GIPR抗体

The glucose-dependent insulinotropic polypeptide receptor (GIPR) is a class B G protein-coupled receptor (GPCR) primarily activated by GIP, an incretin hormone released postprandially from intestinal K-cells. GIPR plays a key role in nutrient metabolism, enhancing glucose-stimulated insulin secretion from pancreatic β-cells and promoting lipid storage in adipocytes. Dysregulation of GIPR signaling is implicated in metabolic disorders, including type 2 diabetes and obesity. GIPR-targeting antibodies have emerged as therapeutic tools to modulate this pathway. Antagonist antibodies aim to block GIPR activity, potentially reducing adiposity and improving insulin sensitivity, as explored in preclinical obesity models. Conversely, agonist antibodies designed to activate GIPR are being investigated for their dual benefit in glucose control and weight management, often in combination with GLP-1 receptor agonists. Recent clinical trials highlight the therapeutic potential of GIPR-directed bispecific antibodies (e.g., tirzepatide), which co-activate GIPR and GLP-1R, demonstrating superior glycemic and weight-loss effects compared to single-receptor agonists. Challenges remain in optimizing receptor selectivity, minimizing off-target effects, and understanding tissue-specific signaling outcomes. Ongoing research focuses on antibody engineering strategies to fine-tune pharmacokinetics and pharmacodynamics for metabolic disease applications.