Dosage: 1.34 mg/ml
Packaging: N1
Release form: solution for subcutaneous administration
Packaging: syringe pen
Manufacturer: PromoMed Rus LLC Manufacturing plant: Medsintez plant (Russia) Active ingredient: Semaglutide
Kvinsenta (semaglutide)
Hypoglycemic agent.
Semaglutide, a GIP-1 receptor agonist (GIP-1R), is synthesized through recombinant DNA technology using a Saccharomyces cerevisiae strain and subsequent purification.
Semaglutide is a GLP-1 analog sharing 94% homology with human GLP-1. It acts as a GLP-1R agonist, selectively binding to and activating GIP-1R, which serves as the target for native GIP-1.
GIP-1 is a physiological hormone with various effects on glucose regulation, appetite, and CCC. Its impact on glucose concentration and appetite is primarily mediated by GIP-1R, located in the pancreas and brain. Pharmacological concentrations of semaglutide reduce blood glucose levels and body weight through a combination of effects described below. GII-1Rs are also found in specific areas of the heart, blood vessels, immune system, and kidneys, where their activation may have cardiovascular and microcirculatory effects.
Unlike native GLP-1, semaglutide has an extended half-life (about 1 week), enabling once-weekly subcutaneous administration. Binding to albumin is the primary mechanism behind semaglutide's prolonged action, leading to decreased renal excretion and protection against metabolic degradation. Additionally, semaglutide is resistant to degradation by the enzyme dipeptidyl peptidase-4. It reduces blood glucose levels through glucose-dependent stimulation of insulin secretion and suppression of glucagon secretion. Consequently, an increase in blood glucose stimulates insulin secretion while suppressing glucagon secretion. The mechanism for lowering glycemic levels also involves a slight delay in gastric emptying during the early postprandial phase. During hypoglycemia, semaglutide reduces insulin secretion without affecting glucagon secretion.
Semaglutide decreases total body weight and adipose tissue mass by reducing energy intake. This involves a general decrease in appetite, increased satiety signals, decreased hunger signals, improved control of food intake, and decreased food cravings. Insulin resistance also decreases, possibly due to reduced body weight. Furthermore, semaglutide reduces the preference for high-fat meals. Animal studies demonstrate semaglutide uptake in specific brain areas, enhancing key satiety signals and suppressing key hunger signals. By acting on isolated brain tissue areas, semaglutide activates neurons associated with satiety and suppresses those associated with hunger.
Clinical studies indicate that semaglutide has positive effects on plasma lipids, reduces systolic blood pressure, and decreases inflammation.
In animal studies, semaglutide inhibits atherosclerosis development, preventing further progression of aortic plaques and reducing inflammation within plaques.