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ChemicalBook--->CAS DataBase List--->222638-67-7

222638-67-7

222638-67-7 Structure

222638-67-7 Structure
IdentificationBack Directory
[Name]

S-(2-BORONOETHYL)-L-CYSTEINE HYDROCHLORIDE
[CAS]

222638-67-7
[Synonyms]

BEC HCl
Reaxys ID: 25974550
S-(2-BORONOETHYL)-L-CYSTEINE HYDROCHLORIDE
BEC hydrochloride - S-(2-Boronoethyl)-L-cysteine hydrochloride
(R)-2-amino-3-((2-boronoethyl)thio)propanoic acid hydrochloride
BEC HCl, 98%, a slow-binding and competitive Arginase II inhibitor
[Molecular Formula]

C5H13BClNO4S
[MDL Number]

MFCD03453539
[MOL File]

222638-67-7.mol
[Molecular Weight]

229.48
Chemical PropertiesBack Directory
[storage temp. ]

Inert atmosphere,Store in freezer, under -20°C
[solubility ]

PBS (pH 7.2): 10 mg/ml
[form ]

A crystalline solid
[color ]

White to yellow
Safety DataBack Directory
[Symbol(GHS) ]


GHS07,GHS02
[Signal word ]

Warning
[Hazard statements ]

H315-H319-H228
[Precautionary statements ]

P240-P210-P241-P264-P280-P302+P352-P370+P378-P337+P313-P305+P351+P338-P362+P364-P332+P313
Hazard InformationBack Directory
[Description]

BEC is a potent slow-binding competitive inhibitor of recombinant rat liver arginase I with Ki values of 0.4 and 0.6 μM from kinetic analyses. It is also a potent inhibitor of human arginase II with Ki values of 310 and 30 nM at pH 7.5 and 9.5, respectively. It does not inhibit murine iNOS at concentrations up to 1 mM. BEC significantly enhances nitric oxide-dependent relaxation of human penile corpus cavernosum smooth muscle in vitro when used at concentrations ranging from 0.1 to 1 mM.
[Uses]

BEC Hydrochloride is Arginase II inhibitor. For the biological study of the inhibition of arginase II, it prevented nitrate tolerance in human umbilical vein endothelial cell and in mouse aorta.
[in vivo]

Administration of the arginase inhibitor BEC decreases arginase activity and causes alterations in NO homeostasis, which are reflected by increases in S-nitrosylated and nitrated proteins in the lungs from inflamed mice. BEC enhances perivascular and peribronchiolar lung inflammation, mucus metaplasia, NF-κB DNA binding, and mRNA expression of the NF-κB-driven chemokine genes CCL20 and KC, and leads to further increases in airways hyperresponsiveness[3].

Animal Model:C57BL/6J wild-type mice, mice deficient in arginase 2 (Arg2-/-), mice deficient in both arginase 1 and 2 (Arg1-/-Arg2-/-), and mice deficient in NOX2 (NOX2-/-
Dosage:20 mg/kg.
Administration:I.V., in 0.9% saline, 1 hour before the injection of LPS.
Result:BEC robustly reduced VEGF expression in neuroglia (72% reduction) and macrophage/microglia (87% reduction).
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