LCKLSL, an N-terminal hexapeptide, acts as a competitive inhibitor of annexin A2 (AnxA2), effectively preventing the binding of tissue plasminogen activator (tPA) to AnxA2 while also inhibiting the generation of plasmin. In addition, LCKLSL exhibits anti-angiogenic properties.

In human retinal microvascular endothelial cells (RMVECs), treatment with LCKLSL (0-2 mg) inhibits the generation of plasmin and suppresses the VEGF-induced activity of tPA under hypoxic conditions[1].

Application of LCKLSL in two in vivo models (in chicken chorioallantoic membrane and murine Matrigel plug assays) of angiogenesis demonstrates suppression of the angiogenic responses. Treatment with the LCKLSL peptide significantly decreases the vascular length. At a dose of 5 μg/mL, the LCKLSL peptide significantly decreases the number of vascular branches, junctions and end-points[1].