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Merck
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重要文件

194751

Sigma-Aldrich

N-叔丁基羟胺盐酸盐

≥98%

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About This Item

線性公式:
(CH3)3CNHOH · HCl
CAS號碼:
分子量::
125.60
Beilstein:
3546053
EC號碼:
MDL號碼:
分類程式碼代碼:
12352100
PubChem物質ID:
NACRES:
NA.22
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化驗

≥98%

形狀

solid

mp

183-185 °C (lit.)

SMILES 字串

Cl.CC(C)(C)NO

InChI

1S/C4H11NO.ClH/c1-4(2,3)5-6;/h5-6H,1-3H3;1H

InChI 密鑰

DCSATTBHEMKGIP-UHFFFAOYSA-N

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應用

N-tert-Butylhydroxylamine hydrochloride was used in spin trapping of short-lived radicals[1]. It was also used in the synthesis of α-ketoamides[2] and 3-spirocyclopropanated 2-azetidinones[3].

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

Eyeshields, Gloves, type N95 (US)


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A New Three-Component Cascade Reaction to Yield 3-Spirocyclopropanated?-Lactams.
Zanobini A, et al.
European Journal of Organic Chemistry, 2006(5), 1251-1255 (2006)
Ludmila A Voloboueva et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 21(14), 4077-4086 (2007-07-28)
Age-related macular degeneration (AMD) is the leading cause of severe visual impairment in the elderly in developed countries. AMD patients have elevated levels of iron within the retinal pigment epithelia (RPE), which may lead to oxidative damage to mitochondria, disruption
C Lagercrantz
Free radical research communications, 14(5-6), 395-407 (1991-01-01)
Spin trapping of short-lived R. radicals is done by use of N-tert-butylhydroxylamine (1) and H2O2. The hydroxylamine is oxidized to the radical t-BuN(O)H (2) which is converted into the spin trap 2-methyl-2-nitrosopropane (3). Simultaneously, hydroxyl radicals .OH are formed from
Yu-Kyung Kim et al.
Clinical hemorheology and microcirculation, 40(4), 315-324 (2009-01-08)
Irradiation has been shown to induce biochemical changes in stored red blood cells (RBCs) and to generate reactive oxygen species (ROS). This study evaluated the hemorheological properties, the degree of lipid peroxidation and the oxidative susceptibility of irradiated RBCs. Furthermore
Hyun Jeong Kim et al.
Redox report : communications in free radical research, 10(6), 287-293 (2006-01-28)
Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Therefore, compounds that scavenge reactive oxygen species may regulate heat shock-induced cell death. Recently, it has been shown that

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