RT20 Retatropeptide RT 100mg*10 bottles 10mg*10 bottles 15mg*10 bottles 20mg*10 bottles 30mg*10 bottles

                                                                     WhatsApp: +85266976540

                                                                                        +85252797286                                                                     Retatrexate (research code LY-3437943) is a novel synthetic, long-acting tri-receptor agonist peptide developed specifically for preclinical studies related to metabolism. It targets three key metabolic receptors: glucagon-like peptide-1 receptor (GLP-1R), glucose-dependent insulinotropic peptide receptor (GIPR), and glucagon receptor (GCGR). Unlike dual-receptor agonists, retatrexate simultaneously activates all three G protein-coupled receptors, thereby producing synergistic biological effects in studies of obesity, glucose metabolism, and energy balance. On the ECHEMI platform, 20 mg lyophilized powder vials are the mainstream laboratory-grade raw material specification, widely used in in vitro cell experiments and animal model studies of metabolic diseases.

Structurally, retatrexate is a peptide modified with 39 amino acids. Its structure is optimized to resist degradation by the DPP-4 enzyme, thus prolonging its metabolic half-life in biological systems. Its receptor binding capacity exhibits differential activity against GLP-1R, GIPR, and GCGR. Preclinical pharmacological data indicate that retatide activates three target receptors in a balanced manner, rather than simply superimposing the effects of a single receptor. This triple agonist property is the core basis of its multidimensional metabolic regulatory function and has attracted widespread attention in current obesity-related pharmacological research.

The primary research function of retatide lies in controlling appetite and food intake through the GLP-1 receptor pathway. Activation of GLP-1R triggers multiple physiological responses, including slowing gastric emptying rate, prolonging food residence time in the stomach, and generating sustained satiety signals at the gastrointestinal level. Simultaneously, activated GLP-1R transmits signals to the hypothalamus appetite regulation center in the brain, inhibiting neural circuits driving food cravings and overeating. In preclinical animal model studies, retatide treatment significantly reduced cumulative food intake in subjects, which was the main driver of the weight loss observed in subsequent trials. Compared to single GLP-1 receptor agonists, combination with a GIPR activator further enhances satiety. GIP receptors act on the central nervous system, enhancing satiety and making it easier for animals to maintain a low-calorie intake state without significant psychogenic feeding compensation (PMC).

Secondly, retatide exerts multi-site glucose homeostasis regulation through the GLP-1R and GIPR pathways. Both receptors mediate glucose-dependent insulin secretion. Only when blood glucose concentration rises can retatide promote the release of more insulin from pancreatic β cells, thereby significantly reducing the risk of hypoglycemia. Simultaneously, it can inhibit excessive glucagon secretion from pancreatic α cells in the postprandial state, thereby inhibiting excessive glucose production in the liver. In animal models of type 2 diabetes, long-term administration observation showed that retatide effectively reduced fasting blood glucose and postprandial blood glucose peaks, and lowered glycated hemoglobin levels. This glucose-dependent mechanism of action makes it an important research tool for exploring intervention strategies for the incretin system to treat insulin resistance and impaired glucose tolerance.

Thirdly, activation of the glucagon receptor (GCGR) endows retatide with unique energy metabolism regulation, distinguishing it from dual-agonist peptides. GCGR mainly acts on the liver and adipose tissue. Moderate activation of GCGR promotes adipose tissue breakdown, reduces lipid storage, and increases systemic energy expenditure. In liver tissue, repaglinide finely modulates hepatic lipid metabolism, providing research material for studies of non-alcoholic fatty liver disease. Its key pharmacological feature lies in the antagonistic effect among three pathways: GCGR itself may increase blood glucose, but the potent hypoglycemic effects of GLP-1R and GIPR completely offset this tendency. This pharmacological balance achieves the dual benefits of fat mobilization and stable glycemic control, an effect that single glucagon receptor agonists cannot achieve. The synergistic effect of reduced food intake and increased energy expenditure creates a larger energy deficit, explaining the significant weight loss observed in preclinical and phase II clinical studies.

Clinical data provide important references for laboratory studies of repaglinide. Dose-dependent weight loss was observed in phase II human clinical trials in overweight and obese subjects. Subjects treated with repaglinide experienced significant average weight loss, with many subjects losing 15%–24% more than their baseline weight.