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Merck

SML0411

Sigma-Aldrich

BAY-X-1005

≥98% (HPLC)

Synonym(e):

α-Cyclopentyl-4-(2-quinolinylmethoxy)-(R)-benzeneacetic acid, (αR)-α-Cyclopentyl-4-(2-quinolinylmethoxy)-benzeneacetic acid, DG 031, Velifapon, Veliflapon

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About This Item

Empirische Formel (Hill-System):
C23H23NO3
CAS-Nummer:
Molekulargewicht:
361.43
MDL-Nummer:
UNSPSC-Code:
12352200
PubChem Substanz-ID:
NACRES:
NA.77

Assay

≥98% (HPLC)

Form

powder

Farbe

white to beige

Löslichkeit

DMSO: 5 mg/mL (clear solution)

Lagertemp.

2-8°C

SMILES String

OC(=O)[C@H](C1CCCC1)c2ccc(OCc3ccc4ccccc4n3)cc2

InChI

1S/C23H23NO3/c25-23(26)22(17-6-1-2-7-17)18-10-13-20(14-11-18)27-15-19-12-9-16-5-3-4-8-21(16)24-19/h3-5,8-14,17,22H,1-2,6-7,15H2,(H,25,26)/t22-/m1/s1

InChIKey

ZEYYDOLCHFETHQ-JOCHJYFZSA-N

Biochem./physiol. Wirkung

Bay-X-1005 is a potent inhibitor of 5-lipoxygenase activating protein (FLAP). Bay-X-1005 inhibits A23187-induced LTB4 production in human leucocytes with an IC50 value of 220 nM, and blocks IgE mediated airway contractions.

Piktogramme

Exclamation mark

Signalwort

Warning

H-Sätze

Gefahreneinstufungen

Acute Tox. 4 Oral

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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Esther Titos et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 17(12), 1745-1747 (2003-09-06)
The existence of an increased number of Kupffer cells is recognized as critical in the initiation of the inflammatory cascade leading to liver fibrosis. Because 5-lipoxygenase (5-LO) is a key regulator of cell growth and survival, in the current investigation
P Roger et al.
Mediators of inflammation, 10(1), 33-36 (2001-04-28)
Increased secretion of mucus is a hallmark of many respiratory diseases and contributes significantly to the airflow limitation experienced by many patients. While the current pharmacological approach to reducing mucus and sputum production in patients is limited, clinical studies have
Inhibition of 5-LO activating protein (FLAP) activity decreases proteinuria in streptozotocin (STZ)-induced diabetic rats.
José M Valdivielso et al.
Advances in experimental medicine and biology, 507, 79-83 (2003-04-01)
Simon Gompertz et al.
Chest, 122(1), 289-294 (2002-07-13)
Patients with COPD classically have neutrophilic bronchial inflammation and raised airway concentrations of the neutrophil chemoattractant leukotriene B(4) (LTB(4)). A small phase II trial was conducted to assess the effects of a leukotriene synthesis inhibitor on bronchial inflammation in patients
Stefano Fiorucci et al.
British journal of pharmacology, 139(7), 1351-1359 (2003-08-02)
(1) Unlike other nonsteroidal anti-inflammatory drugs that inhibit formation of cyclooxygenase (COX)-dependent eicosanoids, acetylation of COX-2 by aspirin switches eicosanoid biosynthesis from prostaglandin E(2) (PGE(2)) to 15-epi-lipoxin A(4) (15-epi-LXA(4) or aspirin-triggered lipoxin, ATL). ATL formation by activated leukocytes (PMN) requires

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