BML-111

• CAT Number: I004354
• CAS Number: 78606-80-1
• Molecular Formula: C8H16O5
• Molecular Weight: 192.21
• Purity: ≥95%
• Synonyms: methyl (5S,6R)-5,6,7-trihydroxyheptanoate
• InChI: InChI=1S/C8H16O5/c1-13-8(12)4-2-3-6(10)7(11)5-9/h6-7,9-11H,2-5H2,1H3/t6-,7+/m0/s1
• InChIKey: RNMFWAFZUNVQOR-NKWVEPMBSA-N
• SMILES: COC(=O)CCCC(C(CO)O)O

BML-111, a lipoxin A4 analog, is a lipoxin A4 receptor agonist. BML-111 represses the activity of angiotensin converting enzyme (ACE) and increases the activity of angiotensinconverting enzyme 2 (ACE2). BML-111 has antiangiogenic, antitumor and anti-inflammatory properties[1][2].
In H22 cells, BML-111 inhibits the production of vascular endothelial growth factor and reduces hypoxia-inducible factor-1α level[1].
BML-111 inhibits leukotriene B4-induced cellular migration with an IC50 of 5 nM[3].
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[1].
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[2].

Reference

[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.
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[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.
 [Content Brief]

[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.
 [Content Brief]