1. Immunology/Inflammation
    NF-κB
    Metabolic Enzyme/Protease
  2. COX
    Reactive Oxygen Species
  3. N-tert-Butyl-α-phenylnitrone

N-tert-Butyl-α-phenylnitrone 

Cat. No.: HY-128463 Purity: >98.0%
Handling Instructions

N-tert-Butyl-α-phenylnitrone is a nitrone-based free radical scavenger that forms nitroxide spin adducts. N-tert-Butyl-α-phenylnitrone inhibits COX2 catalytic activity. N-tert-Butyl-α-phenylnitrone has potent ROS scavenging, anti-inflammatory, neuroprotective, anti-aging and anti-diabetic activities, and can penetrate the blood-brain barrier.

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

N-tert-Butyl-α-phenylnitrone Chemical Structure

N-tert-Butyl-α-phenylnitrone Chemical Structure

CAS No. : 3376-24-7

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100 mg USD 90 In-stock
Estimated Time of Arrival: December 31
250 mg USD 165 In-stock
Estimated Time of Arrival: December 31
500 mg USD 280 In-stock
Estimated Time of Arrival: December 31
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Description

N-tert-Butyl-α-phenylnitrone is a nitrone-based free radical scavenger that forms nitroxide spin adducts. N-tert-Butyl-α-phenylnitrone inhibits COX2 catalytic activity. N-tert-Butyl-α-phenylnitrone has potent ROS scavenging, anti-inflammatory, neuroprotective, anti-aging and anti-diabetic activities, and can penetrate the blood-brain barrier[1][2][3][4].

IC50 & Target[3]

COX-2

 

Reactive oxygen species (ROS)

 

In Vitro

N-tert-Butyl-α-phenylnitrone (PBN) (25-100 µM) treatment leads to a significant decrease in 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)-induced intracellular ROS accumulation. N-tert-Butyl-α-phenylnitrone also attenuates AAPH-induced cytotoxicity, matrix degradation, and apoptosis. N-tert-Butyl-α-phenylnitrone suppresses AAPH-induced activation of ERK/MAPK pathway. N-tert-Butyl-α-phenylnitrone has the potenial for intervertebral disc degeneration (IDD) research[1].

In Vivo

N-tert-Butyl-α-phenylnitrone (PBN; 100 mg/kg; intraperitoneal injection; twice a day; C57Bl/6 mice) treatment not only abolishes the LPS-induced lipid peroxidation, nitrotyrosine residue levels, and GSH depletion, but also decreases the incidence of external malformations[2].

Animal Model: C57Bl/6 mice induced by lipopolysaccharide (LPS)[2]
Dosage: 100 mg/kg
Administration: Intraperitoneal injection; twice a day (on gestational day 8)
Result: Abolished LPS-induced lipid peroxidation, nitrotyrosine residues, and GSH depletion.
Molecular Weight

177.24

Formula

C₁₁H₁₅NO

CAS No.

3376-24-7

SMILES

CC(/[N+]([O-])=C/C1=CC=CC=C1)(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 : 100 mg/mL (564.21 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 5.6421 mL 28.2103 mL 56.4207 mL
5 mM 1.1284 mL 5.6421 mL 11.2841 mL
10 mM 0.5642 mL 2.8210 mL 5.6421 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

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

    Solubility: ≥ 2.5 mg/mL (14.11 mM); Clear solution

  • 2.

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

    Solubility: ≥ 2.5 mg/mL (14.11 mM); Clear solution

  • 3.

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

    Solubility: ≥ 2.5 mg/mL (14.11 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
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Keywords:

N-tert-Butyl-α-phenylnitroneCOXReactive Oxygen SpeciesCyclooxygenaseScavengerantioxidantnitroxidespinadductsROSBBBERKMAPKneuroprotectiveiNOSInhibitorinhibitorinhibit

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Product Name:
N-tert-Butyl-α-phenylnitrone
Cat. No.:
HY-128463
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