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06720

Sigma-Aldrich

2-Aminoethyl hydrogen sulfate

≥98.0% (T)

Synonym(s):

Sulfuric acid mono 2-aminoethylester

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About This Item

Linear Formula:
NH2CH2CH2OSO3H
CAS Number:
Molecular Weight:
141.15
Beilstein:
1704079
EC Number:
MDL number:
UNSPSC Code:
12352100
PubChem Substance ID:
NACRES:
NA.22

Assay

≥98.0% (T)

mp

277 °C (dec.) (lit.)

SMILES string

NCCOS(O)(=O)=O

InChI

1S/C2H7NO4S/c3-1-2-7-8(4,5)6/h1-3H2,(H,4,5,6)

InChI key

WSYUEVRAMDSJKL-UHFFFAOYSA-N

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Pictograms

Exclamation mark

Signal Word

Warning

Hazard Statements

Hazard Classifications

Acute Tox. 4 Oral - Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

Target Organs

Respiratory system

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

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T Táira et al.
Psychopharmacology, 109(1-2), 191-197 (1992-01-01)
Long-term effects of chronic treatment with a GABA-T (GABA-transaminase) inhibitor, ethanolamine O-sulphate (EOS) (200 mg/kg/day for the postnatal days 3-21) on the binding parameters of GABAA receptors, hypothalamic monoamines and subsequent behavior were studied in Wistar rats. At the age
P Baud et al.
Brain research, 452(1-2), 203-211 (1988-06-14)
Locomotor activity in the rat was studied after infusion of GABAergic and enkephalinergic agonists into the nucleus basalis magnocellularis (NBM) of the forebrain. The experiments were designed to find out whether pharmacological blockade of cholinergic neurons in the NBM had
M Qume et al.
British journal of pharmacology, 122(3), 539-545 (1997-11-14)
1. The effects of 2, 8 and 21 day oral treatment with the specific gamma-aminobutyric acid transaminase (GABA-T) inhibitors gamma-vinyl GABA (GVG) and ethanolamine O-sulphate (EOS) on brain GABA levels, GABA-T activity, and basal and stimulated GABA release from rat
M Qume et al.
Biochemical pharmacology, 52(9), 1355-1363 (1996-11-08)
The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is not solely located in the CNS, it and the enzymes responsible for its synthesis (glutamic acid decarboxylase, GAD, EC 4.1.1.15) and catabolism (GABA-transaminase, GABA-T, EC 2.6.1.19) are also present in non-neuronal organs. Following
J Semba et al.
Neuropsychobiology, 21(3), 152-156 (1989-01-01)
We carried out the forced swimming test in mice to investigate the antidepressant potentials of GABA transaminase (GABA-T) inhibitors including aminooxyacetic acid, ethanolamine-O-sulfate, gamma-vinyl GABA (GVG) and valproic acid (VPA). In acute experiments only GVG reduced immobility. Following chronic oral

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