LOX and obesity due to melanocortin 4 receptor deficiency: From a chemical biology standpoint, the profile of LASSBio-1986 is aligned with the growing body of evidence that NAH scaffolds can be tuned to act not only on classical inflammatory targets (such as COX, LOX, iNOS and cytokine networks) but also on metabolic endpoints, including obesity, lipid metabolism and incretin signaling [18,19,20,21,22,24,25,26,27,28].