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Mito-TEMPO

Catalog No. T19428 CAS 1334850-99-5

Mito-TEMPO is a mitochondria-targeted superoxide dismutase mimetic. Mito-TEMPO scavenges superoxide and alkyl radicals and prevents mitochondrial oxidation, necrosis and apoptosis.

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Mito-TEMPO, CAS 1334850-99-5

Pack Size	Availability	Price/USD
5 mg	In stock	$ 51.00
10 mg	In stock	$ 89.00
25 mg	In stock	$ 178.00
50 mg	In stock	$ 343.00
100 mg	In stock	$ 571.00
1 mL * 10 mM (in DMSO)	In stock	$ 58.00

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Purity: 98.5%

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Description	Mito-TEMPO is a mitochondria-targeted superoxide dismutase mimetic. Mito-TEMPO scavenges superoxide and alkyl radicals and prevents mitochondrial oxidation, necrosis and apoptosis.
In vitro	METHODS: Human neuroblastoma cells SH-SY5Y were treated with Mito-TEMPO (25-100 μM) for 24 h. Cell viability was detected using MTT assay. RESULTS: No cytotoxic effect was shown on the cells in the Mito-TEMPO-treated group, and a significant increase in cell viability was detected after Mito-TEMPO treatment. [1] METHODS: Normal rat proximal renal tubular epithelial cell line NRK-52E was pretreated with Mito-TEMPO (10 μM) for 1 h, then stimulated with oxalate (700 μM) for 1 h. The mitochondrial membrane potential was detected by using MMP assay kit (JC-1). RESULTS: The control cells showed bright red fluorescence. Compared with the control, oxalate treatment attenuated the red fluorescence, and these changes were reversed by pretreatment with Mito-TEMPO. The RESULTS suggest that oxalate induces mitochondrial dysfunction, and Mito-TEMPO can inhibit this effect. [2]
In vivo	METHODS: To investigate the protective effect against hepatotoxicity, APAP (300 mg/kg) was intraperitoneally injected into C57BL/6J mice, and Mito-TEMPO (20 mg/kg in saline) was injected intraperitoneally 1.5-3 h later. RESULTS: Mito-TEMPO had a protective effect on the late hepatotoxicity of APAP. [3] METHODS: To investigate the effects on coronary vasodilatation and endothelial SK channel activity, Mito-TEMPO (1 mg/kg in saline) was intraperitoneally injected into C57BL/6J mice with or without diabetes once daily for four weeks. RESULTS: After 4 weeks of treatment with Mito-TEMPO, diabetic mice showed significantly improved endothelium-dependent diastolic responses of coronary arteries to ADP or NS309 and endothelial SK channel currents compared to untreated diabetic mice. [4]

Molecular Weight	510.03
Formula	C29H35N2O2P.Cl
CAS No.	1334850-99-5

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

H2O: 60 mg/mL (117.64 mM), Sonification is recommended.

DMSO: 125 mg/mL (245.08 mM), Sonification is recommended.

References and Literature

1. Mukem S, et al. Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells. Heliyon. 2021 Jun 15;7(6):e07310. 2. Zhang J, et al. MitoTEMPO Prevents Oxalate Induced Injury in NRK-52E Cells via Inhibiting Mitochondrial Dysfunction and Modulating Oxidative Stress. Oxid Med Cell Longev. 2017;2017:7528090. 3. Du K, et al. Mito-tempo protects against acute liver injury but induces limited secondary apoptosis during the late phase of acetaminophen hepatotoxicity. Arch Toxicol. 2019 Jan;93(1):163-178. 4. Xing H, et al. Chronic Inhibition of mROS Protects Against Coronary Endothelial Dysfunction in Mice With Diabetes. Front Cell Dev Biol. 2021 Feb 18;9:643810.

Citations

1. Zhao X, Miao G, Zhang L, et al. Chlamydia pneumoniae Infection Induces Vascular Smooth Muscle Cell Migration and Atherosclerosis Through Mitochondrial Reactive Oxygen Species-Mediated JunB-Fra-1 Activation. Frontiers in Cell and Developmental Biology. 2022, 10: 879023-879023 2. Tian C, Han X, He L, et al. Transient receptor potential ankyrin 1 contributes to the ATP-elicited oxidative stress and inflammation in THP-1-derived macrophage. Molecular and Cellular Biochemistry. 2020: 1-14 3. Wang Y, He X, Xue M, et al.Germacrone protects renal tubular cells against ferroptotic death and ROS release by re-activating mitophagy in diabetic nephropathy.Free Radical Research.2023 (just-accepted): 1-36. 4. Yan Z, Niu L, Wang S, et al.Intestinal Piezo1 aggravates intestinal barrier dysfunction during sepsis by mediating Ca2+ influx.Journal of Translational Medicine.2024, 22(1): 1-12.

Related compound libraries

This product is contained In the following compound libraries：

Anti-Neurodegenerative Disease Compound Library Anti-Aging Compound Library Antioxidant Compound Library NO PAINS Compound Library Bioactive Compounds Library Max Anti-Cancer Compound Library Anti-Fibrosis Compound Library Bioactive Compound Library Mitochondria-Targeted Compound Library Immunology/Inflammation Compound Library

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Keywords

Mito-TEMPO 1334850-99-5 Immunology/Inflammation Metabolism NF-Κb Reactive Oxygen Species Mitochondrial Metabolism inhibit MitoTEMPO Mito TEMPO Inhibitor inhibitor

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