Bioactivity | 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]. | ||||||||||||
Invitro | 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: | ||||||||||||
Name | N-tert-Butyl-α-phenylnitrone | ||||||||||||
CAS | 3376-24-7 | ||||||||||||
Formula | C11H15NO | ||||||||||||
Molar Mass | 177.24 | ||||||||||||
Appearance | Solid | ||||||||||||
Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
Storage |
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Reference | [1]. Zhenggang Zhou, et al. PBN Protects NP Cells From AAPH-induced Degenerative Changes by Inhibiting the ERK1/2 Pathway. Connect Tissue Res. 2020 Mar 30;1-10. [2]. Lei Zhao, et al. Reactive Oxygen Species Contribute to Lipopolysaccharide-Induced Teratogenesis in Mice. Toxicol Sci. 2008 May;103(1):149-57. [3]. Y Kotake, et al. Inhibition of NF-kappaB, iNOS mRNA, COX2 mRNA, and COX Catalytic Activity by phenyl-N-tert-butylnitrone (PBN). Biochim Biophys Acta. 1998 Nov 19;1448(1):77-84. [4]. R A Floyd. Antioxidants, Oxidative Stress, and Degenerative Neurological Disorders. Proc Soc Exp Biol Med. 1999 Dec;222(3):236-45. |