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].

Acetyl Gastric Inhibitory Peptide (human) TFA induces cyclic adenosine monophosphate (cAMP) production in transfected Chinese hamster lung fibroblasts that express human GIP receptors, with an EC50 value of 1.9 nM [1]. Compared to natural GIP, Acetyl Gastric Inhibitory Peptide (human) TFA at concentrations ranging from 10-13 to 10-8 nM demonstrates potent effects in stimulating insulin release [1]. This compound can improve conditions such as glucose intolerance, type 2 diabetes, beta-cell glucose insensitivity, insulin resistance, and reduced insulin secretion [2]. Acetyl Gastric Inhibitory Peptide (human) TFA has the metabolic stability of two fatty acid-derived N-terminal acetylated GIP analogues, along with hypoglycemic and insulinotropic activities, and has been evaluated both in vitro and in vivo [3].

Acetyl Gastric Inhibitory Peptide (human) TFA administered at 25 nmol/kg via intraperitoneal injection as a single dose demonstrated resistance to degradation by plasma dipeptidyl peptidase IV, thereby enhancing its bioactivity and improving its potential as an antidiabetic agent in vivo [1].