Lipoxin A4
(Synonyms: 脂氧素 A4; LXA4) 目录号 : GC18552Produced by the metabolism of 15-HETE or 15-HpETE with leukocytes
Cas No.:89663-86-5
Sample solution is provided at 25 µL, 10mM.
Lipoxin A4 (LXA4) is a trihydroxy fatty acid containing a conjugated tetraene, produced by the metabolism of (±)15-HETE or 15-HpETE with human leukocytes.[1] LXA4 is equipotent to leukotriene B4 in inducing superoxide generation in human neutrophils at 0.1 µM.2 LXA4 is associated with several other biological functions including leukocyte activation, chemotaxis effects, natural killer cell inhibition, and monocyte migration and adhesion.[2],[3],[4] Analytical and biological comparisons of synthetic LXA4 with endogenously derived LXA4 have confirmed its identity as matching the natural product.[5]
Lipoxin A4 (LXA4)是一种三羟基脂肪酸，含有一个共轭四烯，通过人类白细胞代谢(±)15-HETE或15-HpETE产生[1]。在0.1 µM的浓度下，LXA4与白三烯B4具有相同的诱导人类中性粒细胞产生超氧化物的效果[2]。LXA4与许多其他生物学功能有关，包括白细胞激活、趋化效应、自然杀伤细胞抑制、单核细胞迁移和粘附等[2],[3],[4]。合成LXA4与内源性LXA4的分析和生物学比较已经证实其身份与天然产物相匹配[5]。
Reference:
[1]. Serhan, C.N., Nicolaou, K.C., Webber, S.E., et al. Lipoxin A. Stereochemistry and biosynthesis. J. Biol. Chem. 261(35), 16340-16345 (1986).
[2]. Serhan, C.N., Hamberg, M., and Samuelsson, B. Lipoxins: Novel series of biologically active compounds formed from arachidonic acid in human leukocytes. Proc. Natl. Acad. Sci. U.S.A. 81(17), 5335-5339 (1984).
[3]. Ramstedt, U., Serhan, C.N., Nicolaou, K.C., et al. Lipoxin A-induced inhibition of human natural killer cell cytotoxicity: Studies on stereospecificity of inhibition and mode of action. J. Immunol. 138(1), 266-270 (1987).
[4]. Maddox, J.F., and Serhan, C.N. Lipoxin A4 and B4 are potent stimuli for human monocyte migration and adhesion: Selective inactivation by dehydrogenation and reduction. J. Exp. Med. 183(1), 137-146 (1996).
[5]. Serhan, C. . (2007).
| Cas No. | 89663-86-5 | SDF | |
| 别名 | 脂氧素 A4; LXA4 | ||
| 化学名 | 5S,6R,15S-trihydroxy-7E,9E,11Z,13E-eicosatetraenoic acid | ||
| Canonical SMILES | CCCCC[C@H](O)/C=C/C=C\C=C\C=C\[C@@H](O)[C@@H](O)CCCC(O)=O | ||
| 分子式 | C20H32O5 | 分子量 | 352.5 |
| 溶解度 | DMF: 50 mg/mL; Ethanol: 50 mg/mL; PBS pH 7.2: 1 mg/mL | 储存条件 | Store at -80°C, protect form light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.8369 mL | 14.1844 mL | 28.3688 mL |
| 5 mM | 0.5674 mL | 2.8369 mL | 5.6738 mL |
| 10 mM | 0.2837 mL | 1.4184 mL | 2.8369 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Related Biological Data
LXA4 Attenuated Septic AKI via Inhibition of PPAR-g/NF-kB Pathway.As shown in Figure 6B, LXA4 pretreatment significantly inhibited the activation of NFkB p65 (p-p65), p53, and p21, and the changes were reversed by GW9662.
To further explore the renoprotective effect of LXA4 on AKI induced by sepsis, rats were pretreated with LXA4(GlpBio) (100 μg/kg, i.v.) prior to CLP surgery.
Front Immunol 12 (2021) PMID: 33936050 IF: 7.562 -
Related Biological Data
LXA4 was relatively insufficient for the inflammatory response in patients with acute gout.The levels of IL-1b, TNF-a, and LXA4 in the serum of patients with acute gout (n=39), patients with intercritical gout (n=27), and healthy controls (n=30) detected by ELISA.
Moreover, THP-1 macrophages primed with LPS were pretreated with 150 nM LXA4(GlpBio) and tBHQ or auranofin for 1 h, followed by 100 ug/ml MSU stimulation for 24 h.
Front Immunol 13 (2022): 1060441 PMID: 36569930 IF: 7.3 -
Related Biological Data
LXA4 treatment alleviated the increase in body weight and fat mass of mice caused by HFD.LXA4 treatment notably reduced the body weight of mice with HFD (p<0.001, figure 1A), but exerted few effects on food intake (figure 1B) of mice with HFD and the body weight and food intake of normally reared mice (figure 1A-B).
Control + LXA4 group, mice were injected intraperitoneally with 5 ng/g/day LXA4(GlpBio) solution for 3 consecutive days, and then mice subsequently were fed with normal diet for 9 weeks.
bioRxiv (2024): 2024-02