Survodutide

FDA has warned that products containing survodutide sold as 'for research purposes' or 'not for human consumption' are illegally marketed for human use. By September 2026, ClinicalTrials.gov listed multiple Boehringer Ingelheim-sponsored phase 3 survodutide trials, including a completed obesity trial (SYNCHRONIZE-1) and a recruiting compensated-cirrhosis trial (LIVERAGE-Cirrhosis). No approved US product containing survodutide was identified as of the cutoff.^[2][3][4]

Jurisdiction

United States

Product

Survodutide (BI 456906), investigational

Indication

No FDA-approved indication; phase 3 obesity and MASH/cirrhosis trials were registered

Record date

2026-09-08

• A registry sweep of 26 survodutide records was screened for phase/status/sponsor only; it does not summarize trial results. This is a new regulatory-topic claim for survodutide, separate from the existing identity-1 claim's phase 2 trial and its inaccessible correction.

Survodutide was studied as an injected dual glucagon/GLP-1 receptor agonist in a phase 2 obesity trial. A subsequent correction is indexed; this reference withholds precise efficacy figures pending inspection of the corrected report.^[1]

• The correction body could not be accessed, so corrected numerical outcomes remain unverified.

In the 16-week phase 2 trial in type 2 diabetes, at least one treatment-emergent adverse event was reported by 77.8% of the 302 participants given survodutide, 52.5% of those given placebo and 52.0% of those given open-label semaglutide. Gastrointestinal disorders were the most frequent, affecting 55.3% on survodutide, 22.0% on placebo and 28.0% on semaglutide. Adverse events led to treatment discontinuation in 15.9% of the survodutide group, 5.1% of the placebo group and 4.0% of the semaglutide group; most of those discontinuations happened in the first six weeks, during dose escalation, and three-quarters of the survodutide discontinuations were for gastrointestinal disorders. Severe adverse events were reported by 5.3% on survodutide, 6.8% on placebo and none of those given semaglutide, and serious adverse events by 3.6% on survodutide and 5.1% on placebo, again with none on semaglutide. Mean heart rate rose in every group, by 2.3 to 7.3 beats per minute across the survodutide groups, 5.9 with semaglutide and 1.67 with placebo, and the investigators reported no new onset of the highest corrected QT interval categories.^[5]

• Adverse events recorded in one 16-week trial of 411 treated adults. They do not establish the frequency of any event over longer use or in other populations, and they do not establish that survodutide caused any individual event.
• The comparison with semaglutide is not blinded, and the trial was not powered to compare adverse-event rates between the two.
• Survodutide figures are pooled across six dose groups whose individual rates differ, and both discontinuation and gastrointestinal events were more frequent at higher doses.
• The heart-rate and interval findings are group means from a short trial and are not an assessment of cardiovascular risk. The electronic supplementary material listing individual serious events was not inspected.

A separate phase 2 trial studied survodutide in type 2 diabetes rather than obesity. It screened 669 people and treated 411 adults with type 2 diabetes on background metformin for 16 weeks, allocating them to one of six survodutide dose groups, to placebo, or to open-label semaglutide. Mean baseline glycated haemoglobin was 64.7 mmol/mol (8.07%). Adjusted mean glycated haemoglobin fell in every survodutide group, from 9.92 mmol/mol (0.91 percentage points) in the lowest group to 18.72 mmol/mol (1.71 percentage points) in the largest reduction, against 1.62 mmol/mol (0.15 percentage points) in the placebo group, whose confidence interval included no change; the trial reported every survodutide group's reduction as significantly greater than placebo. It also reported that the reduction in the second-lowest dose group, 15.95 mmol/mol (1.46 percentage points), was similar to that in the open-label semaglutide group, 16.07 mmol/mol (1.47 percentage points). Bodyweight fell dose-dependently, by up to 8.7% (95% confidence interval -10.1 to -7.3) in the group receiving the highest twice-weekly dose, and every group except the lowest lost significantly more weight than placebo; the trial reported that the groups given 1.8 mg or more once weekly lost more weight than the semaglutide group, which lost 5.3% (-6.6 to -4.1). The published correction to this report is a single typographical fix to its graphical abstract and changes none of these figures.^[5][6]

• A 16-week dose-finding trial reporting laboratory and bodyweight measures. It says nothing about diabetes complications, cardiovascular events or survival, and 16 weeks is too short to describe durability.
• The semaglutide arm was open-label while the survodutide and placebo arms were blinded, and the trial was not designed to test survodutide against semaglutide formally. Any comparison between them is descriptive.
• The semaglutide comparator was titrated to 1.0 mg once weekly, a type 2 diabetes dose, not the higher dose studied for weight management, so the weight comparison is against that lower comparator dose.
• Nearly one in five treated participants discontinued treatment early, so the week 16 estimates rest on reduced group sizes. The trial reports the timing only for the 53 discontinuations caused by an adverse event, most of which happened in the first six weeks.
• This is a different trial in a different population from the earlier phase 2 obesity trial recorded separately on this page. The two must not be read together as one result.
• The two records cited here are this trial report and its own published correction, not two independent studies.
• Doses appear here only because they identify the randomized groups whose results are reported. They describe the trial, not a recommendation.

A 2025 review of incretin-based treatments for steatotic liver disease describes survodutide as a once-weekly dual agonist with roughly eightfold higher activity at the GLP-1 receptor than at the glucagon receptor, and summarises a phase 2 trial in this condition that this reference has not inspected directly. According to the review, that trial randomised 293 adults with biopsy-proven steatohepatitis and fibrosis stages 1 to 3 to one of three survodutide doses or placebo for 48 weeks. The review reports that the primary endpoint, improvement in steatohepatitis without worsening of fibrosis, was reached by 47%, 62% and 43% of the three survodutide groups against 14% of the placebo group, and that improvement of at least one fibrosis stage was reached by 34%, 36% and 34% against 22% with placebo. It also reports that gastrointestinal effects were more common with survodutide than placebo, including nausea in 66% against 23% and vomiting in 41% against 4%, and that 16% of participants on survodutide discontinued because of gastrointestinal effects, against 1.4% on placebo.^[7]

• Every figure here is a review's account of a trial whose own report this reference has not read. The trial's methods, analysis population, denominators and definitions could not be checked, and a review can transcribe a number incorrectly.
• The review reports the fibrosis comparison without a statistical test, unlike the primary endpoint, so the fibrosis difference from placebo is described rather than tested.
• This is a narrative review whose literature search ran only to June 2024 and which included only trials with liver-biopsy endpoints, so it is not a complete account of the evidence for survodutide.
• A histological endpoint at 48 weeks is a tissue measure. It is not evidence about liver failure, transplantation or survival.
• The receptor-activity ratio is the review's summary of a preclinical pharmacology paper that it cites, not a measurement made in the people the trial enrolled.
• The trial described here is a steatohepatitis trial, a different study in a different population from both the phase 2 obesity trial and the phase 2 type 2 diabetes trial recorded separately on this page.

A Bayesian network meta-analysis published in 2025 pooled 19 randomized controlled trials covering 29,506 adults with a body-mass index of 25 kg/m2 or more, comparing liraglutide, semaglutide, survodutide, tirzepatide, retatrutide and placebo at 36 weeks or later. Its abstract reports that retatrutide and the dual agonists produced equivalent mean weight loss of 11.0 kg, more than the GLP-1 receptor agonists at 9.0 kg, and that for reaching at least 15% weight loss the odds ratios were 54.6 for retatrutide, 16.4 for the dual agonists and 9.0 for the GLP-1 receptor agonists. It also reports that retatrutide carried the highest risk of adverse events, and that in meta-regression the presence of type 2 diabetes was associated with less weight loss. These are indirect comparisons across trials, not head-to-head results.^[8]

• Abstract-only inspection. The included-trial list, risk-of-bias assessment, network structure and heterogeneity statistics were not read, because no lawful full-text copy was reachable.
• The abstract does not name the 19 pooled trials or state their development phase, so this record cannot show which trial of any compound contributed to which estimate. The survodutide and retatrutide results recorded elsewhere in this reference come from phase 2 dose-finding trials, the same records also list completed phase 3 trials of both compounds, and semaglutide and tirzepatide are approved for weight management, so the pooled classes may combine evidence of unequal maturity.
• A network meta-analysis estimates comparisons between treatments that were mostly never tested against each other. Its rankings are model outputs, not measured differences.
• The GLP-1 receptor agonists and the dual agonists are pooled by class in the reported results, so the abstract gives no separate estimate for semaglutide, survodutide or tirzepatide; retatrutide is reported on its own because the abstract treats it as a group of one.
• The meta-regression associations are observational comparisons across trials, not randomized ones.
• This finding is recorded as cross-compound context. It is not evidence about any single compound's own trial results, which are recorded separately on each record.