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Results for "

mitochondria dysfunction

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Adrenergic Receptor (2) Apoptosis (3) AUTACs (1) Autophagy (1) Isotope-Labeled Compounds (1) Mitophagy (1) Paraptosis (1) Potassium Channel (2) Sodium Channel (2)
By Research Areas:	Cancer (6) Cardiovascular Disease (3) Inflammation/Immunology (2) Metabolic Disease (1) Neurological Disease (3)

Inhibitors & Agonists

Screening Libraries

Peptides

Natural
Products

Isotope-Labeled Compounds

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-113341

7β-Hydroxycholesterol 1 Publications Verification	Others	Cardiovascular Disease Neurological Disease Inflammation/Immunology
7β-Hydroxycholesterol is an oxysterol that derived by the oxidation of cholesterol. 7β-hydroxycholesterol is a powerful inducer of oxidative stress, inducing dysfunction of organelles (mitochondria, lysosomes and peroxisomes) that can cause cell death .

HY-147225

TSPO Ligand-Linker Conjugates 1	AUTACs Mitophagy	Neurological Disease Metabolic Disease Cancer
TSPO Ligand-Linker Conjugates 1 contains a ligand for translocator protein (TSPO) and a linker, which is used for the synthesis of mitochondria-targeting autophagy-targeting chimera (AUTAC). AUTAC can bind the TSPO on the outer mitochondrial membrane (OMM) of mitochondria and degrades impaired mitochondria and proteins via mitophagy, and improves mitochondrial activity. TSPO Ligand-Linker Conjugates 1 can be used in mitochondrial dysfunction related research, including neurodegenerative diseases, cancer, and diabetes .

HY-N2858

Alpinumisoflavone acetate	Apoptosis	Cancer
Alpinumisoflavone acetate is a anticancer agent. Alpinumisoflavone acetate shows antiproliferative activity. Alpinumisoflavone acetate decreases the expression of phosphorylation of ERK1/2. Alpinumisoflavone acetate induces mitochondrial dysfunction and mitochondria-mediated Apoptosis. Alpinumisoflavone acetate has the potential for the research of HCC .

HY-P3003

Cereulide	Apoptosis	Neurological Disease Inflammation/Immunology
Cereulide, a toxin depsipeptide, can be produced by Bacillus cereus. Cereulide induces cell apoptosis. Cereulide acts on mitochondria, leading to dysfunction in different organs (liver, pancreatic islet, brain, intestines, etc.) and body systems (immune system and nervous system) .

HY-162344

Ir-CA	Apoptosis Autophagy	Cancer
Ir-CA is an antitumor agent. Ir-CA can accumulate in mitochondria and induces mitochondria dysfunction. Ir-CA induces apoptosis and autophagy. Ir-CA initiates mitophagy and cell cycle arrest to kill Cisplatin (HY-17394)-resistant A549R cells. Ir-CA can effectively inhibit metastasis by inhibiting MMP-2/MMP-9 .

HY-113341S

7ß-Hydroxycholesterol-d7	Isotope-Labeled Compounds
7ß-Hydroxycholesterol-d₇ is the deuterium labeled 7α-Hydroxycholesterol. 7β-Hydroxycholesterol is an oxysterol that derived by the oxidation of cholesterol. 7β-hydroxycholesterol is a powerful inducer of oxidative stress, inducing dysfunction of organelles (mitochondria, lysosomes and peroxisomes) that can cause cell death[1][2].

HY-B0432

Propafenone 1 Publications Verification SA-79	Sodium Channel Adrenergic Receptor Potassium Channel	Cardiovascular Disease Cancer
Propafenone (SA-79), a sodium-channel blocker, acts an antiarrhythmic agent. Propafenone also has high affinity for the β receptor (IC₅₀=32 nM) . Propafenone blocks the transient outward current (Ito) and the sustained delayed rectifier K current (Isus) with IC₅₀ values of 4.9 μm and 8.6 μm, respectively . Propafenone suppresses esophageal cancer proliferation through inducing mitochondrial dysfunction and induce apoptosis .

HY-B0432R

Propafenone (Standard)	Sodium Channel Adrenergic Receptor Potassium Channel	Cardiovascular Disease Cancer
Propafenone (Standard) is the analytical standard of Propafenone. This product is intended for research and analytical applications. Propafenone (SA-79), a sodium-channel blocker, acts an antiarrhythmic agent. Propafenone also has high affinity for the β receptor (IC₅₀=32 nM) . Propafenone blocks the transient outward current (Ito) and the sustained delayed rectifier K current (Isus) with IC₅₀ values of 4.9 μm and 8.6 μm, respectively . Propafenone suppresses esophageal cancer proliferation through inducing mitochondrial dysfunction and induce apoptosis .

HY-155719

fac-[Re(CO)3(L3)(H2O)][NO3]	Paraptosis	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 .

Cat. No.	Product Name

HY-L155

Mitochondrial Toxicity Compound Library	477 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 477 mitochondrial toxic compounds, which can be used as tool compounds for drug development and disease mechanism research.

Mitochondrial Toxicity Compound Library

477 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 477 mitochondrial toxic compounds, which can be used as tool compounds for drug development and disease mechanism research.

HY-L144

Mitochondrial Protection Compound Library	596 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 596 compounds with identified and potential mitochondrial protective activity. MCE Mitochondrial Protection Compound Library is critical for drug discovery and development.

Mitochondrial Protection Compound Library

596 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 596 compounds with identified and potential mitochondrial protective activity. MCE Mitochondrial Protection Compound Library is critical for drug discovery and development.

HY-L064

Glutamine Metabolism Compound Library	924 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 924 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.

Glutamine Metabolism Compound Library

924 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 924 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.

Cereulide	Apoptosis	Neurological Disease Inflammation/Immunology
Cereulide, a toxin depsipeptide, can be produced by Bacillus cereus. Cereulide induces cell apoptosis. Cereulide acts on mitochondria, leading to dysfunction in different organs (liver, pancreatic islet, brain, intestines, etc.) and body systems (immune system and nervous system) .

Cat. No.	Product Name	Category	Target	Chemical Structure