Synonyms: Velgia, Insudive, Queensenta, Ozempic, Rebelsas, Semavik, Semavik Next, Semuglin
Molar mass: 4113.641 g/mol
Formula C187H291N45O59
CAS: 910463-68-2
Semaglutide is a GLP-1 receptor agonist (Glucagon-like peptide-1). Semaglutide is a GLP-1 analog with 94% homology to human GLP-1. Semaglutide acts as a GLP-1R agonist that selectively binds to and activates GLP-1R.
GLP-1 is a physiological hormone that exerts several effects on blood glucose regulation, appetite, and the cardiovascular system. The effects on blood glucose and appetite are specifically mediated by GLP-1 receptors located in the pancreas and brain. Pharmacological concentrations of semaglutide reduce blood glucose levels and body weight through a combination of effects described below. GLP-1 receptors are also present in specific areas of the heart, blood vessels, immune system, and kidneys, where their activation may produce cardiovascular and microcirculatory effects.
Unlike native GLP-1, the extended half-life of semaglutide (about 1 week) allows for subcutaneous administration once a week. Binding to albuminOne of the main proteins of the human body, responsible for maintaining normal blood composition and transporting various substances throughout the body. It also serves as a reserve source of amino acids. Albumins perform two very important functions: managing the distribution of water within the body, helping the blood transport vitamins, minerals, and medications. They are responsible for water exchange — they help retain it in the vessels and prevent it from excessively moving into the tissues (thus preventing the development of edema). Albumins influence the formation of tissue fluid, urine, and lymph, and also control the process of water absorption from the intestines. is the main mechanism of semaglutide’s prolonged action, which reduces its renal excretion and protects it from metabolic degradation. Furthermore, semaglutide is stable against degradation by the dipeptidyl peptidase-4 enzymeEnzymes are proteins that accelerate chemical reactions in the body. They ensure the occurrence of metabolic processes such as food digestion, energy release, cell formation, and many others..
Semaglutide reduces blood glucose levels through glucose-dependent stimulation of insulin secretion and suppression of glucagon secretion. Thus, when blood glucose levels rise, insulin secretion is stimulated and glucagon secretion is suppressed. The mechanism of glycemic reduction also includes a slight delay in gastric emptying in the early postprandial phase. During hypoglycemia, semaglutide reduces insulin secretion and does not suppress glucagon secretion.
Semaglutide reduces total body weight and adipose tissue mass by decreasing energy intake. This mechanism involves an overall reduction in appetite, including enhanced satiety signals and weakened hunger signals, as well as improved control of food intake and reduced food cravings. Insulin resistance is also reduced, possibly due to weight loss. Additionally, semaglutide reduces the preference for high-fat food intake. By acting on isolated areas of brain tissue, semaglutide activates neurons associated with satiety and suppresses neurons associated with hunger.
In clinical studies, semaglutide had a positive effect on blood lipids, reduced systolic blood pressure, and decreased inflammation.
Semaglutide improves pancreatic beta-cell function. After an intravenous glucose bolus in patients with T2DM, semaglutide compared to placebo improved the first and second phase insulin response with a three-fold and two-fold increase, respectively, and increased the maximum secretory capacity of pancreatic beta-cells after an arginine stimulation test. Furthermore, compared to placebo, semaglutide therapy increases fasting insulin concentrations.
Semaglutide caused a slight delay in early gastric emptying, thereby reducing the rate of postprandial glucose entry into the bloodstream.
Weight loss with semaglutide occurred primarily due to loss of adipose tissue, which was 3 times greater than the loss of muscle mass.
Compared to placebo, semaglutide reduced calorie intake by 18–35% during three consecutive ad libitum meals. This was facilitated by semaglutide-induced suppression of appetite both fasting and postprandial, improved control of food intake, reduced food cravings, especially for high-fat foods.
Compared to placebo, semaglutide reduced fasting triglyceride and VLDL cholesterol concentrations by 12% and 21%, respectively. The postprandial increase in triglyceride and VLDL cholesterol concentration in response to a high-fat meal was reduced by more than 40%.
Semaglutide is a modern drug for the treatment of type 2 diabetes (also see Glycation) and weight control. It belongs to the class of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and mimics the action of the natural hormone GLP-1, which regulates blood sugar levels and appetite.
Semaglutide:
Common (usually temporary):
Rare but serious:
Semaglutide is an effective drug for diabetes and obesity but requires medical supervision. Its use should be justified, as serious side reactions are possible.
