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SML0411

Sigma-Aldrich

BAY-X-1005

≥98% (HPLC)

Synonym(s):

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

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5 MG
$148.00
25 MG
$593.00

$148.00

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5 MG
$148.00
25 MG
$593.00

About This Item

Empirical Formula (Hill Notation):
C23H23NO3
CAS Number:
128253-31-6
Molecular Weight:
361.43
MDL number:
MFCD00870329
UNSPSC Code:
12352200
PubChem Substance ID:
329825406
NACRES:
NA.77

$148.00

Please contact Customer Service for Availability

Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 5 mg/mL (clear solution)

storage temp.

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

InChI key

ZEYYDOLCHFETHQ-JOCHJYFZSA-N

Biochem/physiol Actions

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.

Pictograms

Exclamation mark
GHS07

Signal Word

Warning

Hazard Statements

H302

Precautionary Statements

P264 - P270 - P301 + P312 - P501

Hazard Classifications

Acute Tox. 4 Oral

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
0000143140
0000143141
072M4614V

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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
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)
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
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
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