Biological Background

The Glucose-Dependent Insulinotropic Polypeptide Receptor (GIP-R) is a class B GPCR expressed in pancreatic β-cells, adipose tissue, and the gastrointestinal tract. GIP or synthetic agonist activation triggers Gαs coupling and adenylyl cyclase stimulation, increasing intracellular cAMP and enhancing glucose-dependent insulin secretion. GIP-R also modulates lipid metabolism and β-cell proliferation, making it a promising target for type 2 diabetes and obesity research.

GIP-R signals via cAMP and β-arrestin pathways. The cAMP pathway drives insulin exocytosis and β-cell survival; β-arrestin mediates desensitization and pathway diversity. Impaired GIP-R signaling associates with poor glycemic control and reduced β-cell mass, highlighting therapeutic relevance.

Eurofins DiscoverX’s cAMP Hunter™ GIP-RA Bioassay Kit provides a cell-based assay for measuring GIP-RA potency and detecting neutralizing antibodies.

Product Highlights
  • Ready-to-use, functional cell-based assay to monitor cAMP production following GIP-R activation
  • EFC technology delivers robust, highly sensitive detection
  • Two kit formats available: complete kit with positive control agonist or kit without ligand
  • Ready-to-use cryopreserved CHO-K1 GIP-R cells ensure reproducibility and rapid implementation
  • Optimized for 96-well format and easily adaptable to 384-well plate layouts

cAMP Hunter GIP-RA Assay Principle

In the cAMP Hunter™ GIP-RA Bioassay Kit, CHO-K1 cells overexpressing human GIP-R utilize the receptor’s native Gαs coupling to monitor activation. Upon GIP-R engagement, adenylyl cyclase is stimulated to produce 3′–5′ cyclic adenosine monophosphate (cAMP). The resulting rise in intracellular cAMP is quantified via a homogeneous, gain-of-signal competitive immunoassay based on Enzyme Fragment Complementation (EFC) technology.

Signal intensity is directly proportional to cellular cAMP levels, greater GIP-R activation yields higher cAMP and a larger assay readout.

cAMP Hunter GIP-RA assay principle