gip

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

Endogenous truncated form of the incretin hormone GIP. More potent at stimulating glucose-dependent insulin secretion from rat pancreatic β-cells than GIP.

GIP (human) acetate is a stimulator of glucose-dependent insulin secretion and a weak inhibitor of gastric acid secretion. GIP (human) acetate plays a vital role in lipid metabolism and the development of obesity.

GIP (1-39) acetate is a gastric inhibitory peptide (GIP) purified from porcine intestine and stimulates insulin secretion.

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 (3-42), human (Gastric Inhibitory Polypeptide (3-42) (human)) is a peptide that acts as a glucose-dependent proinsulinotropic polypeptide (GIP) receptor antagonist and regulates insulin secretion and the metabolic effects of GIP in vivo, which can be used to study type 2 diabetes.

GIP (1-30) amide, porcine acetate is an agonist of fully glucose-dependent insulinotropic polypeptide (GIP) receptor. GIP (1-30) amide, porcine acetate can weakly inhibit gastric acid secretion and strongly stimulate insulin.

GIP (3-42), human acetate is an antagonist of a glucose-dependent insulinotropic polypeptide (GIP) receptor and regulates insulin secretion and GIP metabolism in vivo.

GIP (1-30) amide, porcine TFA is a high-affinity full agonist of the glucose-dependent insulinotropic polypeptide (GIP) receptor, with potency comparable to native GIP(1-42) [1]. It also exhibits potent insulin-stimulating properties and weakly inhibits gastric acid secretion.

GIP/GLP-1 dual receptor agonist-1 (compound 4), a receptor agonist for both GIP and GLP-1, shows potential for researching metabolic disorders and fatty liver diseases, such as nonalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease (NAFLD) [1].

GIP, human TFA, a 42-amino acid peptide hormone, functions as a glucose-dependent insulin secretion stimulator and a weak gastric acid secretion inhibitor. Released from intestinal K cells following nutrient ingestion, it serves as an incretin hormone [1] [2] [3].

GIP (1-30) amide, human acetate is a fragment of glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone that plays a crucial role in stimulating insulin secretion and mitigating postprandial glycemic excursions. This compound has been shown to enhance insulin secretion in a dose-dependent manner across concentrations of 10^-9 to 10^-6 M [1].

(Pro3) GIP, human ((Pro3) Gastric Inhibitory Peptide, human) is a stable and specific full agonist for the human GIP receptor (hGIPR) with a high binding affinity (K i / K d values of 0.90 nM), demonstrating efficacy in targeting hGIPR, and is thus suitable for obesity-related diabetes research [1] [2].

GIP, rat TFA (glucose-dependent insulinotropic polypeptide), a 42-amino acid peptide secreted by K cells in the duodenum and jejunum, promotes insulin release from pancreatic beta cells, supports beta cell proliferation, and enhances their survival. This rat-origin bioactive peptide, along with GLP (gastric-like peptide), belongs to the intestinal insulinotropic hormone family and is implicated in lipid homeostasis and potentially in the pathogenesis of obesity. Recent research suggests GIP's multifaceted role in these metabolic processes.

GIP (rat) (Glucose-dependent Insulinotropic Polypeptide), also known as Gastric Inhibitory Polypeptide, is a biologically active 42-amino acid peptide secreted by the K cells of the duodenum and jejunum following food consumption. It belongs to the incretin hormone peptide family, which includes GLP (Gastric-like Peptide), and it not only stimulates insulin release from pancreatic islet β-cells but also may encourage β-cell proliferation and survival. Additionally, recent research indicates GIP may have a role in lipid regulation and could contribute to the development of obesity.

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.

Highly potent GIP receptor agonist (EC50 = 630 ± 119 pM). Displays equivalent cAMP stimulating properties and improved resistance to enzymatic degradation compared to native GIP in cells expressing wild type GIP receptor. Improves glucose tolerance, insul

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

[Pro3]-GIP (Mouse) acetate is mouse [Pro3]-GIP. [Pro3]-GIP is a GIP receptor antagonist.

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.

GIP (1-30)-Myr, a modified form of GIP (1-30) with Myr, is a fragment of glucose-dependent insulinotropic polypeptide (GIP). This hormone, classified as an incretin, enhances insulin secretion and reduces postprandial blood glucose fluctuations. GIP (1-30) stimulates insulin secretion in a dose-dependent manner, effective within the 10^-9 to 10^-6 M range.

GIP (22-51) human (Glucose-dependent Insulinotropic Peptide (22-51) human) is a potent pro-atherosclerotic peptide hormone composed of 30 amino acids. It activates the NF-κB signaling pathway, enhances the expression of MMP-8, and induces the expression of pro-inflammatory and pro-atherogenic proteins. Additionally, it increases intracellular free Ca2+ levels in THP-1 induced macrophages. GIP (22-51) human is useful for atherosclerosis research.

GIP/GLP-1 dual receptor agonist-1 (Compound 4) (sodium) functions as a GIP/GLP-1 receptor agonist. This compound is applicable for research into metabolic disorders and liver diseases, including non-alcoholic steatohepatitis (NASH) and non-alcoholic fatty liver disease (NAFLD).

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.