CT-868 (acmopatide)

CT-868, also called acmopatide, is a once-daily injected drug that activates two gut-hormone receptors at once — GLP-1 and GIP. Drugs in this family are familiar from type 2 diabetes and obesity, where they lower glucose, slow the stomach's emptying, and cause substantial weight loss. What makes CT-868 different is intent. According to the American Diabetes Association, it is the first dual GLP-1/GIP agonist developed specifically for type 1 diabetes, rather than a type 2 drug that people with T1D and their doctors have tried off-label and hoped would translate.

The evidence is one trial. It was randomized and placebo-controlled, which matters, and it enrolled 111 adults who had type 1 diabetes and a BMI of at least 27 kg/m² — mean age 41, mean BMI 34, mean starting A1c 7.5%. Participants took acmopatide at 1.8, 4.1 or 6.6 mg once daily, or placebo, for 16 weeks. Everyone stayed on insulin; this is an add-on, not a replacement, and nothing about it changes the fact that a person with type 1 diabetes needs insulin to live.

At the 4.1 mg dose, A1c fell by 0.34% from baseline, and 56% of participants got below 7%. Weight loss was dose-dependent and reached about 7% versus placebo. Daily insulin dose dropped by up to 15% versus placebo.

Those three results are not equally impressive, and it is worth being blunt about which is which. A 0.34% A1c reduction from a baseline of 7.5% is a modest glycemic effect — real, but not transformative, and the trial did not release continuous-glucose time-in-range figures, which is the number most people would actually want. The weight and insulin-dose effects are the substantial ones. For adults with type 1 diabetes who also carry excess weight and insulin resistance — trial participants had BMIs of at least 27 kg/m² (mean 34) — that combination is the point of the drug.

Safety is the question that decides whether any adjunct is worth taking in type 1 diabetes, and here the early news is reassuring. Over the 16 weeks there were no cases of diabetic ketoacidosis and no cases of level 3 (severe) hypoglycemia. Time spent below 54 mg/dL (3.0 mmol/L) did rise numerically in the groups taking the drug, but every group stayed under the recommended ceiling of 1% of the day. The drug was described as generally well tolerated. Set against that: this class slows gastric emptying and reduces food intake, and the trial cut people's insulin doses — a combination that demands care with dose timing, and one that 111 people followed for four months cannot fully characterise.

Two caveats deserve equal weight with the results. First, this is conference data, not a publication. The type 1 findings were presented at the ADA's 86th Scientific Sessions in June 2026 and released by press release; they have not been peer-reviewed. There is a peer-reviewed Phase 2 of CT-868 — but it is in type 2 diabetes, and type 2 evidence does not establish anything about safety or benefit in type 1. Second, Roche removed the programme from its pipeline. Its 23 July 2026 update places RG6641/acmopatide for T1D under “Removed from phase II”.⁵ This page previously misread the table as a move to phase 3. No phase 3 advancement or launch timeline is established.

One quieter reason this belongs on the artificial-pancreas map as well as the pharmacy shelf: an incretin drug blunts the post-meal glucose spike at its source, by slowing how fast food arrives. A closed loop struggles most with meals it was not told about. A drug that flattens the meal curve makes the loop's hardest guess an easier one — the same logic behind pairing insulin with amylin in fully-closed-loop research. That is a hypothesis, not a finding; nobody has yet tested CT-868 inside an automated insulin delivery system.