Mito-TEMPO
Based on 167 publication(s) in Google Scholar
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.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- Pureté: 99.19%
- CAS No.: 1334850-99-5
- Formule: C29H35ClN2O2P
- Masse moléculaire:510.03
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Stockage:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 2 years; -20°C, 1 year (sealed storage, away from moisture)
Publications Citing Use of MedChemExpress (MCE) Mito-TEMPO
More- Science. 2025 Mar 7;387(6738):eadq2509. [Abstract]
- Immunity. 2025 Apr 8;58(4):811-825.e7. [Abstract]
- Immunity. 2024 Jun 19:S1074-7613(24)00305-4. [Abstract]
- Nat Microbiol. 2025 Oct;10(10):2521-2536. [Abstract]
- ACS Nano. 2025 Mar 25;19(11):11029-11048. [Abstract]
- Nat Commun. 2026 Jan 31;17(1):2227. [Abstract]
- Nat Commun. 2025 Aug 26;16(1):7954. [Abstract]
- Nat Commun. 2023 Feb 16;14(1):872. [Abstract]
- Cell Death Differ. 2024 Nov;31(11):1519-1533. [Abstract]
- Acta Pharm Sin B. 2022 Feb;12(2):759-773. [Abstract]
- Autophagy. 2024 Apr;20(4):752-768. [Abstract]
- Adv Sci (Weinh). 2026 Apr;13(19):e16090. [Abstract]
- Adv Sci (Weinh). 2025 Sep 15:e07283. [Abstract]
- Adv Sci (Weinh). 2025 Sep 26:e05486. [Abstract]
- Adv Sci (Weinh). 2023 Mar;10(9):e2207084. [Abstract]
- Nat Plants. 2026 Mar;12(3):635-652. [Abstract]
- Leukemia. 2023 Apr;37(4):765-775. [Abstract]
- Theranostics. 2025 Jan 20;15(6):2360-2374. [Abstract]
- Biomaterials. 2025 Sep:320:123259. [Abstract]
- J Exp Clin Cancer Res. 2025 Jul 4;44(1):193. [Abstract]
- Sci Adv. 2025 Jul 18;11(29):eadw5228. [Abstract]
- J Biomed Sci. 2023 Nov 7;30(1):91. [Abstract]
- Redox Biol. 2025 Sep:85:103750. [Abstract]
- Redox Biol. 2024 Nov 20:78:103439. [Abstract]
- Redox Biol. 2023 Sep:65:102828. [Abstract]
- Redox Biol. 2023 Jun:62:102702. [Abstract]
- Redox Biol. 2023 Feb:59:102587. [Abstract]
- Redox Biol. 2020 Jul;34:101559. [Abstract]
- Environ Sci Technol. 2025 Aug 5;59(30):15705-15719. [Abstract]
- J Hazard Mater. 2024 Jun 7:475:134854. [Abstract]
- J Hazard Mater. 2024 May 15:470:134142. [Abstract]
- J Hazard Mater. 2024 Apr 5:467:133719. [Abstract]
- J Hazard Mater. 2023 Sep 5:457:131750. [Abstract]
- J Hazard Mater. 2022 Feb 15;424(Pt A):127268. [Abstract]
- J Immunother Cancer. 2024 Nov 24;12(11):e009805. [Abstract]
- Mol Biomed. 2025 Oct 2;6(1):75. [Abstract]
- Int J Biol Sci. 2024 Aug 19;20(11):4476-4495. [Abstract]
- Int J Biol Sci. 2024 Apr 29;20(7):2658-2685. [Abstract]
- Int J Biol Sci. 2022 Mar 6;18(6):2261-2276. [Abstract]
- Environ Int. 2023 Aug:178:108138. [Abstract]
- Cell Death Dis. 2026 Mar 27;17(1):413. [Abstract]
- Cell Death Dis. 2025 Jul 1;16(1):482. [Abstract]
- Cell Death Dis. 2020 May 5;11(5):319. [Abstract]
- Genes Dis. 2025 Sep 23.
- Cell Commun Signal. 2023 May 25;21(1):123. [Abstract]
- Dev Cell. 2025 Apr 18:S1534-5807(25)00206-0. [Abstract]
- Int J Biol Macromol. 2026 Apr:355:151129. [Abstract]
- Int J Biol Macromol. 2025 Dec;334(Pt 1):149021. [Abstract]
- Acta Pharmacol Sin. 2025 Jul;46(7):1974-1989. [Abstract]
- Acta Pharmacol Sin. 2024 Aug;45(8):1660-1672. [Abstract]
- Phytomedicine. 2024 Nov 14:136:156260. [Abstract]
- Phytomedicine. 2024 Dec:135:156139. [Abstract]
- Phytomedicine. 2024 Jul:129:155570. [Abstract]
- Free Radic Biol Med. 2026 May:248:255-271. [Abstract]
- Free Radic Biol Med. 2025 Jun 14:237:585-599. [Abstract]
- Free Radic Biol Med. 2025 Apr 5:S0891-5849(25)00215-1. [Abstract]
- Free Radic Biol Med. 2025 Mar 28:S0891-5849(25)00192-3. [Abstract]
- Free Radic Biol Med. 2025 Feb 16:228:183-196. [Abstract]
- Free Radic Biol Med. 2024 Nov 5:225:856-870. [Abstract]
- Free Radic Biol Med. 2024 Jul 9:S0891-5849(24)00552-5. [Abstract]
- Free Radic Biol Med. 2024 Aug 1:220:179-191. [Abstract]
- Free Radic Biol Med. 2024 Feb 20:212:493-504. [Abstract]
- Sci Total Environ. 2023 Dec 20:905:166890. [Abstract]
- Basic Res Cardiol. 2022 Aug 23;117(1):40. [Abstract]
- J Orthop Translat. 2026 Jan 6.
- J Transl Med. 2025 Nov 10;23(1):1254. [Abstract]
- Biomed Pharmacother. 2022 Sep:153:113280. [Abstract]
- Redox Rep. 2026 Dec;31(1):2632434. [Abstract]
- Redox Rep. 2025 Dec;30(1):2550412. [Abstract]
- Redox Rep. 2024 Dec;29(1):2377870. [Abstract]
- Oncogene. 2025 Sep 16:10.1038/s41388-025-03571-1. [Abstract]
- Environ Pollut. 2024 May 15:349:123874. [Abstract]
- Aging Cell. 2026 Jun;25(6):e70573. [Abstract]
- Cell Death Discov. 2023 Nov 18;9(1):419. [Abstract]
- Cell Rep. 2026 Feb 18;45(3):116978. [Abstract]
- Clin Transl Med. 2025 Jun;15(6):e70385. [Abstract]
- Clin Transl Med. 2025 Apr;15(4):e70289. [Abstract]
- Clin Transl Med. 2024 Apr;14(4):e1653. [Abstract]
- Antioxidants (Basel). 2022 Jul 26;11(8):1455. [Abstract]
- Phytother Res. 2025 Feb;39(2):581-592. [Abstract]
- Cell Mol Life Sci. 2025 Jun 5;82(1):226. [Abstract]
- J Agric Food Chem. 2025 Apr 10. [Abstract]
- J Agric Food Chem. 2023 Nov 1;71(43):16310-16322. [Abstract]
- J Agric Food Chem. 2023 Aug 30;71(34):12645-12656. [Abstract]
- Ecotoxicol Environ Saf. 2026 Jan 15:310:119774. [Abstract]
- Ecotoxicol Environ Saf. 2025 Apr 3:295:118139. [Abstract]
- Ecotoxicol Environ Saf. 2024 Mar 15:273:116150. [Abstract]
- Int J Mol Med. 2025 Jun;55(6):96. [Abstract]
- Biochem Pharmacol. 2025 Apr 4:116932. [Abstract]
- Cell Prolif. 2023 Sep;56(9):e13442. [Abstract]
- NanoImpact. 2025 Jun 15:39:100572. [Abstract]
- J Ethnopharmacol. 2025 Nov 28:358:120957. [Abstract]
- Mar Drugs. 2025 Mar 12;23(3):123. [Abstract]
- Chem Biol Interact. 2024 Dec 31:111368. [Abstract]
- Chem Biol Interact. 2025 Jan 5:405:111269. [Abstract]
- J Ethnopharmacol. 2024 Jun 11:118455. [Abstract]
- Life Sci. 2026 Mar 1:388:124199. [Abstract]
- Life Sci. 2025 May 30:123780. [Abstract]
- PLoS Pathog. 2024 Nov 5;20(11):e1012614. [Abstract]
- Int J Mol Sci. 2023 Mar 27;24(7):6309. [Abstract]
- Int Immunopharmacol. 2026 Jan 1;168(Pt 1):115862. [Abstract]
- Eur J Pharmacol. 2025 Oct 15:1005:178118. [Abstract]
- Int Immunopharmacol. 2025 Aug 11:164:115325. [Abstract]
- Int Immunopharmacol. 2025 May 30:160:114984. [Abstract]
- Int Immunopharmacol. 2024 Oct 29;143(Pt 2):113504. [Abstract]
- Eur J Pharmacol. 2024 Apr 15:969:176459. [Abstract]
- Arthritis Res Ther. 2025 Dec 15;27(1):226. [Abstract]
- Hepatol Commun. 2024 Mar 18;8(4):e0399. [Abstract]
- Arthritis Res Ther. 2023 Jul 19;25(1):121. [Abstract]
- Molecules. 2023 Jun 14;28(12):4770. [Abstract]
- Mol Oncol. 2025 Dec 2. [Abstract]
- Cancers (Basel). 2025 Dec 27;18(1):92. [Abstract]
- J Cell Mol Med. 2025 Jul;29(13):e70613. [Abstract]
- Biochim Biophys Acta Mol Basis Dis. 2025 Apr 26;1871(6):167874. [Abstract]
- Biochim Biophys Acta Mol Basis Dis. 2025 Apr 23;1871(6):167866. [Abstract]
- Biochim Biophys Acta Mol Basis Dis. 2023 Aug;1869(6):166740. [Abstract]
- FASEB J. 2023 Jun;37(6):e22954. [Abstract]
- FASEB J. 2022 Aug;36(8):e22475. [Abstract]
- J Inflamm Res. 2025 Aug 14:18:11095-11108. [Abstract]
- Cell Calcium. 2025 Aug 26:132:103071. [Abstract]
- Diabetol Metab Syndr. 2025 Jul 16;17(1):267. [Abstract]
- Aquaculture. 2025 Feb 15.
- Fish Shellfish Immunol. 2024 Jan:144:109261. [Abstract]
- Aging (Albany NY). 2020 Jun 11;12(11):11116-11138. [Abstract]
- Biochim Biophys Acta Mol Cell Res. 2025 Dec;1872(8):120059. [Abstract]
- Cell Signal. 2025 Apr 22:111829. [Abstract]
- Cell Signal. 2022 May:93:110304. [Abstract]
- Biol Trace Elem Res. 2026 Mar 27. [Abstract]
- J Proteome Res. 2025 Aug 1;24(8):4098-4113. [Abstract]
- Biol Trace Elem Res. 2024 Sep;202(9):4180-4190. [Abstract]
- Front Med. 2022 Jul 22:9:887062. [Abstract]
- Mol Hum Reprod. 2020 Oct 1;26(10):773-783. [Abstract]
- Front Oncol. 2022 May 18:12:874900. [Abstract]
- OncoTargets and Therapy Dovepress. 2020 May 18;15:1093-1101. [Abstract]
- Arch Biochem Biophys. 2026 Jun:780:110790. [Abstract]
- Arch Biochem Biophys. 2024 Jul 17:110102. [Abstract]
- J Diabetes Investig. 2023 Jan;14(1):28-36. [Abstract]
- FEBS Lett. 2021 Oct;595(19):2447-2462. [Abstract]
- J Clin Lab Anal. 2026 Mar;40(5):e70172. [Abstract]
- Oral Dis. 2025 Feb;31(2):577-588. [Abstract]
- Mol Pain. 2025 Aug 28:17448069251377633. [Abstract]
- Virus Res. 2023 Dec:338:199238. [Abstract]
- PLoS One. 2020 Oct 1;15(10):e0239659. [Abstract]
- Tissue Cell. 2025 Sep 18:98:103141. [Abstract]
- Placenta. 2023 Nov:143:1-11. [Abstract]
- Vet Sci. 2024 Dec 12;11(12):643. [Abstract]
- Biomol Biomed. 2025 Oct 29. [Abstract]
- Biochem Biophys Rep. 2025 Jan 9:41:101909. [Abstract]
- Biochem Biophys Res Commun. 2023 Nov 5:680:184-193. [Abstract]
- Arch Oral Biol. 2023 Mar:147:105632. [Abstract]
- Dev Neurosci. 2022;44(4-5):309-319. [Abstract]
- Biol Pharm Bull. 2025;48(11):1741-1752. [Abstract]
- Biosci Biotechnol Biochem. 2024 May 8:zbae058. [Abstract]
- bioRxiv. 2026 May 29:2026.05.26.727520. [Abstract]
- bioRxiv. 2025 Nov 11.
- SSRN. 2025 Sep 17.
- Keimyung University. 2025.
- SSRN. 2025 Mar 20.
- Res Sq. 2024 Sep 22.
- Res Sq. 2024 Jun 09.
- Clin Complement Med Pharmacol. 2024 May 21.
- Research Square Preprint. 2024 Mar 19.
- Research Square Preprint. 2024 Mar 19.
- Authorea. 2023 Aug 7.
- Oxid Med Cell Longev. 2023 Feb 10:2023:6726654. [Abstract]
- Oxid Med Cell Longev. 2023 Feb 17:2023:1708251. [Abstract]
- Research Square Preprint. 2022 May.
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Activité biologique
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.
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Cell Line:human podocyte cells (HPC)
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Concentration:200 μM (Target Reagent); 100 nM (Parkin siRNA)
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Incubation Time:24 h (co-treated with TNF-α); 24 h (Parkin siRNA transfection prior to TNF-α and Target Reagent treatment)
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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.
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.
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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]
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Dosage:0.7 mg/kg
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Administration:i.p.; daily; 7 days
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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.
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Animal Model:Sprague-Dawley (female, 10 weeks old at procurement, average weight 220 g; bilateral ovariectomy-induced osteoporosis model)[3]
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Dosage:0.6 mg/kg
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Administration:i.p.; daily; 4 weeks
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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.
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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]
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Dosage:0.7 mg/kg/day
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Administration:i.p.; daily; 2 weeks
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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.
Chemical Information
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CAS No. 1334850-99-5
-
Appearance Solid
-
Masse moléculaire 510.03
-
Formule C29H35ClN2O2P
-
Color Light yellow to orange
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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-]
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Livraison
Room temperature in continental US; may vary elsewhere.
-
Stockage
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 2 years; -20°C, 1 year (sealed storage, away from moisture)
Publications (167)
-
Journal Impact Factor
-
Most Recent
-
Science
2025 Mar 7;387(6738):eadq2509. PMID: 40048515 -
Immunity
Mitochondrial DNA released by senescent tumor cells enhances PMN-MDSC-driven immunosuppression through the cGAS-STING pathway. [Abstract]2025 Apr 8;58(4):811-825.e7. PMID: 40203808 -
Immunity
A metabolic switch orchestrated by IL-18 and the cyclic dinucleotide cGAMP programs intestinal tolerance. [Abstract]2024 Jun 19:S1074-7613(24)00305-4. PMID: 38906145 -
Nat Microbiol
Oxaloacetate sensing promotes innate immune antiviral defence against influenza virus infection. [Abstract]2025 Oct;10(10):2521-2536. PMID: 40983701 -
ACS Nano
Adverse Outcome Pathway-Based Strategies to Mitigate Ag2Se Quantum Dot-Induced Neurotoxicity. [Abstract]2025 Mar 25;19(11):11029-11048. PMID: 40063898 -
Nat Commun
Microbiota-induced EI24 improves homeostasis but impedes function of alveolar macrophages via metabolic regulation. [Abstract]2026 Jan 31;17(1):2227. PMID: 41620436 -
Nat Commun
Helicobacter hepaticus promotes hepatic steatosis through CdtB-induced mitochondrial stress and lipid metabolism reprogramming. [Abstract]2025 Aug 26;16(1):7954. PMID: 40858606 -
Nat Commun
Oxidized mitochondrial DNA induces gasdermin D oligomerization in systemic lupus erythematosus. [Abstract]2023 Feb 16;14(1):872. PMID: 36797275 -
Cell Death Differ
Vps34 sustains Treg cell survival and function via regulating intracellular redox homeostasis. [Abstract]2024 Nov;31(11):1519-1533. PMID: 39117783 -
Acta Pharm Sin B
Targeting glutamine utilization to block metabolic adaptation of tumor cells under the stress of carboxyamidotriazole-induced nutrients unavailability. [Abstract]2022 Feb;12(2):759-773. PMID: 35256945 -
Autophagy
2024 Apr;20(4):752-768. PMID: 37798944 -
Adv Sci (Weinh)
Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism. [Abstract]2026 Apr;13(19):e16090. PMID: 41618855 -
Adv Sci (Weinh)
Redox Cascade in Chicken Skeletal Muscle: SELENOT Suppression in Selenium Deficiency Triggers Disulfidptosis via mtROS-NADPH Dysregulation. [Abstract]2025 Sep 15:e07283. PMID: 40953299 -
Adv Sci (Weinh)
2025 Sep 26:e05486. PMID: 41013886 -
Adv Sci (Weinh)
Extracellularly Detectable Electrochemical Signals of Living Cells Originate from Metabolic Reactions. [Abstract]2023 Mar;10(9):e2207084. PMID: 36737855 -
Nat Plants
2026 Mar;12(3):635-652. PMID: 41644634 -
Leukemia
2023 Apr;37(4):765-775. PMID: 36739349
Mito-TEMPO 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.
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Theranostics
Inhibition of macrophage inflammasome assembly and pyroptosis with GC-1 ameliorates acute lung injury. [Abstract]2025 Jan 20;15(6):2360-2374. PMID: 39990234 -
Biomaterials
Selective and iron-independent ferroptosis in cancer cells induced by manipulation of mitochondrial fatty acid oxidation. [Abstract]2025 Sep:320:123259. PMID: 40112511 -
J Exp Clin Cancer Res
M2 macrophage-secreted KYNU promotes stemness remodeling and malignant behavior in endometrial cancer via the SOD2-mtROS-ERO1α-UPRER axis. [Abstract]2025 Jul 4;44(1):193. PMID: 40616124 -
Sci Adv
2025 Jul 18;11(29):eadw5228. PMID: 40668928 -
J Biomed Sci
Spatiotemporal roles of AMPK in PARP-1- and autophagy-dependent retinal pigment epithelial cell death caused by UVA. [Abstract]2023 Nov 7;30(1):91. PMID: 37936170 -
Redox Biol
EMAP-II from macrophage-derived extracellular vesicles drives neutrophil extracellular traps formation via PI3K/AKT/mtROS in lung ischemia/reperfusion injury. [Abstract]2025 Sep:85:103750. PMID: 40616949 -
Redox Biol
Podocyte SIRPα reduction in diabetic nephropathy aggravates podocyte injury by promoting pyruvate kinase M2 nuclear translocation. [Abstract]2024 Nov 20:78:103439. PMID: 39586122 -
Redox Biol
Epigenetic modulation of Drp1-mediated mitochondrial fission by inhibition of S-adenosylhomocysteine hydrolase promotes vascular senescence and atherosclerosis. [Abstract]2023 Sep:65:102828. PMID: 37517319 -
Redox Biol
BNP protects against diabetic cardiomyopathy by promoting Opa1-mediated mitochondrial fusion via activating the PKG-STAT3 pathway. [Abstract]2023 Jun:62:102702. PMID: 37116257 -
Redox Biol
PM2.5 increases susceptibility to acute exacerbation of COPD via NOX4/Nrf2 redox imbalance-mediated mitophagy. [Abstract]2023 Feb:59:102587. PMID: 36608590 -
Redox Biol
Baicalin combats glutamate excitotoxicity via protecting glutamine synthetase from ROS-induced 20S proteasomal degradation. [Abstract]2020 Jul;34:101559. PMID: 32473460
Mito-TEMPO 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.
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Environ Sci Technol
Chronic Dietary Exposure to Environmental Levels of Glyphosate Increases the Risk of Reproductive Dysfunction in Male Mice. [Abstract]2025 Aug 5;59(30):15705-15719. PMID: 40698942 -
J Hazard Mater
Potential mechanisms of aortic medial degeneration promoted by co-exposure to microplastics and lead. [Abstract]2024 Jun 7:475:134854. PMID: 38889468 -
J Hazard Mater
Environmental cadmium inhibits testicular testosterone synthesis via Parkin-dependent MFN1 degradation. [Abstract]2024 May 15:470:134142. PMID: 38555669 -
J Hazard Mater
Sodium sulfite triggered hepatic apoptosis, necroptosis, and pyroptosis by inducing mitochondrial damage in mice and AML-12 cells. [Abstract]2024 Apr 5:467:133719. PMID: 38335615 -
J Hazard Mater
MDM2 upregulation induces mitophagy deficiency via Mic60 ubiquitination in fetal microglial inflammation and consequently neuronal DNA damage caused by exposure to ZnO-NPs during pregnancy. [Abstract]2023 Sep 5:457:131750. PMID: 37315416 -
J Hazard Mater
Gestational exposure to environmental cadmium induces placental apoptosis and fetal growth restriction via Parkin-modulated MCL-1 degradation. [Abstract]2022 Feb 15;424(Pt A):127268. PMID: 34583167 -
J Immunother Cancer
Propafenone facilitates mitochondrial-associated ferroptosis and synergizes with immunotherapy in melanoma. [Abstract]2024 Nov 24;12(11):e009805. PMID: 39581704 -
Mol Biomed
Iron accumulation in hypothalamus promotes age-dependent obesity and metabolic dysfunction of male mice. [Abstract]2025 Oct 2;6(1):75. PMID: 41037185 -
Int J Biol Sci
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Int J Biol Sci
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Mito-TEMPO 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.
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Oxid Med Cell Longev
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Solvant et solubilité
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)
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.
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.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Select the appropriate dissolution method based on your experimental animal and administration route.
- 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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% 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 μL DMSO 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.
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 μL DMSO 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.
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.
Add each solvent one by one: PBS
Solubility: 50 mg/mL (98.03 mM); Clear solution; Need ultrasonic
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Working solution concentration: 0.22 mg/mL
This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
Pureté et documentation
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Fiche technique (290 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Portuguese - PT (393 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Liu B, et al. MitoTEMPO protects against podocyte injury by inhibiting NLRP3 inflammasome via PINK1/Parkin pathway-mediated mitophagy. Eur J Pharmacol. 2022;929:175136. [Content Brief]
[2]. Olgar Y, et al. MitoTEMPO provides an antiarrhythmic effect in aged-rats through attenuation of mitochondrial reactive oxygen species. Exp Gerontol. 2020;136:110961. [Content Brief]
[3]. Li J, et al. Mitochondria-specific antioxidant MitoTEMPO alleviates senescence of bone marrow mesenchymal stem cells in ovariectomized rats. J Cell Physiol. 2024;239(8):e31323. [Content Brief]
[4]. Akkoca A, et al. Protective effect of MitoTEMPO against cardiac dysfunction caused by ischemia-reperfusion: MCAO stroke model study. Int J Neurosci. 2024;134(12):1582-1593. [Content Brief]
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.
| Optional Solvent | Concentration Solvent Mass | 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.
- Mito-TEMPO
- 1334850-99-5
- Calcium Channel
- Apoptosis
- Mitochondrial Metabolism
- NOD-like Receptor (NLR)
- PINK1/Parkin
- Autophagy
- NLRP3 inflammasome
- chronic kidney disease
- mitochondrial ROS
- ischemic stroke
- mitophagy
- rat BMSCs
- Parkin
- human podocyte cells
- PINK1/Parkin pathway
- postmenopausal osteoporosis
- Inhibitor
- inhibitor
- inhibit