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Merck

SML0411

Sigma-Aldrich

BAY-X-1005

≥98% (HPLC)

别名:

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

经验公式(希尔记法):
C23H23NO3
分子量:
361.43
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 5 mg/mL (clear solution)

儲存溫度

2-8°C

SMILES 字串

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 密鑰

ZEYYDOLCHFETHQ-JOCHJYFZSA-N

生化/生理作用

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.

象形圖

Exclamation mark

訊號詞

Warning

危險聲明

危險分類

Acute Tox. 4 Oral

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°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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