:
Research Areas:
NecroIr2 is an iridium(III) complex, serves as necroptosis inducers in Cisplatin (HY-17394)-resistant lung cancer cells (A549R). NecroIr2 selectively accumulates in mitochondria, leading to oxidative stress and loss of mitochondrial membrane potential (MMP). NecroIr2 activates receptor-interacting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like pseudokinase (MLKL), and regulates CDK4 expression .
Target:
Research Areas:
MPT0B392, an orally active quinoline derivative, induces c-Jun N-terminal kinase (JNK) activation, leading to apoptosis. MPT0B392 inhibits tubulin polymerization and triggers induction of the mitotic arrest, followed by mitochondrial membrane potential loss and caspases cleavage by activation of JNK and ultimately leads to apoptosis. MPT0B392 is demonstrated to be a novel microtubule-depolymerizing agent and enhances the cytotoxicity of sirolimus in sirolimus-resistant acute leukemic cells and the multidrug resistant cell line .
Cat. No.: HY-N1983R
CAS No.: 38395-02-7
Cat. No.: HY-14764
CAS No.: 333963-42-1
Synonyms: SPI 8811
Research Areas:
Cobiprostone (SPI 8811) is a type-2 chloride channel activator. Cobiprostone protects against Indomethacin (HY-14397)-induced depolarization of mitochondrial membrane potential and reverses the loss of mitochondrial membrane potential. Cobiprostone protects against NSAID-induced cellular damage .
Cat. No.: HY-143279
CAS No.: 99140-25-7
Target:
Research Areas:
Topoisomerase II inhibitor 3 (Compound 6 h ) is a acridone derivatives, as well as a Type II DNA topoisomerase (topo II) inhibitor , as a topo IIα/β inhibitor with the value of IC50 is 0.17 μM for topo IIα and the value of IC50 is 0.23 μM for topo IIβ subtypes, caused obvious DNA damage, and induced apoptosis by triggering the loss of mitochondrial membrane potential .
PT-262 is a potent ROCK inhibitor with an IC50 value of around 5 μM. PT-262 induces the loss of mitochondrial membrane potential and elevates the caspase-3 activation and apoptosis. PT-262 inhibits the ERK and CDC2 phosphorylation via a p53-independent pathway. PT-262 blocks cytoskeleton function and cell migration. PT-262 has anti-cancer activity .
Cat. No.: HY-121642
CAS No.: 1169831-01-9
SL-017 is a novel photoacoustic sensitizer and a derivative of photofrin B. It can be taken up by cells to the maximum extent within 30 minutes and is mainly localized in mitochondria. After being activated by visible light or ultrasound, SL-017 can significantly increase the production of reactive oxygen species (ROS). Low concentrations of SL-017 can rapidly cause the loss of mitochondrial membrane potential. SL-017 can also cause mitochondrial fragmentation, a process that occurs after the loss of membrane potential. Epoxyeicosatrienoic acids (EETs) can alleviate the loss of mitochondrial membrane potential caused by SL-017, but the antioxidant ascorbic acid has no such effect. These characteristics indicate that SL-017 mainly targets mitochondria and exerts its cytotoxic effect by triggering the collapse of mitochondrial membrane potential, generating ROS, and causing mitochondrial fragmentation. As a novel photoacoustic sensitizer, SL-017 has potential application value in photodynamic therapy and sonodynamic therapy.
Cat. No.: HY-139828
CAS No.: 2762698-14-4
Anticancer agent 14 is a lead compound (IC50: 0.20 to 0.65 μM) that induces apoptosis, cell cycle arrest, and loss of mitochondrial membrane potential in breast cancer cells.
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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
