hmec

XMD8-92 is an effective and specific BMK1/ERK5 inhibitor (Kd: 80 nM).

E70K is a compound that inhibits the interaction between the chemokine (C-X-C) ligand 8 (CXCL8) and glycosaminoglycans (GAGs) on cell membrane surfaces. It mimics a segment of the CXCL8 protein's GAG-binding region at the C-terminal end, incorporating a glutamate-to-lysine mutation at the 70th position. At a concentration of 50 nM, E70K notably reduces the attachment of primary human neutrophils to human umbilical vein endothelial cells (HUVECs). Moreover, it impedes the CXCL8-triggered movement of these neutrophils across HMEC-1 human microvascular endothelial cell layers within a concentration range of 1 to 1,000 nM.

Quininib is a regulator of Ocular Angiogenesis. Quininib significantly inhibits angiogenic tubule formation in HMEC-1 cells, angiogenic sprouting in aortic ring explants and retinal revascularisation in OIR mice.

Demethoxydeacetoxypseudolaric acid B analog has potent activities against HMEC-1, HL-60, A-549, MB-MDA-468, BEL-7402, HCT116, and Hela cells with IC50s ranging from 0.136 to 1.162 μM. and is semi-synthesized by efficient routines from Pseudolaric acid B.

E70K, a CXCL8 C-terminal peptide, features a lysine (K) substitution for glutamic acid (E) at position 70 and has demonstrated the ability to attenuate neutrophil adhesion and migration in the context of inflammation [1].