1. NF-κB
    Stem Cell/Wnt
    MAPK/ERK Pathway
    Autophagy
    Apoptosis
  2. Keap1-Nrf2
    ERK
    Autophagy
    Apoptosis
    Ferroptosis
  3. TBHQ

TBHQ  (Synonyms: tert-Butylhydroquinone)

Cat. No.: HY-100489 Purity: 99.76%
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TBHQ (tert-Butylhydroquinone) is a widely used Nrf2 activator, protects against Doxorubicin (DOX)-induced cardiotoxicity through activation of Nrf2. TBHQ (tert-Butylhydroquinone) is also an ERK activator; rescues Dehydrocorydaline (DHC)-induced cell proliferation inhibitionin melanoma.

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

TBHQ Chemical Structure

TBHQ Chemical Structure

CAS No. : 1948-33-0

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10 mM * 1 mL in DMSO USD 55 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 40 publication(s) in Google Scholar

Top Publications Citing Use of Products

38 Publications Citing Use of MCE TBHQ

WB

    TBHQ purchased from MCE. Usage Cited in: Biochem Biophys Res Commun. 2018 Jun 7;500(3):790-796.  [Abstract]

    Macrophages are isolated from wild-type mice, treated with tBHQ (100 μM) or not, and induced for 3 h using LPS, IFN-g, IL-4 or IL-13. Western blot analysis of the expression of Nrf2, p65 subunit of NF-kB, phosphorylated p65 and PPARg in the cytoplasm and nucleus.

    TBHQ purchased from MCE. Usage Cited in: Front Pharmacol. 2018 Jun 6;9:540.  [Abstract]

    BHQ promotes higher protein expression of Nrf2 in a time-dependent manner in neonatal rat cardiac fibroblasts (NRCF) while notably downregulated collagen I and collagen III.

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    Description

    TBHQ (tert-Butylhydroquinone) is a widely used Nrf2 activator, protects against Doxorubicin (DOX)-induced cardiotoxicity through activation of Nrf2[1]. TBHQ (tert-Butylhydroquinone) is also an ERK activator; rescues Dehydrocorydaline (DHC)-induced cell proliferation inhibitionin melanoma[2].

    IC50 & Target[1][2]

    Nrf2

     

    ERK

     

    Autophagy

     

    In Vitro

    TBHQ (t-butylhydroquinone; tBHQ; 0-100 μM; 48 hours; H9c2 cells) alone does not affect H9c2 cells viability. Pre-incubation of the H9c2 cells with various concentrations of tBHQ for 24 hours enhances cell viability which is decreased due to exposure to ethanol in a dose-dependent manner. Treatment with tBHQ markedly enhances the viability of H9c2 cardiomyocytes exposed to ethanol[3].
    TBHQ (5 μM; 15 min; H9c2 cells) treatment significantly reduces the amount of apoptotic cells exposed to ethanol[3].
    TBHQ (5 μM; H9c2 cells) pre-treatment markedly inhibites the ethanol-induced increase in caspase-3 and Bax expression, and enhances Bcl-2 expression[3].

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

    Cell Viability Assay[3]

    Cell Line: H9c2 cells
    Concentration: 0 µM, 0.625 µM, 1.25 µM, 2.5 µM, 5 µM, 10 µM, 20 µM, 50 µM and 100 µM
    Incubation Time: 48 hours
    Result: Enhanced the viability of H9c2 cardiomyocytes exposed to ethanol.

    Apoptosis Analysis[3]

    Cell Line: H9c2 cells
    Concentration: 5 μM
    Incubation Time:
    Result: Lowered the amount of apoptotic cells exposed to ethanol.

    Western Blot Analysis[3]

    Cell Line: H9c2 cells
    Concentration: 5 μM
    Incubation Time:
    Result: Inhibited the ethanol-induced increase in caspase-3 and Bax expression, and enhanced Bcl-2 expression.
    In Vivo

    TBHQ treatment (50 mg/kg; Intraperitoneal injection; three injections at intervals of 8 h that began 1-h post ICH; CD-1 mice) augments the DNA-Binding activity of Nrf2, attenuates oxidative brain damage and acute neurological deficits afterintracerebral hemorrhage (ICH), attenuates microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1β). TBHQ has the efficacy of post-injury administration in attenuating acute neurological injury after ICH[4].

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

    Animal Model: Male CD-1 mice (8-10 weeks old)[4]
    Dosage: 50 mg/kg
    Administration: Intraperitoneal injection; three injections at intervals of 8 hours that began 1h post ICH.
    Result: The treatment augmented the DNA-binding activity of Nrf2, attenuated brain oxidative damage, attenuated the microglial activation and the expression of IL-1β.
    Molecular Weight

    166.22

    Formula

    C10H14O2

    CAS No.
    SMILES

    OC1=CC=C(O)C=C1C(C)(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: 

    DMSO : ≥ 56.66 mg/mL (340.87 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 6.0161 mL 30.0806 mL 60.1612 mL
    5 mM 1.2032 mL 6.0161 mL 12.0322 mL
    10 mM 0.6016 mL 3.0081 mL 6.0161 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  50% PEG300    50% saline

      Solubility: 20 mg/mL (120.32 mM); Clear solution; Need ultrasonic

    • 2.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.5 mg/mL (15.04 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.5 mg/mL (15.04 mM); Clear solution

    • 4.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.5 mg/mL (15.04 mM); Clear solution

    *All of the co-solvents are available by MCE.
    Purity & Documentation

    Purity: 99.76%

    References
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    Help & FAQs
    • Do most proteins show cross-species activity?

      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.

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    Product Name:
    TBHQ
    Cat. No.:
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