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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.
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
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
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.
Advances in experimental medicine and biology, 507, 79-83 (2003-04-01)
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
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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