1. Metabolic Enzyme/Protease
    Immunology/Inflammation
    NF-κB
    Autophagy
  2. Reactive Oxygen Species
    Autophagy
  3. Tempol

Tempol (Synonyms: 4-Hydroxy-TEMPO)

Cat. No.: HY-100561 Purity: 99.98%
Handling Instructions

Tempol is a general superoxide dismutase (SOD)-mimetic drug that efficiently neutralizes reactive oxygen species (ROS).

For research use only. We do not sell to patients.

Tempol Chemical Structure

Tempol Chemical Structure

CAS No. : 2226-96-2

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10 mM * 1 mL in Water USD 66 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 5 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Tempol purchased from MCE. Usage Cited in: J Cell Mol Med. 2020 Sep;24(17):9545-9559.

    After 1-h pre-treatment with Tempol (3 mM), RNF4 expression is measured by Western blot after H2O2 or ATO treatment in NMCMs. RNF4 elevated initially and then attenuated after H2O2 or ATO treatment, while Tempol partially reversed the oxidative stimulus-induced elevation of RNF4 in vitro.
    • Biological Activity

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    Description

    Tempol is a general superoxide dismutase (SOD)-mimetic drug that efficiently neutralizes reactive oxygen species (ROS).

    IC50 & Target

    ROS[1]

    In Vitro

    Tempol significantly attenuates H2O2-mediated decrease in mitochondrial respiration and increase in LDH release from rat PT cells, indicating a reduction in cell injury and death. The beneficial actions of Tempol are similar to those obtained using the Fe2+ chelator DEF. However, coadministration of DEF and Tempol does not produce any additional beneficial actions against renal ischemia/reperfusion injury or against oxidative stress-mediated PT cell injury/death[2].

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

    In Vivo

    SOD-mimetic Tempol is able to mimic resveratrol’s effects on heart function. Tempol is administered daily by gavage. Mice treated with Met or Tmp had decreased PR and QTc intervals and increased heart rates compared to peroral vehicle (VEH). These results are similar to that obtained by treatment with RSV. Pre- and post-treatment profiles of individual mice are illustrated[1]. Tempol, a membrane-permeable radical scavenger, reduces oxidant stress-mediated renal dysfunction and injury in the rat. Tempol significantly reduces the increase in urea, creatinine, γGT, AST, NAG, and FENa produced by renal ischemia/reperfusion, suggesting an improvement in both renal function and injury. Tempol also significantly reduces kidney MPO activity and MDA levels, indicating a reduction in PMN infiltration and lipid peroxidation, respectively. Tempol reduces the histologic evidence of renal damage associated with ischemia/reperfusion and caused a substantial reduction in the staining for nitrotyrosine and PARS, suggesting reduced nitrosative and oxidative stress[2].

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

    Clinical Trial
    Molecular Weight

    172.24

    Formula

    C₉H₁₈NO₂*

    CAS No.
    SMILES

    [O]N1C(C)(C)CC(O)CC1(C)C

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage
    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    H2O : 50 mg/mL (290.29 mM; Need ultrasonic)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 5.8059 mL 29.0293 mL 58.0585 mL
    5 mM 1.1612 mL 5.8059 mL 11.6117 mL
    10 mM 0.5806 mL 2.9029 mL 5.8059 mL
    *Please refer to the solubility information to select the appropriate solvent.
    References
    Cell Assay
    [2]

    To investigate the effect of Tempol, DEF, and DEF coadministered with Tempol on H2O2-mediated cell injury and death, confluent cultures of PT cells are preincubated (10 min at 37°C) with Tempol (0.03 to 10 mM), DEF (0.03 to 10 mM), or DEF (3 mM) in combination with Tempol (3 mM). The ranges of concentrations of Tempol and DEF are based on those previously shown in this laboratory to reduce on H2O2-mediated cell injury and death in (1) cultured rat cardiac myoblasts (Tempol) and (2) primary cultures of rat PT cells (DEF ). PT cell cultures are then incubated with H2O2 (1 mM) for four hours, after which cellular injury and death are assessed. Upon completion of incubations, cellular injury and death are assessed using the spectrophotometric assays described later in this article[2].

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

    Animal Administration
    [1][2]

    Mice[1]
    Female or male BALB/c mice (5-7 weeks of age) are used. Mice are infected intraperitoneally (i.p.) with 102 blood trypomastigote forms of the type I Colombian strain of T. cruzi. Treatments are performed daily for 30 days from the establishment of CCC (60 dpi) by i.p. injection of 15 mg/kg trans-resveratrol (10% ethanol/PBS), vehicle (10% ethanol/PBS), 5 mg/Kg EX527 (0.1% DMSO), or peroral administration of 40 mg/Kg Resveratrol (10%ethanol-PBS), 500 mg/kg Metformin (dissolved in water), 100 mg/kg Tempol (dissolved in water), Benznidazole (25 mg/Kg, dissolved in water) and vehicle (water or 10%ethanol-PBS).
    Rats[2]
    83 male Wistar rats weighing 230 to 320 g are used.Upon completion of surgical procedures, the animals are randomly allocated to the eight groups. At one minute before commencement of reperfusion, animals received a bolus injection of either vehicle (saline, 4 mL/kg, IV), Tempol (30 mg/kg in saline, IV), DEF (40 mg/kg in saline, IV), or DEF (40 mg/kg in saline, IV) in combination with Tempol (30 mg/kg in saline, IV). The corresponding groups then received a continuous infusion of one of the following throughout the reperfusion period: vehicle (saline, 4 mL/kg/h, IV), Tempol (30 mg/kg/h in saline, IV), DEF (40 mg/kg/h in saline, IV), or Tempol and DEF in combination (30 and 40 mg/kg/h, respectively, in saline, IV). To elucidate the effects of Tempol or DEF on cardiovascular hemodynamics and organ function in sham-operated rats, respective groups of animals received the treatments described previously in this article and as outlined. The concentration of Tempol administered in vivo is based on those previously demonstrated by us to provide significant protection against myocardial ischemia/reperfusion injury in an in vivo rat model. Similarly, the concentration of DEF used is identical to that which we have previously used to provide significant protection against hepatic ischemia/reperfusion injury in in vivo rat and rabbit models.

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

    References

    Purity: 99.98%

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    Keywords:

    Tempol4-Hydroxy-TEMPOReactive Oxygen SpeciesAutophagyInhibitorinhibitorinhibit

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