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A8036

Sigma-Aldrich

N-Acetylheparin sodium salt

~90%

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About This Item

MDL number:
UNSPSC Code:
12352201
NACRES:
NA.25

Assay

~90%

form

solid

Application

N-Acetylheparin, derivitized porcine mucosal heparin without anticoagulant properties, may be used to protect cardiac, vascular and neural tissues by inhibiting complement activation and neutrophil infiltration of the damage site.

Preparation Note

Prepared from porcine mucosal heparin by a modification of the method of Nagasawa, K. and Inoue, Y., Methods Carb. Chem., 8, 291 (1980).

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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J L Park et al.
Pharmacology, 58(3), 120-131 (1999-02-02)
The ability of the heparin derivative, N-acetylheparin (NHEP) to protect the heart from regional ischemia/reperfusion injury was examined in vivo. NHEP (2 mg/kg i.v.) or vehicle was administered 2 h before occlusion of the left circumflex coronary (LCX) artery. Open-chest
P C Kouretas et al.
Journal of molecular and cellular cardiology, 30(12), 2669-2682 (1999-02-17)
Heparin, which is widely used clinically, has recently been shown to have specific properties affecting the vascular endothelium. We hypothesized that heparin stimulates endothelial nitric oxide synthase (eNOS) activity by a mechanism independent of its anticoagulant properties and dependent on
P C Kouretas et al.
Circulation, 99(8), 1062-1068 (1999-03-02)
Coronary endothelial dysfunction after brief ischemia-reperfusion (IR) remains a clinical problem. We investigated the role of heparin and N-acetylheparin, a nonanticoagulant heparin derivative, in modulating coronary endothelial function after IR injury, with an emphasis on defining the role of the
Y Hua et al.
Journal of neurosurgery, 92(6), 1016-1022 (2000-06-06)
Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. Erythrocyte lysis may be mediated by the complement cascade, which then triggers parenchymal injury. In this study the authors examine whether the

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