| 靶点: |
Lipoxin A4 receptor;Angiotensin converting enzyme (ACE) |
| 体内研究: |
BML-111 (1 mg/kg; intraperitoneal injection; for 15 days; male Imprinting Control Region mice) treatment suppresses tumor-related angiogenesis and tumor growth in vivo. BML-111 also enhances the in situ apoptosis while inhibiting macrophage infiltration in tumor tissue. BML-111 protects LPS-induced acute lung injury and LPS/D-GalN-induced acute liver injury. BML-111 represses the activity of ACE, but increases the activity of ACE2. BML-111 decreases the expression levels of ACE, AngII, and AngII type 1 receptor (AT1R), meanwhile increases the levels of ACE2, angiotensin-(1-7) (Ang-1-7), and Mas. |
| 参考文献: |
1. Ying Chen, et al. Lipoxin A4 and Its Analogue Suppress the Tumor Growth of Transplanted H22 in Mice: The Role of Antiangiogenesis. Mol Cancer Ther. 2010 Aug;9(8):2164-74. 2. Qiong-Feng Chen, et al. BML-111, a Lipoxin Receptor Agonist, Protects Against Acute Injury via Regulating the Renin Angiotensin-Aldosterone System. Prostaglandins Other Lipid Mediat. 2019 Feb;140:9-17. 3. T H Lee, et al. Inhibition of Leukotriene B4-induced Neutrophil Migration by Lipoxin A4: Structure-Function Relationships. Biochem Biophys Res Commun. 1991 Nov 14;180(3):1416-21. |
| 溶解性: |
H2O: ≥20mg/mL |
| 保存条件: |
-80℃(运输条件:冰袋低温运输) |
| 配置溶液浓度参考: |
|
1mg |
5mg |
10mg |
| 1 mM |
5.203 ml |
26.013 ml |
52.026 ml |
| 5 mM |
1.041 ml |
5.203 ml |
10.405 ml |
| 10 mM |
0.52 ml |
2.601 ml |
5.203 ml |
| 50 mM |
0.104 ml |
0.52 ml |
1.041 ml |
|
| 注意: |
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