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.

Product information

CAS Number: 78606-80-1

Molecular Weight: 192.21

Formula: C8H16O5

Chemical Name: methyl (5S,6R)-5,6,7-trihydroxyheptanoate

Smiles: COC(=O)CCC[C@H](O)[C@H](O)CO

InChiKey: RNMFWAFZUNVQOR-NKWVEPMBSA-N

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

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 ^oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 ^oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

In Vitro:

In H22 cells, BML-111 inhibits the production of vascular endothelial growth factor and reduces hypoxia-inducible factor-1α level. BML-111 inhibits leukotriene B4-induced cellular migration with an IC50 of 5 nM.

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. 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.

Products are for research use only. Not for human use.