Allo-aca, a leptin peptidomimetic, acts as a potent antagonist peptide that selectively inhibits leptin receptor activity, effectively disrupting leptin signaling in various in vitro and in vivo models [1] [2].

At a concentration of 50 pM, Allo-aca inhibits leptin-induced proliferation of MDA-MB-231 cells. It also suppresses leptin-induced proliferation of MCF-7 cells with an IC50 of 200 pM [1]. At 250 nmol/L, Allo-aca reduces the expression of VEGF-dependent leptin mRNA below baseline levels in both cell lines. Additionally, Allo-aca inhibits the mitogenic effects induced by VEGF. In RF/6A retinal endothelial cells, Allo-aca obstructs VEGF-induced chemotaxis and haptotaxis [2].

In the MDA-MB-231 orthotopic mouse xenograft model, subcutaneous administration of Allo-aca at doses of 0.1 and 1 mg/kg/day significantly extended the average survival time from 15.4 days (untreated control group) to 24 days and 28.1 days, respectively [1].