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ADA 2026 obesity studies

CE / CME

Translating Emerging Obesity Evidence Into Clinical Action: Highlights From ADA 2026

Physician Assistants/Physician Associates: 1.00 AAPA Category 1 CME credit

Pharmacists: 1.00 contact hour (0.1 CEUs)

ABIM MOC: maximum of 1.00 Medical Knowledge MOC point

Physicians: maximum of 1.00 AMA PRA Category 1 Credit™

Nurse Practitioners/Nurses: 1.00 Nursing contact hour

Released: July 21, 2026

Expiration: July 20, 2027

Donna H. Ryan
Donna H. Ryan, MD
CME/CE Information

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CagriSema and Appetite Signaling: Why It Matters

Finally, a mechanistic study was presented at ADA 2026, which examined the effects of CagriSema on self-reported appetite, brain responses, and eating behaviors. This is important because the brain is a central regulator of eating behavior, including appetite, satiety, reward, and food-cue responses.11

CagriSema is a once-weekly, injectable, fixed-dose combination of cagrilintide (an amylin analogue) and semaglutide (a GLP-1 RA).12 This OMM may provide complementary mechanisms that influence appetite, satiety, and food-related reward pathways in the brain.

Study outcomes were measured via patient-reported outcomes (PROs) and functional magnetic resonance imaging (fMRI). Overall, the findings support appetite regulation and food-reward biology as clinically relevant treatment domains. Although the results are encouraging, tolerability remains an important consideration and long-term data are needed for real-world use of CagriSema in overweight or obesity.4

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CagriSema and Appetite Signaling: Study Design

This was a randomized, placebo-controlled mechanistic study that enrolled 130 adults with obesity or overweight (BMI >27 kg/m²). Those with type 2 diabetes or weight change of more than 5 kg within the prior 90 days were excluded.

Enrolled patients were randomized to receive once-weekly CagriSema 2.4 mg/2.4 mg or placebo via SC injection.

The primary endpoint was change in postprandial appetite scores per visual analogue scale at 22 weeks. Key secondary endpoints included change in energy intake throughout the day, total body weight, PROs assessing eating behaviors, and brain responses to food cues per fMRI at 22 weeks.4

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CagriSema and Appetite Signaling: Baseline Characteristics

Across both study arms, the mean age was 38 years, body weight was approximately 99 kg, and BMI was approximately 34 kg/m². Almost half (53%-57%) of patients were female and, as shown via A1C levels, none had type 2 diabetes.4

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CagriSema and Appetite Signaling: Change in Postprandial Appetite Scores (VAS) at 22 Weeks

Appetite was assessed before and after a standardized meal throughout the day, with scoring based on hunger, prospective food consumption, satiety, and fullness.

Baseline appetite scores were generally comparable between study arms. At 22 weeks, CagriSema produced a marked reduction in appetite scores compared with placebo. More specifically, postprandial appetite scores decreased by 47% with CagriSema vs 8% with placebo (P <.0001).

These outcomes demonstrate substantial improvements in hunger, fullness, and satiety with CagriSema and closely reflect what I have observed in clinical practice among patients who are already receiving this therapy.4

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CagriSema and Appetite Signaling: Key Secondary Endpoints

The study’s secondary endpoint outcomes at 22 weeks further support the effects of CagriSema on eating behavior. Compared with placebo, patients treated with CagriSema consumed approximately 1000 fewer kilocalories per day (P <.0001). In addition, patients in the CagriSema arm saw a substantially reduced intake of high-fat sweets vs the placebo arm (P <.0010).

In terms of weight loss, mean change in total body weight was -16.4% with CagriSema compared with -0.95% with placebo (P <.0001). Alongside this level of weight loss, patients treated with CagriSema also continued to report reduced hunger, increased satiety, and lower energy intake, all of which are findings that contrast with the metabolic adaptations that often accompany weight loss.4

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CagriSema and Appetite Signaling: PROs and fMRI Outcomes

PRO measures also demonstrated CagriSema’s ability to reduce food cravings, Eating Drive Index composite, hunger, and appetite. It improved patients’ craving control, mood, and postmeal satiety, as well. Of note, some patients also reported decreased food noise (ie, intrusive thoughts, feelings, and motivations related to eating) with CagriSema.

Per fMRI, investigators observed changes in responses by the brain to high-calorie food cues with CagriSema.4

These findings support the biologic effects of an OMM that combines an amylin analogue and GLP-1 RA on the neural pathways involved in appetite regulation, satiety, and food reward. Taken together, this evidence provides mechanistic support for CagriSema via observed reductions in appetite and food intake.

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CagriSema and Appetite Signaling: Safety

Like the other OMMs discussed, the safety findings for CagriSema were as expected. Most AEs were gastrointestinal in nature and predominantly mild to moderate in severity. There were no unexpected safety findings reported.4

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CagriSema and Appetite Signaling: Clinical Interpretation

This mechanistic study of CagriSema reinforces the need to discuss appetite, cravings, and food noise with patients because these are the biologic features of obesity that can help assess treatment response. Furthermore, the addition of an amylin analogue to a GLP-1 RA may ultimately benefit patients who have an incomplete response to existing incretin-based therapies, although additional clinical evidence is needed to confirm this.

Overall, this study demonstrated that CagriSema influences multiple aspects of appetite regulation, including PROs, food intake, and brain responses to food cues, providing mechanistic support for this novel therapeutic approach.4

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