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Bromoenol lactone
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Bromoenol lactone图片
CAS NO:88070-98-8
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议

产品介绍
Bromoenol lactone ((6E)-Bromoenol lactone) 是一种基于自杀的不可逆、选择性、有效的钙非依赖性磷脂酶 A2 (iPLA2β) 抑制剂,IC50 值约为 7 μM,可抑制抗原刺激的肥大细胞胞吐作用而不阻断 Ca2 + 涌入。
Cas No.88070-98-8
别名(6E)-Bromoenol lactone
化学名6E-(bromomethylene)tetrahydro-3-(1-naphthalenyl)-2H-pyran-2-one
Canonical SMILESBr/C=C1\CCC(C(=O)O\1)c1cccc2ccccc12
分子式C16H13BrO2
分子量317.2
溶解度≤2mg/ml in ethanol;25mg/ml in DMSO;50mg/ml in dimethyl formamide
储存条件Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

Bromoenol lactone is a potent and irreversible inhibitor of myocardial cytosolic calcium-independent phospholipase A2 (iPLA2) [1].

The iPLA2 has been involved in stimulus-induced arachidonic acid release and lysophospholipid generation. The catalytic action of iPLA2 is responsible for phospholipid remodeling as a housekeeping function. Arachidonic acid and lysophospholipid generated by iPLA2 act as a signaling molecule in cellular functions, including eicosanoid production, glucose-induced insulin secretion, Fas-induced apoptosis, cellular proliferation, membrane traffic in fusion, contribution to myocardial ischemia, and others [2].

BEL promoted apoptosis in a variety of cell lines, including U937, THP-1, and MonoMac (human phagocyte), RAW264.7 (murine macrophage), Jurkat (human T lymphocyte), and GH3 (human pituitary). Long term treatment with BEL (up to 24 h) increased annexin-V binding to the cell surface and nuclear DNA damage. BEL induced the proteolysis of procaspase-9 and procaspase-3 and increased cleavage of poly (ADP-ribose) polymerase [1]. BEL inhibited cellular phosphatidic acid phosphohydrolase (PAP) activity in intact P388D1 macrophages with an IC50 of ~8 μM. BEL blocked triacylglycerol biosynthesis in P388D1 cells by decreasing diacylglycerol availability [3].

References:
[1] Fuentes L, Pérez R, Nieto M L, et al.  Bromoenol lactone promotes cell death by a mechanism involving phosphatidate phosphohydrolase-1 rather than calcium-independent phospholipase A2[J]. Journal of Biological Chemistry, 2003, 278(45): 44683-44690.
[2] Akiba S, Sato T.  Cellular function of calcium-independent phospholipase A2[J]. Biological and Pharmaceutical Bulletin, 2004, 27(8): 1174-1178.
[3] Balsinde J, Dennis E A.  Bromoenol lactone inhibits magnesium-dependent phosphatidate phosphohydrolase and blocks triacylglycerol biosynthesis in mouse P388D1 macrophages[J]. Journal of Biological Chemistry, 1996, 271(50): 31937-31941.