BML-111

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]. IC50 & Target: Lipoxin A4 receptor^[1]
Angiotensin converting enzyme (ACE)^[2] In Vitro: 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]. In Vivo: 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].