34 Results for "

mitochondria dysfunction

" in MedChemExpress (MCE) Product Catalog:
Products (34)

34 Results for "mitochondria dysfunction" in MCE Product Catalog:

Cat. No.: HY-N8617
CAS No.: 135247-94-8
Trijuganone C is a tanshinone-type diterpenoid compound. Trijuganone C can be isolated from the roots of Salvia miltiorrhiza Bunge. Trijuganone C induces chromatin condensation, DNA fragmentation, activation of Caspase-3, -8 and -9, as well as cleavage of PARP. Trijuganone C activates Bid and Bax, leading to loss of mitochondrial membrane potential and inducing the release of cytochrome c from mitochondria into the cytosol. Trijuganone C exerts antiproliferative effects through Apoptosis induction mediated by Mitochondrial dysfunction and Caspase activation. Trijuganone C exhibits significant antiproliferative activity against leukemia cells and colon cancer cells .
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Cat. No.: HY-158726
CAS No.: 2480150-28-3
Complex 3 is a fluorescent dithiocarbazate-copper complex with anticancer activity, which localizes to mitochondria. Complex 3 displays excitation/emission maxima of 455-495/535 nm, respectively. Complex 3 inhibits the growth of BxPC-3, AsPC-1, PANC-1, and WI38 pancreatic cancer cells with IC50 values of 0.74, 0.41, 0.62, and 2.06 µM, respectively. Complex 3 induces lipid peroxidation and mitochondrial rupture and shrinkage in AsPC-1 cells. Complex 3 also induces mitochondrial apoptosis and cytokine-cytokine receptor interaction dysfunction in AsPC-1 cells. Complex 3 reduces tumor volume in an AsPC-1 mouse xenograft model .
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Cat. No.: HY-155719
Target:  

Paraptosis

Domaines de recherche:  

Cancer

fac-[Re(CO)3(L3)(H2O)][NO3] (compound 3), the rhenium(I) tricarbonyl aqua complex, is an anticancer agent associated with mitochondrial dysfunction. fac-[Re(CO)3(L3)(H2O)][NO3] is cytotoxic to prostate cancer cells with IC50=0.32 μM (PC-3 cells). fac-[Re(CO)3(L3)(H2O)][NO3] mainly accumulates in mitochondria, down-regulates ATP production in PC3 cells, and promotes paraptosis. However, fac-[Re(CO)3(L3)(H2O)][NO3] did not induce necrosis, apoptosis and autophagy .
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Cat. No.: HY-113402B
Synonyms: γ-Glu-Cys ammonium
Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
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Cat. No.: HY-184173
OXPHOS-IN-3 is a mitochondria-targeted dual OXPHOS/glycolysis inhibitor. OXPHOS-IN-3 exhibits potent antiproliferative activity against pancreatic cancer cells. OXPHOS-IN-3 induces mitochondrial dysfunction, ferroptosis, and immunogenic cell death (ICD). OXPHOS-IN-3 shows potent antitumor activity in pancreatic ductal adenocarcinoma (PDAC) models .
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Cat. No.: HY-L155
545 compounds

Mitochondria, as the main place of energy supply in life, is essential to maintain normal life activities. Mitochondrial dysfunction is associated with common diseases, such as cardiovascular diseases, neurodegenerative diseases, diabetes and cancer. The heart, brain and liver rely heavily on mitochondrial function as the main organs for drug metabolism. In addition, mitochondria is also a target of many drugs, some of which induce organotoxicity by inducing mitochondrial toxicity.

MCE contains 545 mitochondrial toxic compounds, which can be used as tool compounds for drug development and disease mechanism research.

Cat. No.: HY-P10707
Target:  

Endogenous Metabolite

Domaines de recherche:  

Inflammation/Immunology

Tpp-CAQK can bind to mitochondria, enabling the construction of an engineered mitochondrial compound, Mito-Tpp-CAQK, with excellent bioactivity. Mito-Tpp-CAQK can be internalized by macrophages, thereby enhancing the phagocytosis of myelin debris, alleviating mitochondrial dysfunction, and reducing proinflammatory profiles, ultimately facilitating tissue repair and functional recovery in mice after spinal cord injury .
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Cat. No.: HY-P10707A
Target:  

Endogenous Metabolite

Domaines de recherche:  

Inflammation/Immunology

Tpp-CAQK TAF can bind to mitochondria, enabling the construction of an engineered mitochondrial compound, Mito-Tpp-CAQK TFA, with excellent bioactivity. Mito-Tpp-CAQK TFA can be internalized by macrophages, thereby enhancing the phagocytosis of myelin debris, alleviating mitochondrial dysfunction, and reducing proinflammatory profiles, ultimately facilitating tissue repair and functional recovery in mice after spinal cord injury .
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Cat. No.: HY-182266
FBP is a mitochondria-targeted, selective anticancer agent. FBP induces oxidative stress and mitochondrial dysfunction, leading to Apoptosis. FBP generates ROS and causes double-strand DNA breaks in cancer cells. FBP exhibits cytotoxic efficacy against cancer cells, with cervical cancer cells being the most sensitive. FBP can be used for the research of cervical cancer, lung cancer, melanoma and breast cancer .
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Cat. No.: HY-L144
1,112 compounds

Normal mitochondrial function is critical for maintaining cellular homeostasis because mitochondria produce ATP and are the major intracellular source of free radicals. Cellular dysfunctions induced by intracellular or extracellular insults converge on mitochondria and induce a sudden increase in permeability on the inner mitochondrial membrane, the so-called mitochondrial membrane permeability transition (MMPT). MMPT is caused by the opening of pores in the inner mitochondrial membrane, matrix swelling, and outer membrane rupture. The MMPT is an endpoint to initiate cell death because the pore opening together with the release of mitochondrial cytochrome c activates the apoptotic pathway of caspases.

The normal operation of mitochondrial function is important for maintaining normal cell death and treatment of mitochondrial diseases. MCE offers a unique collection of 1,112 compounds with identified and potential mitochondrial protective activity. MCE Mitochondrial Protection Compound Library is critical for drug discovery and development.

Cat. No.: HY-D3148
CAS No.: 1804107-88-7
Target:  

Fluorescent Dye

Domaines de recherche:  

Others

TPE-Ph-In is a mitochondria-targeted voltage-sensitive probe that can be used for mitochondrial membrane potential detection, mitochondrial imaging of animal and plant cells and tissues, mouse sperm activity indication, and detection of mitochondrial membrane potential changes associated with early apoptosis. TPE-Ph-In is non-fluorescent in solution, but emits strong fluorescence when aggregated via restriction of intramolecular rotation/movement, and its fluorescence intensity is directly correlated with local probe concentration or mitochondrial membrane potential level. TPE-Ph-In can penetrate cell membranes, target mitochondria through charge-dependent accumulation, has low cytotoxicity and high photostability, and enables super-resolution imaging of plant mitochondrial fission, fusion and cristae structures. The excitation wavelengths of TPE-Ph-In include 450 nm, 488 nm, and 489 nm, while its emission wavelengths include 551-661 nm, 660 nm, and 694 nm. TPE-Ph-In can be used for studies on mitochondrial dysfunction associated with early apoptosis .
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Cat. No.: HY-112879R
CAS No.: 1334850-99-5
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/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 .
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Cat. No.: HY-184265
CAS No.: 1993461-76-9
Synonyms: Mito-Esc
Mito-Esculetin (Mito-Esc) is an orally active mitochondria-targeted derivative of Esculetin (HY-N0284). Mito-Esculetin inhibits LPS-induced phosphorylation of STAT3 Tyr-705, partially reverses LPS-mediated depletion of SIRT3, and enhances the AMPK-SIRT1 signaling axis. Mito-Esculetin inhibits PAI-1 activity, regulates miRNA, and induces phosphorylation of IRS and AKT. Mito-Esculetin suppresses oxidant-induced endothelial dysfunction, Ang-II (HY-13948)- and high glucose-induced atherosclerotic plaque formation, Palmitate (HY-N0830)-induced insulin resistance, as well as high glucose-mediated endothelial cell senescence and inflammatory responses. Mito-Esculetin reduces body weight and non-esterified fatty acid (NEFA) levels. Mito-Esculetin can be used in research related to acute coronary syndrome, type 2 diabetes, and hyperglycemia-induced atherosclerosis .
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Cat. No.: HY-L064
1,827 compounds

Glutamine is an important metabolic fuel that helps rapidly proliferating cells meet the increased demand for ATP, biosynthetic precursors, and reducing agents. Glutamine Metabolism pathway involves the initial deamination of glutamine by glutaminase(GLS), yielding glutamate and ammonia. Glutamate is converted to the TCA cycle intermediate α-ketoglutarate (α-KG) by either glutamate dehydrogenase (GDH) or by the alanine or aspartate transaminases (TAs), to produce both ATP and anabolic carbons for the synthesis of amino acids, nucleotides and lipids. During periods of hypoxia or mitochondrial dysfunction, α-KG can be converted to citrate in a reductive carboxylation reaction catalyzed by IDH2. The newly formed citrate exits the mitochondria where it is used to synthesize fatty acids and amino acids and produce the reducing agent, NADPH.

Cancer cells display an altered metabolic circuitry that is directly regulated by oncogenic mutations and loss of tumor suppressors. Mounting evidence indicates that altered glutamine metabolism in cancer cells has critical roles in supporting macromolecule biosynthesis, regulating signaling pathways, and maintaining redox homeostasis, all of which contribute to cancer cell proliferation and survival. Thus, intervention in glutamine metabolic processes could provide novel approaches to improve cancer treatment.

MCE owns a unique collection of 1,827 compounds targeting the mainly proteins and enzymes involved in glutamine metabolism pathway. Glutamine Metabolism compound library is a useful tool for intervention in glutamine metabolic processes.