Searches for “Mounjaro type 1 diabetes” keep returning a question the clinical record has not fully answered. Type 1 diabetes is an autoimmune disease in which the body’s insulin-producing cells are destroyed, so insulin is not optional. Yet many adults living with it also have overweight or obesity, creating a difficult treatment problem: how to manage body weight and insulin resistance without compromising glucose control.
GLP-1 drugs already treat type 2 diabetes and obesity. Some patients with type 1 diabetes also receive them, particularly when obesity is present. But none has been approved specifically as an insulin add-on to treat type 1 diabetes, and the evidence for long-term safety in that role remains incomplete.
A phase 2 trial published in Diabetes Care on October 28, 2026, offers another piece of that evidence. It tested acmopatide, also known as CT-868, a once-daily injected dual GLP-1 and GIP receptor agonist, in 111 adults with type 1 diabetes and a body mass index of at least 27.
Acmopatide is not tirzepatide, the molecule sold as Mounjaro and Zepbound. The drugs target the same two receptor families, but the results of a trial involving one molecule cannot automatically be attributed to the other.
All the trial results discussed below come from human studies. The question is not whether incretin drugs can affect weight or glucose in type 1 diabetes. It is whether those benefits can be sustained without introducing unacceptable risks.
What the New Acmopatide Trial Showed
Participants were randomly assigned to acmopatide at 1.8 mg, 4.1 mg or 6.6 mg, or to a matching placebo, for 16 weeks. All continued insulin treatment. The average starting HbA1c, a measure of blood-sugar control over approximately three months, was 7.5%. Average BMI was 34.3.
The primary endpoint was change in HbA1c. On that measure, the drug moved the needle modestly: HbA1c fell between 0.4 and 0.6 percentage points across the acmopatide groups, compared with 0.3 points on placebo.
Only the 4.1 mg group showed a nominally statistically significant improvement versus placebo, with an additional 0.3-percentage-point reduction. Nominal significance matters here: it should not be mistaken for definitive proof of a dose-response relationship or a fully confirmed finding across multiple comparisons.
At week 16, 55.6% of participants receiving 4.1 mg reached an HbA1c below 7%, compared with 33.3% receiving placebo.
The weight results were larger. Participants receiving acmopatide lost between 3.3% and 6.7% of baseline body weight, depending on dose, while the placebo group gained approximately 0.3%.
Total daily insulin requirements also declined, with reductions ranging from 3.4% to 14.9% greater than placebo at the two higher doses. Systolic blood pressure fell as well, although placebo recipients also experienced a reduction, making that comparison less straightforward.
The glucose improvement was modest. The weight loss and reduction in insulin requirements were more pronounced.
Then comes the safety result that deserves the most attention. Adverse events were primarily gastrointestinal, and investigators reported no diabetic ketoacidosis and no severe hypoglycemia during the study.
That is encouraging, particularly in a disease where either complication can be life-threatening. It is also a result from just 111 participants followed for 16 weeks. An absence of events in a small trial cannot establish that uncommon complications will not appear with wider or longer exposure.
Why Mounjaro, Type 1 Diabetes and Off-Label Use Keep Colliding
Tirzepatide is marketed as Mounjaro for type 2 diabetes and as Zepbound for indications including chronic weight management. Semaglutide is similarly marketed under different brands, including Ozempic and Wegovy, for different approved uses.
There is an important regulatory distinction. An obesity medicine may be prescribed to an eligible person who also has type 1 diabetes without being approved specifically to improve glucose control in type 1 diabetes. That is different from an approval to use the drug as an adjunct to insulin for treating the autoimmune disease itself.
The distinction matters because insulin remains essential. An incretin drug may reduce appetite, body weight or insulin requirements, but it cannot replace the insulin that a person with type 1 diabetes needs.
Meanwhile, research interest continues to grow. A September 2026 narrative review in Diabetes Technology & Therapeutics examined studies of adjunctive treatments in people using automated insulin delivery systems.
It found that adding semaglutide or tirzepatide was associated with weight loss, lower daily insulin requirements and more time spent within the target glucose range. The reviewed studies did not show clear increases in hypoglycemia or diabetic ketoacidosis, but the evidence base was limited and the authors called for larger, longer investigations.
The history offers a reason not to assume that encouraging early results will be enough.
In 2016, Novo Nordisk’s ADJUNCT ONE trial evaluated liraglutide added to insulin in 1,398 adults with type 1 diabetes over 52 weeks. HbA1c improved, insulin requirements declined and body weight fell by as much as 4.9 kilograms relative to placebo.
Those benefits came with safety problems. At the highest liraglutide dose, symptomatic hypoglycemia was approximately 31% more frequent than with placebo, while episodes of hyperglycemia with ketosis occurred at more than twice the placebo rate. The higher risk of symptomatic hypoglycemia was also significant at the middle dose.
These were episodes of hyperglycemia with ketosis, not necessarily episodes meeting the definition of diabetic ketoacidosis. The distinction is important, but the safety signal was still sufficient for the investigators to conclude that the findings limited liraglutide’s clinical use in type 1 diabetes.
Liraglutide never received an approval specifically for treating type 1 diabetes.
What a Biased GLP-1/GIP Agonist Is Supposed to Fix
Acmopatide is described by its developers as a fully signal-biased GLP-1/GIP receptor agonist.
Receptors do not necessarily trigger one biological response when activated. They can initiate several intracellular signaling pathways, with different effects on hormone activity, receptor behavior and cellular responses.
A biased agonist is designed to favor selected signaling pathways over others.
The development hypothesis is that a carefully engineered signaling profile might preserve useful metabolic effects while improving tolerability or limiting unwanted receptor responses. Similar ideas are being explored across other hormone-receptor programs.
But calling a drug biased describes its pharmacology, not a proven clinical advantage. The new acmopatide study did not directly compare it against tirzepatide or another dual agonist to establish whether signaling bias improves safety.
Sixteen weeks, with approximately 27 to 29 people in each study arm, can demonstrate early efficacy and identify common adverse events. It cannot establish whether nausea is meaningfully less frequent than with another drug, whether insulin reductions persist for years, or whether rare serious complications emerge in a much larger population.
A receptor engineered to behave differently still has to prove that those differences matter to patients.
The Measurements That Would Settle the Evidence
Three questions would move this field from short-term promise toward a reliable treatment strategy.
First, can a drug sustain reductions in insulin requirements and improvements in glucose control for a year or longer? That requires continuous glucose monitoring, careful insulin adjustments and a comparison group maintained throughout follow-up.
Second, what happens to hypoglycemia and diabetic ketoacidosis when hundreds or thousands of patients receive treatment? These outcomes are too consequential to infer long-term safety from a 16-week study in which no events occurred.
Third, what happens when treatment stops?
That question has already produced a small but revealing dataset. An extension analysis of the ADJUST-T1D semaglutide trial, published online in August 2026, followed 16 adults who discontinued semaglutide and 22 previously assigned to placebo who remained off GLP-1 treatment.
Over approximately 12 weeks, time spent within the target glucose range fell by a median 3.6 percentage points in the former semaglutide group, compared with a 1.5-point increase in the placebo group. Measures of glucose variability also worsened more after semaglutide withdrawal.
The study found no significant between-group differences in hypoglycemia-related monitoring measures. Its sample was small, and a sensitivity analysis adjusting for end-of-treatment glucose metrics weakened the statistical certainty of some findings.
Still, the results suggest that at least some glycemic benefits observed during treatment may not persist after discontinuation.
The benefit may travel with the drug. The question is what happens when the drug leaves.
How to Read Any of This as a Patient
None of the findings in these studies constitutes an insulin-adjustment or incretin-dosing guide. GLP-1 and dual GIP/GLP-1 medicines are not approved specifically as adjunctive treatments for glucose management in type 1 diabetes.
Adding one of these medicines can change food intake, body weight and insulin requirements. Those changes make clinical supervision particularly important, because both insufficient insulin and excessive insulin can produce dangerous outcomes.
Decisions about weight-management medicines in people with type 1 diabetes belong with a qualified diabetes clinician who can review glucose-monitoring data, insulin delivery, hypoglycemia history and ketone-related risks.
It is also useful to separate three claims that are often blurred together.
First, some incretin drugs have produced meaningful weight loss in people with type 1 diabetes in clinical studies. That is supported by randomized and observational human evidence.
Second, reductions in insulin use and improvements in time within the glucose target range have been observed, particularly in smaller studies involving automated insulin delivery. Those benefits require confirmation across broader populations.
Third, whether routine long-term use as an insulin adjunct is sufficiently safe remains unresolved. The ADJUNCT ONE experience is a reminder that favorable efficacy results do not automatically produce an acceptable safety profile.
Insulin is not optional in type 1 diabetes, regardless of how effective an additional medicine may eventually become.
Where the Field Stands
Acmopatide is part of a growing effort to study incretin-based medicines specifically in type 1 diabetes rather than assuming that their results in type 2 diabetes or obesity can be transferred to a different disease.
The October Diabetes Care publication provides randomized, placebo-controlled evidence of improvements in weight, insulin requirements and modestly better glucose control over 16 weeks. It does not establish long-term clinical benefit or uncommon safety risks.
The study was supported by the drug developer and included company-affiliated researchers, making independent replication and larger trials particularly valuable.
There is a substantial population behind this question. The U.S. Centers for Disease Control and Prevention estimated in its 2026 National Diabetes Statistics Report that approximately 1.8 million American adults aged 20 or older had diagnosed type 1 diabetes.
Many face the additional challenge of overweight or obesity. An effective adjunct could have meaningful clinical value, but only if the benefits are demonstrated alongside the safety of continued insulin treatment.
Grey Pepper has previously examined the opposite side of GLP-1 biology in its coverage of avexitide, a GLP-1 receptor blocker being studied for post-bariatric hypoglycemia, and the distinct question of type 2 diabetes remission without medication in young adults. Both stories underscore how much context matters when interpreting changes in glucose metabolism.
The next generation of incretin trials in type 1 diabetes will need to answer a harder question than whether participants lose weight. Researchers must show that improved weight and glucose outcomes can coexist with safe, reliable insulin delivery over years of treatment.
For people living with type 1 diabetes, the encouraging part is that the science is moving. The unresolved part is whether the evidence can support a new treatment indication.
The question is no longer whether incretin drugs can do something in type 1 diabetes. It is whether they can do enough, safely enough, for long enough.
Sources
- Klein KR, Pettus J, et al. Diabetes Care. “A Phase 2, Double-Blind, Randomized, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Acmopatide (CT-868), a Fully Biased GLP-1/GIP Receptor Agonist, in Adults With Type 1 Diabetes and Overweight or Obesity.” Published October 28, 2026. Primary clinical trial.
- American Diabetes Association. “First Dual GLP-1/GIP Receptor Agonist Developed for Type 1 Diabetes Shows Promising Benefits in Blood Glucose Control.” June 5, 2026. ADA announcement.
- Frandsen CS, et al. Diabetes Care. “Efficacy and Safety of Liraglutide Added to Insulin Treatment in Type 1 Diabetes: The ADJUNCT ONE Treat-To-Target Randomized Trial.” 2016. Primary clinical trial.
- Kitsios K, Trakatelli CM. Diabetes Technology & Therapeutics. “Adjunctive Treatments for Patients with Type 1 Diabetes Using Automated Insulin Delivery Systems. A Narrative Review.” September 4, 2026. Review.
- Montaser E, et al. Diabetes, Obesity and Metabolism. “Glycaemic Changes After Semaglutide Discontinuation in Adults With Type 1 Diabetes Using Automated Insulin Delivery: Analysis of the ADJUST-T1D Extension Study.” Published online August 31, 2026. Extension study.
- Centers for Disease Control and Prevention. National Diabetes Statistics Report. Updated September 16, 2026. National prevalence estimates.
- Eli Lilly. Zepbound Prescribing Information. Official U.S. prescribing information.
