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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 Ca2+ 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.
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.
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.
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 Ca2+ 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[1][2][3][4].
体外実験
Mito-TEMPO (200 μM; 24 h) inhibits the activation of the NLRP3 inflammasome and protects human podocytes (HPC) from TNF-α-induced injury[1]. Mito-TEMPO (200 μM; 24 h) improves mitochondrial function and induces PINK1/Parkin pathway-mediated mitophagy in TNF-α-injured human podocytes (HPC)[1]. Mito-TEMPO (200 μM; 24 h) inhibits the activation of the NLRP3 inflammasome in TNF-α-injured human podocytes (HPC) in a Parkin-dependent manner[1]. Mito-TEMPO (0.1-10 μM; 2 days) 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]. Mito-TEMPO (1 μM; 7 days) 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]. Mito-TEMPO (1 μM; 2 days) 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]. Mito-TEMPO (1 μM; 2 days) 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]. Mito-TEMPO (1 μM; 2 days) 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]. Mito-TEMPO (1 μM; 2 days) 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]. Mito-TEMPO (1 μM; 2 days) restores mitochondrial membrane potential in bone marrow mesenchymal stem cells (BMSCs) from ovariectomized (LT-OVX) rats and alleviates estrogen deficiency-induced mitochondrial dysfunction[3]. Mito-TEMPO (1 μM; 2 days) 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.
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.
体内実験
Mito-TEMPO (0.7 mg/kg; i.p.; once daily for 7 consecutive days) 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]. Mito-TEMPO (0.6 mg/kg; i.p.; once daily for 4 weeks) alleviates trabecular bone loss and reduces the expression of senescence and mitochondrial stress markers in ovariectomized rats with osteoporosis[3]. Mito-TEMPO (0.7 mg/kg/day; i.p.; once daily for 14 consecutive days) 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; 2 weeks
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.
DMSO : 100 mg/mL (196.07 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : 60 mg/mL (117.64 mM; Need ultrasonic)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
1.9607 mL
9.8033 mL
19.6067 mL
5 mM
0.3921 mL
1.9607 mL
3.9213 mL
10 mM
0.1961 mL
0.9803 mL
1.9607 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year (sealed storage, away from moisture). When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
*
Note: If you choose water as the stock solution, please dilute it to the working solution,
then filter and sterilize it with a 0.22 μm filter before use.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.5 mg/mL (4.90 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 3
Add each solvent one by one: 10% DMSO 90% Corn Oil
Solubility: ≥ 2.5 mg/mL (4.90 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 900 μLCorn oil, and mix evenly.
For the following dissolution methods, please prepare the working solution directly.
It is recommended to prepare fresh solutions and use them promptly within a short period of time. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution.
If precipitation or phase separation occurs during preparation,
heat and/or sonication can be used to aid dissolution.
Protocol 1
Add each solvent one by one: PBS
Solubility: 50 mg/mL (98.03 mM); Clear solution; Need ultrasonic
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Calculation results:
Working solution concentration:
mg/mL
This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact MedChemExpress (MCE).
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year (sealed storage, away from moisture). When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Optional Solvent
ConcentrationSolventMass
1 mg
5 mg
10 mg
25 mg
H2O / DMSO
1 mM
1.9607 mL
9.8033 mL
19.6067 mL
49.0167 mL
5 mM
0.3921 mL
1.9607 mL
3.9213 mL
9.8033 mL
10 mM
0.1961 mL
0.9803 mL
1.9607 mL
4.9017 mL
15 mM
0.1307 mL
0.6536 mL
1.3071 mL
3.2678 mL
20 mM
0.0980 mL
0.4902 mL
0.9803 mL
2.4508 mL
25 mM
0.0784 mL
0.3921 mL
0.7843 mL
1.9607 mL
30 mM
0.0654 mL
0.3268 mL
0.6536 mL
1.6339 mL
40 mM
0.0490 mL
0.2451 mL
0.4902 mL
1.2254 mL
50 mM
0.0392 mL
0.1961 mL
0.3921 mL
0.9803 mL
60 mM
0.0327 mL
0.1634 mL
0.3268 mL
0.8169 mL
80 mM
0.0245 mL
0.1225 mL
0.2451 mL
0.6127 mL
100 mM
0.0196 mL
0.0980 mL
0.1961 mL
0.4902 mL
*
Note: If you choose water as the stock solution, please dilute it to the working solution,
then filter and sterilize it with a 0.22 μm filter before use.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
Customer Validation
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.
Customer Validation
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.
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