Ozempic (semaglutide) is a glucagon-like peptide 1 (GLP-1) receptor agonist.
Ozempic is specifically indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.
Ozempic is supplied as a solution for subcutaneous injection into the abdomen, thigh or upper arm. The recommended starting dose is 0.25 mg once weekly. After 4 weeks, the dose should be increased to 0.5 mg once weekly. If after at least 4 weeks additional glycemic control is needed, increase the dose to 1 mg once weekly. Ozempic should be administered once weekly at any time of day, with or without meals. If a dose is missed administer within 5 days of missed dose.
The FDA approval of Ozempic was based on the results from a global Phase IIIa clinical trial comprised eight clinical trials involving more than 8,000 adults with type II diabetes, including a two-year cardiovascular outcomes trial that evaluated safety in adults with type II diabetes at high risk of cardiovascular events. Ozempic showed clinically meaningful and statistically significant reductions in A1c compared with placebo, sitagliptin and exenatide extended-release. As a secondary endpoint in the trials, treatment with Ozempic resulted in reductions in body weight.
Adverse effects associated with the use of Ozempic may include, but are not, limited to, the following:
The Ozempic drug label comes with the following Black Box Warning:
RISK OF THYROID C−CELL TUMORS. In rodents, semaglutide causes thyroid C-cell tumors. It is unknown whether Ozempic causes thyroid C-cell tumors, including medullary thyroid carcinoma, in humans as the human relevance of semaglutide-induced rodent thyroid C-cell tumors has not been determined. Ozempic is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2).
Ozempic (semaglutide) is a glucagon-like peptide 1 (GLP-1) receptor agonist that selectively binds to and activates the GLP-1 receptor, the target for native GLP-1. GLP-1 is a physiological hormone that has multiple actions on glucose, mediated by the GLP-1 receptors. The principal mechanism of protraction resulting in the long half-life of semaglutide is albumin binding, which results in decreased renal clearance and protection from metabolic degradation. Furthermore, semaglutide is stabilized against degradation by the DPP-4 enzyme. Semaglutide reduces blood glucose through a mechanism where it stimulates insulin secretion and lowers glucagon secretion, both in a glucose-dependent manner. Thus, when blood glucose is high, insulin secretion is stimulated and glucagon secretion is inhibited. The mechanism of blood glucose lowering also involves a minor delay in gastric emptying in the early postprandial phas
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