270 Results for "

Mitochondrial Dysfunction

" in MedChemExpress (MCE) Product Catalog:
Products (270)

270 Results for "Mitochondrial Dysfunction" in MCE Product Catalog:

Cat. No.: HY-184749
Target:  

Topoisomerase Apoptosis

Research Areas:  

Cancer

Topoisomerase I-IN-24 (compound 5l) is a topoisomerase I (topoisomerase I) inhibitor. Topoisomerase I-IN-24 inhibits topoisomerase I activity in a concentration-dependent manner, suppresses cancer cell migration, induces apoptosis (apoptosis), and arrests the cell cycle at the G1 phase. Topoisomerase I-IN-24 can be used in the research of lung cancer, hepatocellular carcinoma and cervical adenocarcinoma .
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Cat. No.: HY-187518
CAS No.: 3134912-65-2
Research Areas:  

Infection

NMT-IN-9 is an arylpyrrolidone-based NMT inhibitor with an IC50 of 93.20 nM and a KD of 5.57 × 10 -9 M against NMT. NMT-IN-9 exhibits broad-spectrum antifungal activity against Candida albicans, Candida glabrata, Candida tropicalis, Cryptococcus neoformans and Aspergillus fumigatus, with an MIC of 2-16 μg/mL, and retains activity against fluconazole-resistant Candida isolates, with an MIC of 8-16 μg/mL. NMT-IN-9 induces intracellular ROS accumulation, mitochondrial membrane depolarization, DNA damage, apoptosis and necrotic cell death in fungal cells, and disrupts fungal cell integrity. NMT-IN-9 can be used for studies on NMT-targeted antifungal mechanisms and fluconazole-resistant Candida infections .
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Cat. No.: HY-155719
Target:  

Paraptosis

Research Areas:  

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-176149
Research Areas:  

Cancer

Fluoxetine-Conjugated Platinum(IV) prodrug-1 (Compound 8) is an eEF2K inhibitor. Fluoxetine-Conjugated Platinum(IV) prodrug-1 inhibits cancer cell proliferation, induces DNA damage, cell cycle arrest at S phase and apoptosis. Fluoxetine-Conjugated Platinum(IV) prodrug-1 induces ROS accumulation and mitochondrial dysfunction. Fluoxetine-Conjugated Platinum(IV) prodrug-1 inhibits TNBC cell migration and invasion by inhibiting MMP-2 activity. Fluoxetine-Conjugated Platinum(IV) prodrug-1 induces autophagy in TNBC cells by activating AMPK. Fluoxetine-Conjugated Platinum(IV) prodrug-1 has antitumor activity and activates immunosuppression in the 4T1-Luc mouse model. Fluoxetine-Conjugated Platinum(IV) prodrug-1 can be used in triple-negative breast cancer (TNBC) research .
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Cat. No.: HY-N2160
CAS No.: 77690-92-7
6'''-Feruloylspinosin is an orally active RORα activator that crosses the blood-brain barrier, with a Kd of 0.308 μM, and is found in natural sources. 6'''-Feruloylspinosin modulates AMPK and mTOR phosphorylation. 6'''-Feruloylspinosin promotes autophagy through the AMPK/mTOR signaling pathway, inhibits GSK3β phosphorylation at Tyr216, and activates the PGC-1α/Nrf2/HO-1 pathway. 6'''-Feruloylspinosin regulates neurotransmitter levels, enhances mRNA expression of GABAA α1, α5, and GABAB R1 receptor subunits, increases brain 5-HT and GABA, restores melatonin levels, and ameliorates anxiety-like behaviors. 6'''-Feruloylspinosin regulates oxidative stress homeostasis, inhibits mitochondrial dysfunction, decreases MDA while increasing GSH. 6'''-Feruloylspinosin can be used for research on Alzheimer's disease, acute myocardial infarction, heart failure with insomnia, and insomnia .
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Cat. No.: HY-N3201
CAS No.: 630057-39-5
Neoprzewaquinone (NEO) is an orally active phenanthraquinone derivative isolated from Salvia miltiorrhiza Bunge. Neoprzewaquinone A inhibits IL-15Rα, blocks the ROCK2/STAT3 pathway to impair the migration and invasion abilities of triple-negative breast cancer cells; induces apoptosis of hepatocellular carcinoma cells by inhibiting the PI3K-AKT pathway; suppresses LPS-induced inflammation via binding to TLR4/MD2, and inhibits IL-15-induced proliferation, migration and phagocytosis of microglial cells; protects osteoblasts from mitochondrial dysfunction and apoptosis in diabetic osteoporosis by activating PRKD2 and the ELF5/PRKD2/PI3K/AKT/mTOR axis. Neoprzewaquinone A can be used in the research of diseases including rheumatoid arthritis, hepatocellular carcinoma, diabetic osteoporosis and triple-negative breast cancer .
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Cat. No.: HY-183805
Target:  

5-HT Receptor FAAH

Research Areas:  

Neurological Disease

5-HT6R/FAAH modulator 2 is a dual 5-HT6R antagonist and FAAH inhibitor with human 5-HT6R pKi 7.24, human FAAH pIC50 5.47, and blood-brain barrier penetration.5-HT6R/FAAH modulator 2 modulates serotonergic signaling, blocks 5-HT6R function, inhibits endocannabinoid degradation via FAAH catalytic activity suppression.5-HT6R/FAAH modulator 2 exhibits neuroprotective effects against mitochondrial dysfunction, amyloid-β, and glutamate-induced toxicity, reverses memory deficits.5-HT6R/FAAH modulator 2 shows reduced cytotoxicity relative to oxygen-containing lead compounds.5-HT6R/FAAH modulator 2 can be used for the research of Alzheimer's disease .
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Cat. No.: HY-N0430
CAS No.: 3486-66-6
Synonyms: Coptisin
Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
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Cat. No.: HY-181413
CAS No.: 3093642-25-9
PROTAC EZH2 Degrader-44 (compound 60) is a highly efficient PROTAC degrader targeting the EZH2-PRC2 complex. By recruiting the CRBN E3 ligase and relying on the proteasome system, PROTAC EZH2 Degrader-44 simultaneously induces the degradation of core components EZH2, SUZ12 and EED, thereby significantly reducing the levels of H3K27me3 and CARM1. PROTAC EZH2 Degrader-44 exerts antiproliferative effects through a dual mechanism: on the one hand, it triggers mitochondrial dysfunction leading to decreased membrane potential; on the other hand, it strongly promotes apoptosis by regulating Bcl-2 family proteins (upregulating Bax, Caspase-3 and PARP, and downregulating Bcl-2). PROTAC EZH2 Degrader-44 exhibits only extremely low cytotoxicity in human normal mammary epithelial, liver and kidney cells, showing a favorable safety window. PROTAC EZH2 Degrader-44 is an ideal tool molecule for exploring the mechanisms of targeted therapy for triple-negative breast cancer .
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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.