# What Is Semaglutide? The GLP-1 Peptide Explained > What is semaglutide? A GLP-1 receptor agonist peptide — an engineered copy of a gut hormone, FDA-approved for type 2 diabetes and chronic weight management. The structure, class and approvals, explained plainly and cited. An engineered copy of a gut hormone, built to last a week — what it is, what class it belongs to, and what it is approved to do. ## The short version If you are asking what is semaglutide, the simplest answer is: it is a medicine that copies a natural gut hormone to lower blood sugar and quiet appetite. The hormone it copies is GLP-1 (glucagon-like peptide-1), which your gut releases after you eat. GLP-1 tells the pancreas to release insulin, slows how fast your stomach empties, and signals your brain that you are full. The problem with the natural hormone is that the body destroys it within about two minutes. Semaglutide is re-engineered so it lasts about a week instead, which is why a single weekly injection works. It comes as a once-weekly shot and a once-daily pill. The FDA has approved it to treat type 2 diabetes, to manage long-term weight, to lower heart-attack and stroke risk in people with heart disease, and (in 2025) to treat a fatty-liver disease called MASH. This page explains what it is and how it is built. It is a plain-language primer, not medical advice. ## Semaglutide peptide: what it is made of The semaglutide peptide is a 31-amino-acid acylated analogue of human GLP-1 — meaning it is a chain of building blocks that closely mirrors the natural hormone, sharing about 94% of its sequence, with a fatty-acid chain attached [11]. Three engineered changes give it staying power. First, the building block at position 8 is swapped for a non-standard one (alpha-aminoisobutyric acid, or Aib) that blocks DPP-4, the enzyme that normally chews up GLP-1 in minutes. Second, a building block at position 34 is changed to keep the molecule stable. Third, and most important for its weekly schedule, a long C18 fatty di-acid side chain is attached; this lipid "tail" binds tightly but reversibly to albumin (a carrier protein in the blood), which shields the peptide from being filtered out by the kidneys and slows its breakdown [11]. The net result of that design is an elimination half-life of roughly one week, so steady drug levels persist and one weekly dose is enough. By chemistry it is a peptide; by function it is a GLP-1 receptor agonist. ## What class of drug it is Semaglutide belongs to a class called GLP-1 receptor agonists (GLP-1 RAs), sometimes called incretin mimetics. An incretin is a gut hormone — GLP-1 is one — that boosts insulin release in response to food; a receptor agonist is simply a molecule that switches a receptor on. So a GLP-1 receptor agonist is a drug that turns on the same receptor the natural incretin hormone uses, mimicking its effects. Related medicines in the same family include liraglutide and dulaglutide. A pharmaceutical-sciences review describes semaglutide as a newer GLP-1 receptor agonist whose structure-based long half-life supports once-weekly or once-daily dosing across its indications [11]. A separate, related medicine — tirzepatide — goes one step further by activating two gut-hormone receptors (GIP and GLP-1) rather than one; the head-to-head comparison is covered on the [Semaglutide research](/research) page [7]. This site uses generic compound names only. ## What it is approved to do Semaglutide is a fully FDA-approved prescription medicine, not an experimental or research-only compound — a distinction worth stating plainly. It is approved across several indications and two formulations: type 2 diabetes, chronic weight management, reduction of major adverse cardiovascular events in adults with established cardiovascular disease and overweight or obesity, and (2025) metabolic dysfunction-associated steatohepatitis (MASH) [21]. Each indication rests on a dedicated trial. Weight management is anchored by STEP 1, which showed a mean -14.9% body-weight change at 68 weeks [1]. The cardiovascular indication rests on SELECT, a 17,604-person trial showing a 20% reduction in heart attacks, strokes and cardiovascular death [3]. The kidney evidence comes from FLOW, showing a 24% reduction in major kidney events in type 2 diabetes with chronic kidney disease [6]. The liver indication rests on the 2025 ESSENCE trial [12]. What people actually experience on it — the benefits and downsides — is summarized on the [Semaglutide effects](/effects) page. ## Approved product versus compounded versions One distinction matters for anyone reading about semaglutide. The clinical evidence summarized across this site was generated with the approved, manufactured product. During a federally declared shortage from roughly 2022 into early 2025, compounding pharmacies were permitted to produce semaglutide; regulators documented dosing errors, adverse events, and products with unverified or non-pharmaceutical ingredients during that window, and the compounding pathway was curtailed once the shortage was declared resolved. Compounded or non-pharmaceutical versions fall outside the approved-product evidence base. This site describes that regulatory context for completeness; it sells nothing, recommends no source, and is not medical advice. --- A measured, fully cited reading of the semaglutide trial record, with the weight-management evidence read first and the open questions kept in plain sight — an editorial digest, not a clinic, a prescriber, or a vendor.