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Chemical Structure| 1948-33-0 Chemical Structure| 1948-33-0

Structure of TBHQ
CAS No.: 1948-33-0

Chemical Structure| 1948-33-0

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TBHQ (tert-Butylhydroquinone) is a widely used Nrf2 activator that protects against Doxorubicin (DOX)-induced cardiotoxicity by activating Nrf2. Additionally, TBHQ is an ERK activator that counteracts Dehydrocorydaline (DHC)-induced inhibition of cell proliferation in melanoma.

Synonyms: tert-Butylhydroquinone

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Product Details of TBHQ

CAS No. :1948-33-0
Formula : C10H14O2
M.W : 166.21
SMILES Code : OC1=CC=C(O)C=C1C(C)(C)C
Synonyms :
tert-Butylhydroquinone
MDL No. :MFCD00002344
InChI Key :BGNXCDMCOKJUMV-UHFFFAOYSA-N
Pubchem ID :16043

Safety of TBHQ

GHS Pictogram:
Signal Word:Warning
Hazard Statements:H302-H315-H319-H335
Precautionary Statements:P261-P305+P351+P338

Related Pathways of TBHQ

MAPK

Isoform Comparison

Biological Activity

In Vitro:

Cell Line
Concentration Treated Time Description References
Human intestinal epithelial cells (HIEC) 10 μM 48 h TBHQ significantly decreased LDH release and cell death in 5-FU-treated HIECs and improved their proliferative ability. Cell Mol Biol Lett. 2021 Nov 18;26(1):48.
L02 cells 10 μM 24 h tBHQ pretreatment significantly increased Nrf2 expression, inhibited EC-induced lipid peroxidation, and restored GSH levels, indicating that tBHQ suppressed EC-induced ferroptosis by activating the Nrf2 pathway. Redox Biol. 2022 Jul;53:102349.
Human primary small airway epithelial cells (SAE) 25 µM 15 h TBHQ treatment resulted in a significant increase in CSE enzymatic activity and CSE mRNA levels Antioxidants (Basel). 2022 Aug 16;11(8):1582.
Human primary small airway epithelial cells (SAE) 25 µM 15 h TBHQ treatment led to a significant increase in CSE enzymatic activity and mRNA levels, with a 400% increase in activity and a 10-12-fold increase in mRNA levels. Antioxidants (Basel). 2022 Aug 16;11(8):1582.
HCT116 cells 5 μM 24 h TBHQ significantly reversed the downregulation of GPX4 and NQO1 caused by PRDX1 silencing, indicating that NRF2 plays a critical role in suppressing ferroptosis induced by PRDX1 knockdown. Int J Biol Sci. 2024 Sep 23;20(13):5070-5086.
SW620 cells 5 μM 24 h TBHQ significantly reversed the downregulation of GPX4 and NQO1 caused by PRDX1 silencing, indicating that NRF2 plays a critical role in suppressing ferroptosis induced by PRDX1 knockdown. Int J Biol Sci. 2024 Sep 23;20(13):5070-5086.
Hep3B cells 60 μM 8 h TBHQ increased CUL4A mRNA levels, while WDR23, DDB1, and RBX1 mRNA levels remained unchanged. J Biol Chem. 2021 Jan-Jun;296:100704.

In Vivo:

Species
Animal Model
Administration Dosage Frequency Description References
C57/BL6 mice 5-FU-induced intestinal mucositis model Intraperitoneal injection 10 mg/kg Once daily for 8 days TBHQ significantly attenuated 5-FU-induced intestinal mucositis in mice, reducing weight loss, diarrhea score, and increasing colon length. Cell Mol Biol Lett. 2021 Nov 18;26(1):48.
Balb/c mice EC-induced liver injury model Intraperitoneal injection 20 mg/kg Once daily for 21 days TBHQ pretreatment significantly improved EC-induced liver injury and inflammation, restored Nrf2 expression, and inhibited ferroptosis-related markers, indicating that tBHQ suppressed EC-induced hepatic ferroptosis by activating the Nrf2 pathway. Redox Biol. 2022 Jul;53:102349.
Mice CaOx nephrocalcinosis model Intraperitoneal injection 10 mg/kg 3 days pretreatment followed by 7 days maintenance To investigate the effect of TBHQ on CaOx-induced kidney injury and crystal deposition, TBHQ partially reversed kidney injury and crystal deposition. Adv Sci (Weinh). 2024 Dec;11(48):e2408945
Mice CaOx nephrocalcinosis model Intraperitoneal injection 75, 100, 125 mg/kg Once daily for 7 days To evaluate the effect of ferroptosis inhibition on CaOx-induced kidney injury, it was found that the ferroptosis inhibitor Fer reduced CaOx-induced crystal deposition and kidney injury. Adv Sci (Weinh). 2024 Dec;11(48):e2408945
Mice CT26PRDX1-KD xenograft model Intraperitoneal injection 10 mg/kg Daily until the end of the experiment TBHQ significantly restored the expression of NRF2 and GPX4 in the CT26PRDX1-KD group and reversed the inhibitory effect of PRDX1 knockdown on tumor growth, indicating that NRF2 activation suppresses ferroptosis induced by PRDX1 knockdown in vivo. Int J Biol Sci. 2024 Sep 23;20(13):5070-5086.

Protocol

Bio Calculators
Preparing Stock Solutions 1mg 5mg 10mg

1 mM

5 mM

10 mM

6.02mL

1.20mL

0.60mL

30.08mL

6.02mL

3.01mL

60.16mL

12.03mL

6.02mL

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