Semaglutide is an approved GLP-1 medicine — here is what the trials establish, read in full.

The short version

Semaglutide is a real, approved medicine — not an experimental compound. It belongs to a drug family called GLP-1 receptor agonists, which copy a gut hormone your body makes after a meal to lower blood sugar and quiet appetite. It is given as a once-weekly shot under the skin or a once-daily pill, and doctors prescribe it for type 2 diabetes, long-term weight management, lowering heart-attack and stroke risk in certain people, and — newly in 2025 — a serious form of fatty liver disease called MASH (a liver condition where fat, inflammation, and scarring build up). In one large 2025 liver trial, the inflammation cleared in roughly 6 of 10 people on the drug. The benefits are well measured, but so are the downsides: nausea is common, weight comes back if you stop, and "compounded" versions made outside the approved supply have caused documented safety problems. What people report — including the downsides — is on the effects page.

What the semaglutide record establishes

Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist — a 31-amino-acid analogue of the gut incretin hormone GLP-1 (a hormone the intestine releases after eating that prompts insulin, calms hunger, and slows the stomach), engineered to circulate for about a week rather than the roughly two minutes of the natural hormone. It is FDA-approved across several indications and two formulations: a once-weekly subcutaneous (under-the-skin) injection and a once-daily oral tablet. This site is a documentation-grade reading of the published evidence; it summarizes that record and does not provide medical advice, prescribe, or sell anything.

The leading finding here is hepatic. In the 2025 ESSENCE phase-3 trial of biopsy-confirmed metabolic dysfunction-associated steatohepatitis (MASH) with stage 2-3 fibrosis, once-weekly semaglutide 2.4 mg resolved steatohepatitis without worsening fibrosis in 62.9% of participants versus 34.3% on placebo, and improved fibrosis without worsening steatohepatitis in 36.8% versus 22.4% ^[1]. That liver result sits on top of an unusually broad metabolic record built over a decade of large trials.

The weight evidence is anchored by STEP 1, in which once-weekly subcutaneous semaglutide 2.4 mg produced a mean body-weight change of -14.9% from baseline to week 68 versus -2.4% with placebo in adults with overweight or obesity without diabetes ^[2]. The cardiovascular evidence spans two populations: in SUSTAIN-6, semaglutide reduced the composite of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke (hazard ratio 0.74; 95% CI 0.58-0.95) in type 2 diabetes at high risk ^[3], and in SELECT (n=17,604) it reduced that same composite by 20% (HR 0.80; 95% CI 0.72-0.90) in adults with established cardiovascular disease and obesity but without diabetes ^[4]. The kidney evidence comes from FLOW (n=3,533), where semaglutide 1.0 mg reduced major kidney-disease events by 24% (HR 0.76; 95% CI 0.66-0.88) in type 2 diabetes with chronic kidney disease ^[5].

The point of staging the record this way is honesty about evidence strength. Each of the findings above is a controlled-human-trial result. The same record carries genuine cautions — gastrointestinal intolerance, weight regain after discontinuation, signals under surveillance — and a clear line between the approved manufactured product and compounded preparations made outside it.

Semaglutide as a documented molecule

The molecule is precisely characterized. Semaglutide shares approximately 94% sequence homology with native human GLP-1, with molecular formula C187H291N45O59, a molecular weight of 4113.64 Da, and CAS number 910463-68-2. Three engineered features give it its week-long action: an alpha-aminoisobutyric-acid (Aib) substitution at position 8 that blocks the degrading enzyme DPP-4 (dipeptidyl peptidase-4), a lysine-to-arginine swap at position 34, and a C18 fatty di-acid side chain on the remaining lysine at position 26 that binds tightly and reversibly to serum albumin, slowing clearance.

For a plain-English account of the class and structure, see what is semaglutide; for the central appetite-circuit mechanism, see how does semaglutide work. The full study-by-study staging — population, dose, route, outcome, and evidence status for each trial — is on the Semaglutide research page, and the complete source list is in the Semaglutide references.

Approved product versus compounded preparations

An important distinction runs through this record. The evidence summarized here — STEP, SUSTAIN, SELECT, FLOW, ESSENCE — was generated with the approved manufactured product. During a federally declared shortage from roughly 2022 to early 2025, compounding pharmacies were permitted to prepare semaglutide; the FDA documented dosing errors, adverse events requiring hospitalization, and products with unverified or non-pharmaceutical active ingredients in that pathway. After the shortage was declared resolved in early 2025, those compounding pathways were curtailed.

Compounded or non-pharmaceutical sources therefore fall outside the approved-product evidence base and carry documented quality and safety concerns. This site does not evaluate, rank, or point to any source; it reads the published literature. The reported benefits and adverse effects people describe, with cited safety reasoning, are documented on the Semaglutide effects page.