LEAP-2 acetate (Human liver expressed antimicrobial peptide-2) is an endogenous antagonist of the ghrelin receptor GHS-R1a with an IC50 of 6.0 nM, suppressing the orexigenic effects of ghrelin, attenuating ghrelin-induced growth hormone release, reducing basal food intake. LEAP-2 acetateexhibit direct antimicrobial activity against model microorganisms, thereby serving as a multifunctional peptide for mechanistic studies of obesity, metabolism, and infection biology.

GHSR1a:1-3 nM (Ki)

In metabolic mouse models, LEAP-2 acetate functions as a satiety signal. Its plasma levels are inversely correlated with Ghrelin; levels decrease during fasting and rise upon re-feeding. Administration of LEAP-2 acetate suppresses appetite and prevents Ghrelin-induced hyperglycemia by blocking the reduction of insulin secretion. In diet-induced obese mice, chronic administration or overexpression of LEAP-2 acetate leads to reduced food intake and body weight loss [1].