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S7198

Sigma-Aldrich

Sivelestat sodium salt hydrate

≥98% (HPLC), solid

Synonym(s):

EI 546 sodium salt hydrate, Elaspol sodium salt hydrate, LY 544349 sodium salt hydrate, Ono-5046 sodium salt hydrate, o-(p-Hydroxybenzenesulfonamido)hippuric acid, pivalate (ester) sodium salt hydrate

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About This Item

Empirical Formula (Hill Notation):
C20H22N2O7S · xNa+ · yH2O
CAS Number:
127373-66-4
Molecular Weight:
434.46 (anhydrous free acid basis)
UNSPSC Code:
12352200
NACRES:
NA.77

assay

≥98% (HPLC)

form

solid

color

white to off-white

solubility

DMSO: 10 mg/mL, clear

storage temp.

room temp

InChI

1S/C20H22N2O7S/c1-20(2,3)19(26)29-13-8-10-14(11-9-13)30(27,28)22-16-7-5-4-6-15(16)18(25)21-12-17(23)24/h4-11,22H,12H2,1-3H3,(H,21,25)(H,23,24)

InChI key

BTGNGJJLZOIYID-UHFFFAOYSA-N

Application

Sivelestat sodium salt hydrate may be used to inhibit human neutrophil elastase-mediated cell signaling.

Biochem/physiol Actions

Sivelestat is a competitive human neutrophil elastase (HNE) inhibitor (IC50 = 44 nM, Ki = 0.2 μM). It also inhibits leukocyte elastase obtained from rabbit, rat, hamster and mouse (IC50 = 19 to 49 nM). However, it does not inhibit trypsin, thrombin, plasmin, plasma kallikrein, pancreas kallikrein, chymotrypsin and cathepsin G even at 100 μM. In in-vivo studies, it suppressed lung hemorrhage in hamster (ID50 = 82 μg/kg) by intratracheal administration and increase of skin capillary permeability in guinea pig (ID50 = 9.6 mg/kg) by intravenous administration, both of which were induced by human neutrophil elastase.

Storage Class

11 - Combustible Solids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

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Biswajit Khatua et al.
Journal of leukocyte biology, 91(4), 641-655 (2012-01-14)
PA is an opportunistic pathogen that is commonly associated with severe infection in immunocompromised hosts. Siglec-9 binds with Sias by cis interaction on the neutrophil surface, thereby reducing immunological activity. However, neutrophils bind with pathogens through trans interactions of siglec-9
Linshui Zhou et al.
Journal of cellular and molecular medicine, 24(20), 11998-12007 (2020-09-17)
The transition of alveolar type II epithelial cells into fibroblasts has been reported to cause and/or aggravate pulmonary fibrosis (PF), which is characterized by fibroblast proliferation, an enhanced production and accumulation of ECM (extracellular matrix), alveolar wall damage and functional
Katja Herges et al.
Multiple sclerosis (Houndmills, Basingstoke, England), 18(4), 398-408 (2012-02-22)
The pathology of neuromyelitis optica (NMO), in contrast to multiple sclerosis, comprises granulocyte infiltrates along extensive lengths of spinal cord, as well as optic nerve. Furthermore, IFN-β treatment worsens NMO. We recently found that experimental autoimmune encephalomyelitis (EAE) induced with
Naoya Fujino et al.
Experimental lung research, 38(1), 28-36 (2011-12-14)
Excess production of neutrophil elastase contributes to the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). However, the role of neutrophil elastase in the repair process following ALI/ARDS is not well understood. The objective of this
Shuoqi Zhang et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 35(9), e21835-e21835 (2021-08-28)
Circulating neutrophil extracellular traps (NETs) resistant to t-PA have not been studied completely although NETs in thrombi may contribute to tissue plasminogen activator (t-PA) resistance. This research intended to elucidate whether circulating NETs are associated with t-PA resistance and the
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