Amylin receptor 3 (AMY3 receptor)

Amylin receptor 3 is a heterodimeric G protein-coupled peptide hormone receptor formed by the combination of the calcitonin receptor with the accessory protein RAMP3. It is one of three major subtypes in this family—AMY1, AMY2, and AMY3—each defined by its specific RAMP partner. The principal endogenous ligand for all amylin receptors is amylin (islet amyloid polypeptide), but they also respond to related peptides such as calcitonins and CGRP. The AMY receptors are widely distributed in both peripheral tissues and the central nervous system. AMY receptors mediate diverse physiological functions including regulation of satiety, energy homeostasis, glycemic control, and neuronal signaling. They have emerged as therapeutic targets for metabolic diseases like obesity and type 2 diabetes due to their role in appetite suppression and glucose regulation[6][7]. There is also growing evidence implicating these receptors in neurodegenerative processes associated with Alzheimer’s disease; both human amylin and amyloid-beta can activate these receptors leading to potentially harmful intracellular cascades[3]. Pharmacologically, pramlintide—a synthetic analog of human amylin—is an FDA-approved drug that acts on these receptors for diabetes management. Novel dual agonists targeting both calcitonin and amylin activity are under development for obesity therapy[6]. Experimental antagonists have shown promise in blocking neurotoxicity mediated by amyloidogenic peptides. The molecular structure consists specifically of a class B GPCR core provided by the calcitonin receptor dimerized with RAMP proteins—in this case RAMP3—which confers unique pharmacological properties compared to other family members[4][5].

Other names

AMY3Amylin receptor subtype 3CALCR/RAMP3 complexCalcitonin receptor–RAMP3 complex

Agonists activate the AMY3 receptor to mimic or enhance amylin’s physiological effects such as reducing food intake and regulating blood glucose. Antagonists block the binding of amylin or amyloid-beta to prevent downstream neurotoxic signaling.