MitoPQ (Synonyms: MitoParaquat) |
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Catalog No.GC44204
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MitoPQ es un ciclador redox dirigido a las mitocondrias. MitoPQ produce superÓxido por ciclo redox en el sitio de flavina del complejo I, aumentando selectivamente la producciÓn de superÓxido dentro de las mitocondrias. MitoPQ se puede utilizar en el estudio de antioxidantes.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1821370-28-8
Sample solution is provided at 25 µL, 10mM.
MitoPQ (MitoParaquat) is a mitochondria-targeted redox cycler that selectively increases superoxide production within the mitochondrial matrix in vivo and in cells[1]. MitoPQ accumulates in the mitochondrial matrix and generates O2- through redox cycling at the flavin site of complex I (Fig. 1)[1,2]. MitoPQ is commonly used to study the role of mitochondrial superoxide production in health and disease in both cells and in vivo[3,4].

Fig. 1. Rationale for the development of MitoParaquat[1,2]. MitoParaquat (MitoPQ) is composed of a redox cycling paraquat moiety, and a hydrophobic carbon chain linking it to a mitochondria-targeting triphenylphosphonium cation. MitoPQ is accumulated by mitochondria driven by the plasma (Δψp) and mitochondrial (Δψm) membrane potentials. Within the matrix, the dicationic viologen component of MitoPQ is reduced to a radical monocation by one-electron reduction at the flavin site of complex I. The radical monocation then reacts very rapidly with O2 to generate superoxide. This localized redox cycling leads to the selective production of superoxide within the mitochondrial matrix.
In vitro, treatment of C2C12 myoblasts with MitoPQ (5μM) for 20min time-dependently and significantly increased MitoSOX fluorescence intensity, whereas paraquat (PQ) at equivalent conditions failed to increase MitoSOX oxidation within this timeframe. Treatment of HCT116 cells with MitoPQ (1-10μM) for 24h induced cell death in a dose-dependent manner, with significantly higher toxicity compared to PQ[1]. Treatment of Raw264.7 cells with MitoPQ (0.5μM) for 16h significantly disrupted the mitochondrial membrane potential, an effect that was attenuated by the addition of 10mM N-acetylcysteine (NAC)[5]. Treatment of 3T3-L1 adipocytes with MitoPQ (10μM) for 2h specifically increased mitochondrial superoxide and hydrogen peroxide levels without affecting global cellular respiration[6].
In vivo, acute intraperitoneal injection of MitoPQ (0.16mg/kg) into wild-type mice fasted for 16h significantly impaired glucose tolerance 2h post-injection. Intraperitoneal injection of MitoPQ (0.16mg/kg) in wild-type mice for 1.5h impaired hepatic insulin signaling in vivo, as evidenced by reduced levels of phosphorylated insulin receptor (IR), AKT, and GSK3α[7]. Daily intraperitoneal injection of MitoPQ (0.1mg/kg/day) for 7 days in cardiomyocyte-specific Nrf3 knockout mice significantly reduced survival rates and attenuated the beneficial effects of Nrf3 gene deletion on cardiac function and remodeling after myocardial infarction[8].
References:
[1] ROBB E L, GAWEL J M, AKSENTIJEVIĆ D, et al. Selective superoxide generation within mitochondria by the targeted redox cycler MitoParaquat[J]. Free Radical Biology and Medicine, 2015, 89: 883-894.
[2] COCHENÉ H M, MURPHY M P. Complex I is the major site of mitochondrial superoxide production by paraquat[J]. Journal of Biological Chemistry, 2008, 283(4): 1786-1798.
[3] ANTONUCCI S, MULVEY J F, BURGER N, et al. Selective mitochondrial superoxide generation in vivo is cardioprotective through hormesis[J]. Free Radical Biology and Medicine, 2019, 134: 678-687.
[4] GOLEVA T N, LYAMZAEV K G, ROGOV A G, et al. Mitochondria-targeted 1, 4-naphthoquinone (SkQN) is a powerful prooxidant and cytotoxic agent[J]. Biochimica et Biophysica Acta (BBA)-Bioenergetics, 2020, 1861(8): 148210.
[5] CHOWDHURY A R, ZIELONKA J, KALYANARAMAN B, et al. Mitochondria-targeted paraquat and metformin mediate ROS production to induce multiple pathways of retrograde signaling: A dose-dependent phenomenon[J]. Redox Biology, 2020, 36: 101606.
[6] FAZAKERLEY D J, MINARD A Y, KRYCER J R, et al. Mitochondrial oxidative stress causes insulin resistance without disrupting oxidative phosphorylation[J]. Journal of Biological Chemistry, 2018, 293(19): 7315-7328.
[7] GONCALVES R L, WANG Z B, RIVEROS J K, et al. CoQ imbalance drives reverse electron transport to disrupt liver metabolism[J]. Nature, 2025.
[8] CHEN Q, ZHENG A, XU X, et al. Nrf3-Mediated mitochondrial superoxide promotes cardiomyocyte apoptosis and impairs cardiac functions by suppressing Pitx2[J]. Circulation, 2025, 151(14): 1024-1046.
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Cell experiment [1]: |
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Cell lines |
C2C12 cells (mouse myoblasts cell line) |
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Preparation Method |
In C2C12 myoblasts, mitochondrial superoxide and hydrogen peroxide production were monitored by live cell imaging using the fluorescent dye MitoSOX. Individual cells were tracked through time, and fluorescence intensity was analyzed using Fiji imaging processing and analysis software. C2C12 cells were treated with 5μM MitoPQ or PQ, and changes in MitoSOX fluorescence intensity were observed over 20min. |
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Reaction Conditions |
5μM; 20min |
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Applications |
MitoPQ increased MitoSOX fluorescence, and this oxidation increased over time. In contrast, PQ was unable to increase MitoSOX oxidation over this timescale, even at a thousand times greater concentration than used for MitoPQ. |
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Animal experiment [2]: |
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Animal models |
C57BL/6J |
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Preparation Method |
Mice were fasted for 16h and then received 0.16mg/kg MitoPQ by i.p. injection. 1.5h later, mice were anaesthetized with 100mg/kg ketamine and 10mg/kg xylazine and then injected with 0.75U/kg insulin into the portal vein. Livers were collected 3min later and immediately frozen in liquid N2. Epididymal adipose tissue and gastrocnemius were next collected and frozen until protein extraction. |
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Dosage form |
0.16mg/kg; i.p. |
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Applications |
MitoPQ decreased hepatic insulin signalling in vivo, as indicated by the reduced levels of phosphorylated insulin receptor (IR), AKT and GSK3α in the liver. |
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References: [1] Robb EL, Gawel JM, Aksentijević D, Cochemé HM, Stewart TS, Shchepinova MM, Qiang H, Prime TA, Bright TP, James AM, Shattock MJ. Selective superoxide generation within mitochondria by the targeted redox cycler MitoParaquat. Free Radical Biology and Medicine. 2015 Dec 1;89:883-94. [2] Goncalves RL, Wang ZB, Riveros JK, Parlakgül G, Inouye KE, Lee GY, Fu X, Saksi J, Rosique C, Hui ST, Coll M. CoQ imbalance drives reverse electron transport to disrupt liver metabolism. Nature. 2025 May 28:1-9. |
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| Cas No. | 1821370-28-8 | SDF | |
| Sinónimos | MitoParaquat | ||
| Chemical Name | 1-methyl-1'-(10-(triphenylphosphonio)decyl)-[4,4'-bipyridine]-1,1'-diium iodide | ||
| Canonical SMILES | C[N+](C=C1)=CC=C1C(C=C2)=CC=[N+]2CCCCCCCCCC[P+](C3=CC=CC=C3)(C4=CC=CC=C4)C5=CC=CC=C5.[I-].[I-].[I-] | ||
| Formula | C39H46N2P • 3I | M.Wt | 954.5 |
| Solubility | 10mM in ethanol or 100mM in DMSO | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.0477 mL | 5.2383 mL | 10.4767 mL |
| 5 mM | 209.5 μL | 1.0477 mL | 2.0953 mL |
| 10 mM | 104.8 μL | 523.8 μL | 1.0477 mL |
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Quality Control & SDS
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- Purity: >98.00% Appearance: A solid
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Average Rating: 5 (Based on Reviews and 17 reference(s) in Google Scholar.)















