GIP (1-30) amide (Human) is an insulin-dependent glucose-dependent polypeptide.The sugar-dependent insulin polypeptide (GIP) is an insulin secreting hormone, which can stimulate the secretion of insulin and reduce the occurrence of postpranal-glycemic dis
Potent insulinotropic hormone synthesized by duodenal K-cells. High affinity GIP receptor agonist (EC50 = 0.81 nM) that inhibits gastric acid secretion and stimulates pancreatic insulin release in response to glucose. Also affects lipid metabolism and dis
GIP (1-30) amide, porcine TFA is a high-affinity full agonist of the glucose-dependent insulinotropic polypeptide (GIP) receptor, having a similar potency as the native GIP(1-42) [1]. Furthermore, GIP (1-30) amide, porcine displays weak inhibitory effects on gastric acid secretion while exhibiting potent insulin-stimulating properties.
GIP (1-30) amide (Human) TFA is a glucose-dependent insulinotropic polypeptide fragment. Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone that stimulates insulin secretion and reduces postprandial glycaemic excursions.
Endogenous truncated form of the incretin hormone GIP. More potent at stimulating glucose-dependent insulin secretion from rat pancreatic β-cells than GIP.
GIP receptor antagonist (IC50 = 2.6μM). Inhibits GIP-stimulated insulin release from pancreatic β cells in vitro. In ob/ob mice, blocks the effects of GIP on insulin release and plasma glucose levels. Also improves intraperitoneal glucose tolerance, insul
High affinity rat GIP receptor partial agonist (Kd = 13 nM). Increases cAMP accumulation in COS-7 cells transfected with rat GIP receptor, while also acting as a competitive antagonist of GIP.
This GIP fragment has potent insulinotropic activity in the isolated, perfused rat pancreas but greatly reduced somatostatinotropic activity in the isolated perfused rat stomach. The site responsible for insulinotropic activity apparently lies between residues 19 and 30 of GIP.