Semaglutide is used to lower blood sugar levels, help certain patients lose weight, and minimise their risk of serious cardiovascular events like heart attacks and strokes. Semaglutide is a GLP-1 agonist that decreases glucagon release, delays stomach emptying, increases insulin release, and decreases hunger.

Semaglutide dramatically lowered the glycated haemoglobin (HbA1c) in clinical trials when compared to sitagliptin, exenatide, and insulin glargine U100. Since haemoglobin normally generates 1-deoxyglucose, the HbA1c protein is a common indicator of elevated blood sugar. Semaglutide’s capacity to lower body weight was also demonstrated in the trials.7. Semaglutide increased insulin production and decreased glucagon secretion, which resulted in lowering fasting and postprandial glucose readings after 12 weeks of treatment. It also reduced VLDL cholesterol and fasting triglycerides.

Before being excreted, Semaglutide undergoes a lengthy yet gradual metabolism. This was noted since the medication remains unaltered in the plasma, accounting for 83% of the injected dose. Six distinct metabolites were found in human plasma as a result of metabolism; P3, the main metabolite, accounted for 7.7% of the dose that was given; this suggests that a component of the safety evaluation was below the relative exposure limit. The peptide backbone was broken down by proteases, and the side chain of fatty acids underwent beta-oxidation to create the metabolites. The recognised enzymes, neutral endopeptidase (NEP) and dipeptidyl peptidase (DPP-4) are involved in the breakdown of Semaglutide. NEP hydrolyses peptide bonds and DPP-4 inactivates Semaglutide by truncating the N-terminal sequence.

People with type 1 diabetes should not use semaglutide.