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Results for "

mitochondrial membrane lipid peroxidation

" in MedChemExpress (MCE) Product Catalog:

13

Inhibitors & Agonists

3

Fluorescent Dyes

1

Biochemical Assay Reagents

2

Peptides

1

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-125623
    MitoPerOx
    3 Publications Verification

    Fluorescent Dye Others
    MitoPerOx is a mitochondrial-targeted, lipid peroxidation-indicating fluorescent probe with BODIPY581/591 fluorophores. The triphenylphosphine cation (TPP+) of MitoPerOx can be selectively enriched in mitochondria (depending on membrane potential) and can be used to detect lipid peroxidation in the inner mitochondrial membrane. Under the action of lipid peroxides, the BODIPY581/591 fluorophores of MitoPerOx shift their emission wavelength from 590 nm (reduced state) to 520 nm (oxidized state), and ratiometric detection can be performed at an excitation wavelength of 488 nm. MitoPerOx can specifically monitor the peroxidation of mitochondrial phospholipids (especially cardiolipin) and is used in the study of oxidative stress-related diseases (such as aging, neurodegenerative diseases, and mitochondrial dysfunction)[1][2].
    MitoPerOx
  • HY-N0663

    Mitochondrial Metabolism Cyclophilin Potassium Channel Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Talatisamine is an orally active cyclophilin D activator isolated from the roots of Aconitum carmichaeli Debx. Talatisamine exerts biological functions by activating cyclophilin D, inhibiting Ca 2+-dependent opening of the mitochondrial permeability transition pore (mPTP) (IC50=78 μM), and blocking delayed rectifier K + channels (IC50=146 μM). Talatisamine possesses both antioxidant and membrane-stabilizing properties, effectively inhibits lipid peroxidation and protects mitochondrial membrane function. Talatisamine exhibits multiple activities including antiarrhythmic, hypotensive, anti-inflammatory, anticancer and neuroprotective effects. Talatisamine finds applications in the research of ischemic diseases, rheumatoid arthritis, inflammation-related diseases and Alzheimer's disease .
    Talatisamine
  • HY-DY1073

    Fluorescent Dye Others
    MitoPerOx (solution) is a mitochondrial-targeted, lipid peroxidation-indicating fluorescent probe with BODIPY581/591 fluorophores. The triphenylphosphine cation (TPP+) of MitoPerOx can be selectively enriched in mitochondria (depending on membrane potential) and can be used to detect lipid peroxidation in the inner mitochondrial membrane. Under the action of lipid peroxides, the BODIPY581/591 fluorophores of MitoPerOx shift their emission wavelength from 590 nm (reduced state) to 520 nm (oxidized state) , and ratiometric detection can be performed at an excitation wavelength of 488 nm. MitoPerOx can specifically monitor the peroxidation of mitochondrial phospholipids (especially cardiolipin) and is used in the study of oxidative stress-related diseases (such as aging, neurodegenerative diseases, and mitochondrial dysfunction) .
    Solvent and concentration: DMSO: 2 mM
    MitoPerOx (solution)
  • HY-P1723
    Spexin
    2 Publications Verification

    Neuropeptide Q

    Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Neurological Disease
    Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .
    Spexin
  • HY-W040255

    PGPC

    Ferroptosis FABP Caspase Interleukin Related Apoptosis Inflammation/Immunology
    1-Palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine is an oxidized phospholipid. 1-Palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine reduces the viability of HUVECs, increases the levels of ferrous ions and lipid peroxidation, promotes the production of superoxide anions, and decreases the levels of glutathione and GPX4 in cells. 1-Palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine upregulates the mRNA and protein levels of FABP3 in HUVECs, impairs mitochondrial membrane potential, and induces ferroptosis-related changes as well as mitochondrial dysfunction and damage. 1-Palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine activates caspase-11 and promotes the continuous release of IL-1β from macrophages and dendritic cells. 1-Palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine inhibits the proliferation of aortic smooth muscle cells and induces apoptosis in these cells. 1-Palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine is applicable to relevant research on atherosclerosis .
    1-Palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine
  • HY-P1723A

    Neuropeptide Q TFA

    Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy Cardiovascular Disease Metabolic Disease
    Spexin (Neuropeptide Q) TFA is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin TFA can function through both central and peripheral actions. Spexin TFA upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin TFA improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin TFA can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .
    Spexin TFA
  • HY-W686216

    Dopamine Receptor Neurological Disease
    VK-28 is a blood-brain barrier-permeable iron chelator. VK-28 inhibits mitochondrial membrane lipid peroxidation and the iron-dependent generation of reactive hydroxyl radicals. VK-28 exhibits neuroprotective activity and protects rats against 6-OHDA-induced striatal dopaminergic damage. VK-28 can be used in studies related to Parkinson's disease .
    VK-28
  • HY-179016

    Ferroptosis Apoptosis Mitochondrial Metabolism Calcium Channel Cancer
    Ferroptosis/apoptosis inducer-3 (Compound 34) is a Ferroptosis and Apoptosis inducer. Ferroptosis/apoptosis inducer-3 induces both Ferroptosis and Apoptosis by causing G2/M phase cell cycle arrest, disrupting mitochondrial membrane potentials, promoting lipid peroxidation, and increasing the levels of Ca 2+ and Fe 2+ through the activation of calcium/calmodulin signaling. Ferraplasm/apoptosis inducer-3 shows anticancer effects against cervical cancer, adenocarcinoma, breast cancer, colon cancer, and colorectal carcinoma .
    Ferroptosis/apoptosis inducer-3
  • HY-D3381

    Fluorescent Dye Others
    MitoCLox is a mitochondria-targeted ratiometric fluorescent probe for measuring mitochondrial inner membrane lipid peroxidation .
    MitoCLox
  • HY-182295

    Reactive Oxygen Species (ROS) Apoptosis MMP Bacterial Parasite Cardiovascular Disease Infection Neurological Disease
    Negundoside is an iridoid glycoside compound. Negundoside exhibits hepatoprotective effects, reduces ROS, lipid peroxidation and intracellular calcium ion levels, and prevents the decrease of mitochondrial membrane potential (MMP) and apoptosis (apoptosis). Negundoside has neuroprotective effects, improves behavioral deficits, alleviates oxidative damage, and ameliorates cerebral infarction. Negundoside also possesses antibacterial and antiparasitic activities .
    Negundoside
  • HY-183621

    Parasite Reactive Oxygen Species (ROS) Autophagy Infection
    Antileishmanial agent-43 is a 3,4,5‑trisubstituted isoxazole with selective antileishmanial activity. Antileishmanial agent-43 shows IC50 values of 12.7 μM against Leishmania amazonensis promastigotes and 0.96 μM against intracellular amastigotes. Antileishmanial agent-43 induces ROS elevation, oxidative stress and mitochondrial dysfunction, resulting in lipid peroxidation, mitochondrial depolarization and ATP imbalance. Antileishmanial agent-43 causes cell shrinkage, phosphatidylserine externalization, plasma membrane permeabilization, and promotes autophagy. Antileishmanial agent-43 can be used for the research of leishmaniasis .
    Antileishmanial agent-43
  • HY-182802

    Ferroptosis Glutathione Peroxidase Reactive Oxygen Species (ROS) Mitochondrial Metabolism Cancer
    Ferroptosis inducer-15 is a ferroptosis inducer. Ferroptosis inducer-15 downregulates GPX4 expression, triggers lipid peroxidation via ROS accumulation, and disrupts mitochondrial membrane potential to drive ferroptosis. Ferroptosis inducer-15 increases splenic CD4 + T cell proportion, promotes CD8 + cytotoxic T cell tumor infiltration, and activates antitumor immune responses. Ferroptosis inducer-15 exerts antiproliferative activity against colorectal cancer cells and inhibits tumor growth in xenograft mice models without significant body weight loss. Ferroptosis inducer-15 can be used for the research of cancer, such as colorectal cancer .
    Ferroptosis inducer-15
  • HY-W715812

    Fungal Apoptosis Caspase Reactive Oxygen Species (ROS) MDM-2/p53 SOD Bcl-2 Family PERK JNK p38 MAPK Cardiovascular Disease Infection Endocrinology Cancer
    Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability . Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process . Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction .
    Bromuconazole

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