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Semaglutide is indicated to improve glycemic control in adults with type 2 diabetes mellitus as an adjunct of diet and exercise. The approved therapeutic doses are 0.5 mg and 1 mg.7 Diabetes mellitus type 2 is a long-term metabolic disorder characterized by high blood sugar, insulin resistance and lack of insulin. Its onset is determined by the loss ability of beta cells to respond to an increased plasma glucose. This disease is predominantly caused by lifestyle factors like overweight and obesity. The key feature on type 2 diabetes is the presence of insulin resistance which reduced the capacity of insulin to exert its functions at normal at any given concentration. The secretion of insulin is stimulated by the action of incretins in the gut like glucagon-like peptide 1, which also delays gastric emptying and induces satiety, and glucose-dependent insulinotropic polypeptide.
Mode of Action:

Drugs like semaglutide affect the glucose control through several different mechanisms like the increase of insulin secretion, slow of gastric emptying, and reduction of postprandial glucagon and food intake. The glucose homeostasis depends on hormones like insulin and amylin secreted in pancreatic beta cells, glucagon secreted in pancreatic alpha cells and gastrointestinal peptides like glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide. When glucose is administered orally, GLP-1 will stimulate the synthesis of insulin by stimulating pancreatic islets, it will also slow the gastric emptying, inhibit post-meal glucagon release and reduce food intake. GLP-1 has a major role in glucose management and semaglutide presents an analog structure which allows it to perform all the activities of GLP-1.3 The innovative section of semaglutide is the presence of structural modifications (amino acid substitution at position 8) that generate superior stability against dipeptidyl peptidase-4 which is an enzyme that degrades incretins like GLP-1. The structure of semaglutide (lysine acylation with a spacer and C-18 fatty di-acid at position 26) also permits an increased and specific binding to plasma albumin; as well as a modification (amino acid substitution at position 34) that prevents C-18 fatty di-acid binding in wrong sites. All these characteristics donate semaglutide with an extended half-life, increasing patient compliance and quality of life.


In clinical trials, semaglutide reduced significantly the glycated hemoglobin (HbA1c) compared to other medications like sitagliptin, exenatide and insulin glargine U100. The HbA1c protein is a standard measure of high glucose as in normal conditions the hemoglobin forms 1-deoxyfructose. In the trials, it was also showed the ability of semaglutide to reduce the body weight.7 After 12 weeks of treatment, semaglutide lowered fasting and postprandial glucose concentrations by increasing insulin production and decreasing glucagon secretion. It also lowered fasting triglycerides and VLDL cholesterol.


The metabolism of semaglutide is slowly but extensively metabolized prior to excretion. This was observed as 83% of the administered dose found in the plasma is composed of the unchanged drug. As a product of the metabolism, six different metabolites were identified in human plasma in which the major metabolite, named P3, accounted for 7.7% of the administered dose, thus indicating a component below the relative exposure limit in the safety assessment. The metabolites were formed following proteolytic cleavage of the peptide backbone and beta-oxidation of the fatty acid side chain. The known enzymes to be involved in the degradation of semaglutide are dipeptidyl peptidase (DPP-4) and neural endopeptidase (NEP). DPP-4 inactivates semaglutide truncating the N-terminal sequence and NEP hydrolyze peptide bonds.


In preclinical toxicity studies with semaglutide, there was observed the presence of mild c-cell hyperplasia, nests and dilated ultimobranchial ducts after three months of exposure with a 17X of the clinical dose. There was also reports of liver necrosis and centrilobular hypertrophy mainly in man in the same doses. Some ECG abnormalities and multifocal vacuolation and degeneration were observed in high dose studies (27X).

17-{[(1R)-3-[(2-{2-[({2-[2-({[(5S)-5-[(2S)-2-[(2S)-2-[(2S)-2-{2-[(2S)-2-[(2S)-2-[(2S)-2-[(2S)-2-[(2S)-2-[(2S)-2-[(2S)-2-[(2S)-2-[(2S,3R)-2-[(2S)-2-[(2S,3R)-2-{2-[(2S)-2-{2-[(2S)-2-amino-3-(1H-imidazol-4-yl)propanamido]-2-methylpropanamido}-4-carboxybutanamido]acetamido}-3-hydroxybutanamido]-3-phenylpropanamido]-3-hydroxybutanamido]-3-hydroxypropanamido]-3-carboxypropanamido]-3-methylbutanamido]-3-hydroxypropanamido]-3-hydroxypropanamido]-3-(4-hydroxyphenyl)propanamido]-4-methylpentanamido]-4-carboxybutanamido]acetamido}-4-carbamoylbutanamido]propanamido]propanamido]-5-{[(1S)-1-{[(1S)-1-{[(1S,2S)-1-{[(1S)-1-{[(1S)-1-{[(1S)-1-{[(1S)-1-{[(1S)-4-carbamimidamido-1-[({[(1S)-4-carbamimidamido-1-[(carboxymethyl)carbamoyl]butyl]carbamoyl}methyl)carbamoyl]butyl]carbamoyl}-2-methylpropyl]carbamoyl}-3-methylbutyl]carbamoyl}-2-(1H-indol-3-yl)ethyl]carbamoyl}ethyl]carbamoyl}-2-methylbutyl]carbamoyl}-2-phenylethyl]carbamoyl}-3-carboxypropyl]carbamoyl}pentyl]carbamoyl}methoxy)ethoxy]ethyl}carbamoyl)methoxy]ethoxy}ethyl)carbamoyl]-1-carboxypropyl]carbamoyl}heptadecanoic acid
Molecular Mass:
Average: 4113.641 Monoisotopic: 4111.11537713
General Reference:
General Reference:

Gotfredsen CF, Molck AM, Thorup I, Nyborg NC, Salanti Z, Knudsen LB, Larsen MO: The human GLP-1 analogs liraglutide and semaglutide: absence of histopathological effects on the pancreas in nonhuman primates. Diabetes. 2014 Jul;63(7):2486-97. doi: 10.2337/db13-1087. Epub 2014 Mar 7. [PubMed:24608440]
Blundell J, Finlayson G, Axelsen M, Flint A, Gibbons C, Kvist T, Hjerpsted JB: Effects of once-weekly semaglutide on appetite, energy intake, control of eating, food preference and body weight in subjects with obesity. Diabetes Obes Metab. 2017 Sep;19(9):1242-1251. doi: 10.1111/dom.12932. Epub 2017 May 5. [PubMed:28266779]
Lee YS, Jun HS: Anti-diabetic actions of glucagon-like peptide-1 on pancreatic beta-cells. Metabolism. 2014 Jan;63(1):9-19. doi: 10.1016/j.metabol.2013.09.010. Epub 2013 Oct 17. [PubMed:24140094]
Jensen L, Helleberg H, Roffel A, van Lier JJ, Bjornsdottir I, Pedersen PJ, Rowe E, Derving Karsbol J, Pedersen ML: Absorption, metabolism and excretion of the GLP-1 analogue semaglutide in humans and nonclinical species. Eur J Pharm Sci. 2017 Jun 15;104:31-41. doi: 10.1016/j.ejps.2017.03.020. Epub 2017 Mar 16. [PubMed:28323117]
Barnett A. (2012). Type 2 diabetes (2nd ed.). Oxford.
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