gip, human

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 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].

(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 (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, 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].

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

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

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.

(Pro3) GIP, human acetate (299898-52-5 Free base) is a potent, stable, and specific full agonist peptide for the human GIP receptor (GIPR). (Pro3) GIP, human acetate (299898-52-5 Free base) is the acetate salt form of a modified analog of natural GIP in which three alanine (Ala) residues have been mutated to proline (Pro). (Pro3) GIP, human acetate (299898-52-5 Free base) is a glucose-dependent insulin secretion (GIP) agonist and a weak inhibitor of gastric acid secretion.

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.

Tirzepatide sodium is the sodium salt form of a dual glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor agonist peptide drug that enhances insulin secretion and improves glycemic control by simultaneously activating GIP and GLP-1 receptors. In research and clinical settings, Tirzepatide sodium has also demonstrated effects in reducing body weight and improving metabolic parameters, and is used in studies related to type 2 diabetes and metabolic disorders.

[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.

human GIP(3-30), amide is a high-affinity human GIP receptor antagonist and a natural metabolite of DPP-4 cleavage of GIP(1-30)NH₂. Human GIP(3-30), amide inhibits insulin secretion in vitro and suppresses cAMP and β-arrestin 1/2 recruitment induced by GIP(1-42).

Taspoglutide, acting as an agonist for the glucagon-like peptide-1 receptor (GLP-1R; Ki = 1.1 nM for the human receptor), induces cAMP accumulation in CHO-K1 cells expressing human GLP-1R (EC50 = 0.06 nM). In oral glucose tolerance tests conducted on Zucker diabetic fatty rats, Taspoglutide (administered weekly at 1 mg/animal) significantly reduced blood glucose levels and increased insulin levels. Additionally, in the same model, it also lowered blood levels of gastric inhibitory polypeptide (GIP), plasma triglycerides, and body weight.