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1072-13-5

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1072-13-5 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 1072-13-5 includes 7 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 4 digits, 1,0,7 and 2 respectively; the second part has 2 digits, 1 and 3 respectively.
Calculate Digit Verification of CAS Registry Number 1072-13:
(6*1)+(5*0)+(4*7)+(3*2)+(2*1)+(1*3)=45
45 % 10 = 5
So 1072-13-5 is a valid CAS Registry Number.
InChI:InChI=1/C6H16N6S2.2BrH/c7-5(8)11-1-3-13-14-4-2-12-6(9)10;;/h1-4H2,(H4,7,8,11)(H4,9,10,12);2*1H

1072-13-5SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 19, 2017

Revision Date: Aug 19, 2017

1.Identification

1.1 GHS Product identifier

Product name GUANIDINOETHYL DISULFIDE

1.2 Other means of identification

Product number -
Other names Bis(2-guanidinoethyl) persulfide

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:1072-13-5 SDS

1072-13-5Downstream Products

1072-13-5Related news

In vitro and in vivo suppression of cellular activity by GUANIDINOETHYL DISULFIDE (cas 1072-13-5) released from hydrogel microspheres composed of partially oxidized hyaluronan and gelatin07/25/2019

This paper describes the preparation of oxidized hyaluronan crosslinked gelatin microspheres for drug delivery. Microspheres were prepared by a modified water-in-oil-emulsion crosslinking method, where three-dimensional crosslinked hydrogel microspheres formed in the absence of any extraneous cr...detailed

1072-13-5Relevant articles and documents

Pharmacological characterization of guanidinoethyldisulphide (GED), a novel inhibitor of nitric oxide synthase with selectivity towards the inducible isoform

Szabo, Csaba,Bryk, Ruslana,Zingarelli, Basilia,Southan, Garry J.,Gahman, Timothy C.,Bhat, Venkat,Salzman, Andrew L.,Wolff, Donald J.

, p. 1659 - 1668 (1996)

1 Guanidines, amidines, S-alkylisothioureas, and recently, mercaptoalkylguanidines have been described as inhibitors of the generation of nitric oxide (NO) from L-arginine by NO synthases (NOS). We have recently demonstrated that guanidinoethyldisulphide (GED), formed from the dimerisation of mercaptoethylguanidine (MEG), is a novel inhibitor of nitric oxide synthases. Here we describe the pharmacological properties of GED on purified NOS isoforms, various cultured cell types, vascular ring preparations, and in endotoxin shock. 2 GED potently inhibited NOS activity of purified inducible NOS (iNOS), endothelial NOS (ecNOS), and brain NOS (bNOS) enzymes with K(i) values of 4.3, 18 and 25 μM, respectively. Thus, GED has a 4 fold selectivity for iNOS over ecNOS at the enzyme level. The inhibitory effect of GED on ecNOS and iNOS was competitive vs. L-arginine and non-competitive vs. tetrahydrobiopterin. 3 Murine J774 macrophages, rat aortic smooth muscle cells, murine lung epithelial cells, and human intestinal DLD-1 cells were stimulated with appropriate mixtures of pro-inflammatory cytokines or bacterial lipopolysaccharide to express iNOS. In these cells, GED potently inhibited nitrite formation (EC50 values: 11, 9, 1 and 30 μM, respectively). This suggests that uptake of GED may be cell type- and species- dependent. The inhibitory effect of GED on nitrite production was independent of whether GED was given together with immunostimulation or 6 h afterwards, indicating that GED does not interfere with the process of iNOS induction. 4 GED caused relaxations in the precontracted vascular ring preparations (EC50: 20 μM). Part of this relaxation was endothelium-dependent, but was not blocked by methylene blue (100 μM), an inhibitor of soluble guanylyl cyclase. In precontracted rings, GED enhanced the acetylcholine-induced, endothelium-dependent relaxations at 10 μM and caused a slight inhibition of the relaxations at 100 μM. The vascular studies demonstrate that the inhibitory potency of GED on ecNOS in the ring preparations is considerably lower than its potency against iNOS in the cultured cells. These data suggest that the selectivity of GED towards iNOS may lie, in part, at the enzyme level, as well as differential uptake by cells expressing the various isoforms of NOS. 5 In a rat model of endotoxin shock in vivo, administration of GED, at 3 mg kg-1 bolus followed by 10 mg kg-1 h-1 infusion, starting at 90 min after bacterial lipopolysaccharide (LPS, 15 mg kg-1, i.v.), prevented the delayed fall in mean arterial blood pressure, prevented the development of the vascular hyporeactivity to noradrenaline of the thoracic aorta ex vivo and protected against the impairment of the endothelium-dependent relaxations associated with this model of endotoxaemia. The same bolus and infusion of the inhibitor did not alter blood pressure or ex vivo vascular reactivity in normal animals over 90 min. 6 Administration of GED (10 mg kg-1, i.p.) given at 2 h after LPS (120 mg kg-1, i.p.) and every 6 h thereafter caused a significant improvement in the survival rate in a lethal model of endotoxin shock in mice between 12 and 42 h. 7 In conclusion, we found that GED is a competitive inhibitor of iNOS activity. Its selectivity towards iNOS may lie both at the enzyme level and at the level of cell uptake. GED has beneficial effects in models of endotoxin shock that are driven by iNOS. GED or its derivatives may be useful tools in the experimental therapy of inflammatory conditions associated with NO overproduction due to iNOS expression.

Radiation-protective agents. I. Studies on N-alkylated-2-(2-aminoethyl)thiopseudoureas and 1,1-(dithioethylene)diguanidines.

Hino,Tana-ami,Yamada,Akaboshi

, p. 1193 - 1201 (2007/10/04)

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