gip , human

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 (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, 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 (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.

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 (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.

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

[Tyr0] Gastric Inhibitory Peptide (23-42), human, is a glucose-dependent insulinotropic polypeptide (GIP) that modestly inhibits gastric acid secretion while enhancing insulin secretion, making it relevant for research on diabetes and obesity [1] [2].

Acetyl Gastric Inhibitory Peptide (human) TFA, a fatty acid-derivatized analog of the glucose-dependent insulinotropic polypeptide, exhibits enhanced antihyperglycemic and insulinotropic properties. It is utilized in the research of diabetes, insulin resistance, and obesity [1] [2] [3].

Gastric inhibitory peptide (GIP) (22-51), a pro-atherogenic peptide comprised of 30 amino acids from the residues 22-51 of its precursor protein proGIP, is present in human plasma. It activates the degradation of IκB-α and the nuclear translocation of NF-κB in both macrophage-differentiated THP-1 cells and human aortic endothelial cells at a concentration of 1 µM. Additionally, in ApoE-/- mice, GIP (22-51) escalates the area of atherosclerotic lesions and plaque development in vivo.