2. Metabolic Enzyme/Protease Neuronal Signaling Autophagy Immunology/Inflammation Membrane Transporter/Ion Channel Apoptosis
  3. Mitochondrial Metabolism PINK1/Parkin NOD-like Receptor (NLR) Autophagy Calcium Channel Apoptosis
  4. MitoTEMPO hydrate

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 Ca2+ 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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CAS No. : 1569257-94-8

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Based on 164 publication(s) in Google Scholar

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MitoTEMPO hydrate Related Antibodies

Top Publications Citing Use of Products

164 Publications Citing Use of MCE MitoTEMPO hydrate

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IF

    MitoTEMPO hydrate purchased from MedChemExpress. Usage Cited in: Leukemia. 2023 Apr;37(4):765-775.  [Abstract]

    Mito-TEMPO (MTTP; 50 nM; 48 h) efficiently reduces total and mitochondrial ROS content in PDX AML cells. CellROX dye, left panel, MitoSOX dye, right panel.

    MitoTEMPO hydrate purchased from MedChemExpress. Usage Cited in: Redox Biol. 2020 Jul;34:101559.  [Abstract]

    GS carbonylation in astrocytes under OGD/R. Mito-TEMPO decreases GS carbonylation in astrocytes.

    MitoTEMPO hydrate purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2020 May 5;11(5):319.  [Abstract]

    Western blot assay shows the expression of nestin, PINK1, LC3 and p62 in the MPCs, which are pretreated with Mito-TEMPO and exposed to lupus nephritis plasma for 24 h.

    View All NOD-like Receptor (NLR) Isoform Specific Products:

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    NLRP3 NLRP1 NOD1 NOD2

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    N-type calcium channel L-type calcium channel P/Q-type calcium channel T-type calcium channel Calcium Channel

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    Description

    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 Ca2+ 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[1][2][3][4].

    In Vitro

    MitoTEMPO (200 μM; 24 h) hydrate inhibits the activation of the NLRP3 inflammasome and protects human podocytes (HPC) from TNF-α-induced injury[1].
    MitoTEMPO (200 μM; 24 h) hydrate improves mitochondrial function and induces PINK1/Parkin pathway-mediated mitophagy in TNF-α-injured human podocytes (HPC)[1].
    MitoTEMPO (200 μM; 24 h) hydrate inhibits the activation of the NLRP3 inflammasome in TNF-α-injured human podocytes (HPC) in a Parkin-dependent manner[1].
    MitoTEMPO (0.1-10 μM; 2 days) hydrate significantly reduces mitochondrial superoxide levels in bone marrow mesenchymal stem cells (BMSCs) of rats in the sham-operated group, short-term ovariectomized (ST-OVX) group, and long-term ovariectomized (LT-OVX) group, with the most prominent effect on BMSCs in the LT-OVX group at the concentration of 1 μM[3].
    MitoTEMPO (1 μM; 7 days) hydrate upregulates the activity of alkaline phosphatase (ALP), an early osteogenic marker, in bone marrow mesenchymal stem cells (BMSCs) of rats with long-term ovariectomy (LT-OVX), and reverses the activity reduction caused by estrogen deficiency[3].
    MitoTEMPO (1 μM; 2 days) hydrate alleviates premature senescence of bone marrow mesenchymal stem cells (BMSCs) in ovariectomized (LT-OVX) rats by reducing the expression of senescence markers, decreasing DNA damage, and ameliorating cell proliferation impairment[3].
    MitoTEMPO (1 μM; 2 days) hydrate restores lysosomal acidity, reduces mature CTSB levels, and alleviates lysosomal dysfunction in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats induced by estrogen deficiency[3].
    MitoTEMPO (1 μM; 2 days) hydrate enhances mitophagy in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats, which is evidenced by increased colocalization of mitochondrial markers and lysosomal markers[3].
    MitoTEMPO (1 μM; 2 days) hydrate inhibits the activation of mitochondrial unfolded protein response (UPRmt) in bone marrow mesenchymal stem cells (BMSCs) of ovariectomized (LT-OVX) rats induced by estrogen deficiency by reducing the expression of HSP60 and CLPP proteins[3].
    MitoTEMPO (1 μM; 2 days) hydrate restores mitochondrial membrane potential in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats and alleviates estrogen deficiency-induced mitochondrial dysfunction[3].
    MitoTEMPO (1 μM; 2 days) hydrate improves mitochondrial respiratory function, including basal respiration, ATP-coupled respiration, and maximal respiration, in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats[3].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    MitoTEMPO hydrate Related Antibodies

    Western Blot Analysis[1]

    Cell Line: human podocyte cells (HPC)
    Concentration: 200 μM (Target Reagent); 100 nM (Parkin siRNA)
    Incubation Time: 24 h (co-treated with TNF-α); 24 h (Parkin siRNA transfection prior to TNF-α and Target Reagent treatment)
    Result: Lost the ability to significantly reduce the levels of NLRP3, cleaved caspase-1, or mature IL-1β in Parkin-silenced HPC, reversing the inhibitory effect observed in non-silenced cells.
    In Vivo

    MitoTEMPO (0.7 mg/kg; i.p.; once daily for 7 consecutive days) hydrate significantly improves renal function, alleviates podocyte injury, inhibits NLRP3 inflammasome activation, and induces PINK1/Parkin pathway-mediated mitophagy in rats with chronic kidney disease (CKD)[1].
    MitoTEMPO (0.6 mg/kg; i.p.; once daily for 4 weeks) hydrate alleviates trabecular bone loss and reduces the expression of senescence and mitochondrial stress markers in ovariectomized rats with osteoporosis[3].
    MitoTEMPO (0.7 mg/kg/day; i.p.; once daily for 14 consecutive days) hydrate exerts protective effects against ischemia-reperfusion-induced cardiac and neurological dysfunction in male Wistar albino rats, as evidenced by the normalization of hemodynamic, electrocardiographic, biochemical and histological parameters compared with the IR group[4].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: Sprague-Dawley (male, 6-8 weeks old, 180-220 g, CKD induced by subcutaneous injection of 1 mg C-BSA emulsion followed by tail vein injection of 0.5 mg C-BSA every other day for 21 days)[1]
    Dosage: 0.7 mg/kg
    Administration: i.p.; daily; 7 days
    Result: Significantly reduced 24-hour urinary protein levels at 35 days post-modeling.
    Decreased serum creatinine (SCR) and blood urea nitrogen (BUN) levels compared to CKD model rats.
    Reduced mean density of podocyte injury marker desmin by ~55% compared to CKD model rats.
    Increased mean density of slit diaphragm protein podocin compared to CKD model rats.
    Suppressed podocyte foot process fusion and reduced thickened glomerular basement membrane (GBM) thickness compared to CKD model rats.
    Reduced colocalization of NLRP3 and ASC in glomeruli compared to CKD model rats.
    Decreased protein levels of NLRP3, cleaved caspase-1, and mature IL-1β compared to CKD model rats.
    Lowered mRNA levels of IL-1β and TNF-α compared to CKD model rats .
    Increased LC3 II/I ratio, PINK1, and Parkin protein levels compared to CKD model rats.
    Decreased p62 protein levels compared to CKD model rats.
    Enhanced colocalization of LC3 and mitochondrial marker COX IV compared to CKD model rats.
    Animal Model: Sprague-Dawley (female, 10 weeks old at procurement, average weight 220 g; bilateral ovariectomy-induced osteoporosis model)[3]
    Dosage: 0.6 mg/kg
    Administration: i.p.; daily; 4 weeks
    Result: Significantly inhibited trabecular bone loss in OVX rats.
    Improved trabecular bone thickness and density in treated OVX rats compared to vehicle-treated OVX rats.
    Restored bone mineralization and deposition capabilities in treated OVX rats.
    Reduced the expression of senescence-related marker p53 in the trabecular bone region of the proximal tibia.
    Significantly decreased the expression of HSP60 and CLPP, markers of mitochondrial unfolded protein response, in OVX rats.
    Animal Model: Wistar Albino (17-week-old male, initial body weight 250-304 g, middle cerebral artery occlusion followed by 3 days of reperfusion)[4]
    Dosage: 0.7 mg/kg/day
    Administration: i.p.; daily; 14 days
    Result: Increased final body weight to 302.57 g, compared to 285.75 g for the distilled water group.
    Reduced heart weight/body weight ratio to 3.01 mg/g, which was statistically significantly lower than the ischemia-reperfusion (IR) group's 3.39 mg/g.
    Normalized volume of electrically participating tissue, left ventricular ejection time, and heart rate to levels not significantly different from the sham group, and statistically significantly different from the IR group.
    Normalized P-R interval, QTc, T-wave time, T-wave repolarization time, and R-R interval to levels not significantly different from the sham group, and statistically significantly different from the IR group.
    Increased blood serum total antioxidant status (TAS) compared to the IR group; decreased total oxidant status (TOS) and oxidative stress index (OSI) compared to the IR group.
    Increased heart left ventricle cyclic adenosine monophosphate (cAMP) and inositol triphosphate (IP3) levels to values close to the sham group and statistically significantly higher than the IR group.
    Decreased brain right cerebral hemisphere catalase levels compared to the IR group.
    Improved heart left ventricle tissue morphology to show mostly normal cardiac muscle cells with minimal myofibril degeneration, compared to widespread abnormalities in the IR group.
    Improved brain right cerebral hemisphere tissue morphology to show mostly normal neurons and glial cells with fewer degenerative changes than the IR group.
    Molecular Weight

    528.04

    Formula

    C29H37ClN2O3P
    CAS No.
    Appearance

    Solid

    Color

    Orange to red

    SMILES

    [O]N1C(C)(C)CC(NC(C[P+](C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4)=O)CC1(C)C.[Cl-].O
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    -20°C, sealed storage, away from moisture

    *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

    Purity & Documentation
    References
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    MitoTEMPO hydrate Related Classifications

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    Keywords:

    MitoTEMPO1569257-94-8Mitochondrial MetabolismPINK1/ParkinNOD-like Receptor (NLR)AutophagyCalcium ChannelApoptosisPTEN-induced kinase 1/ParkinCa2+ channelsCa channelsNLRP3 inflammasomechronic kidney diseasemitochondrial ROSischemic strokemitophagyrat BMSCsParkinhuman podocyte cellsPINK1/Parkin pathwaypostmenopausal osteoporosisInhibitorinhibitorinhibit

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