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Also: Glucophage XR · Fortamet · Glumetza · Riomet · Diabex · Diaformin · Obimet · Glycomet · Janumet · Synjardy · Xigduo · Kombiglyze · Invokamet · Jentadueto · met · Gluco · the diabetes pill
Four separate measurements, never averaged. Independent evidence counts only studies with no sponsor attached. Methodology version v2.0-2026-10 · how we grade evidence
Approved to improve glycaemic control in type 2 diabetes. It is claimed — but not approved — to produce modest weight loss or prevent weight gain, and to reduce progression from prediabetes to type 2 diabetes.
It is not approved for obesity or weight loss by any regulator, anywhere, in any population. Every weight-loss use is off-label. The 2020 independent meta-analysis of metformin in obesity opens by noting precisely that.
This is the one compound in the cluster whose weight evidence is strongest on the independent side and absent on the regulatory side. The diabetes-prevention evidence is strong and independent — a 3,234-participant NIH-funded trial with ten- and fifteen-year follow-up. The weight evidence is real but small and comes from secondary and post-hoc outcomes: about 2.1 kg versus 0.1 kg with placebo in that trial, where weight change was a secondary endpoint, and a pooled BMI reduction of roughly 1 kg/m² in independent meta-analysis whose own authors doubt it reaches the threshold guidelines ask of a weight-loss drug.
Its harm profile is categorically milder than the incretins’ and the centrally acting combinations’: no thyroid C-cell boxed warning, no documented lean-mass-loss signal, no gallbladder signal and no pancreatitis signal. Gastrointestinal intolerance is the dominant and very common problem, lactic acidosis the classic rare serious risk, and vitamin B12 deficiency with long-term use is well documented. Its problem is efficacy, not safety.
At a glance
Metformin reduces hepatic gluconeogenesis and increases peripheral insulin sensitivity. AMPK activation, inhibition of mitochondrial complex I and of glycerophosphate dehydrogenase, and gut-mediated effects including GLP-1 secretion and bile-acid and microbiome changes are all proposed as proximate causes. The weight effect is usually attributed to reduced appetite and gastrointestinal effects rather than to increased energy expenditure. The glucose-lowering effect and reduced hepatic glucose output are demonstrated in humans. The molecular mechanism remains contested after nearly seventy years of clinical use, and **the mechanism by which metformin reduces body weight is not established** — AMPK activation is not a settled human explanation for weight loss.
Dated determinations, each flagged for whether it is final and whether it covers safety only. A safety review is not an efficacy finding, and most reporting in this category conflates the two.
Drugs@FDA lists the original approval of Glucophage as 3 March 1995. Secondary sources commonly state FDA approval in 1994 with the US launch in 1995; these two dates conflict in the sources and which the agency itself considers the approval date has not been resolved here. Paediatric age floors vary by product. The NDA is now held by EMD Serono Inc. and those products are listed as discontinued; metformin is long since genericised.
Metformin is not approved for obesity or weight loss by any regulator, anywhere, in any population. Every weight-loss use is off-label, as is its widespread use in polycystic ovary syndrome and in antipsychotic-associated weight gain. The 2020 independent meta-analysis of metformin in obesity opens by noting precisely this. The date on this row is the date of the US approval whose indication is limited to glycaemic control; no refusal or determination on obesity exists to point at, because no application for that indication has been approved anywhere. This is the one compound in the cluster whose weight evidence is strongest on the independent side and absent on the regulatory side.
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