CE/CME accredited
1. The activity has been scientifically rigorous and evidence-based * (choose only one of the following options)
Overview
GLP-1 receptor agonists have transformed obesity care, yet obesity is driven by many hormones acting on the brain [Kusminski 2024; Müller 2022]. Which other signals matter, and where do emerging therapies act?
Time to watch: 2 mins 20 secs
Respond to the questions below to unlock the next part of the activity which builds on the contents of this animation, including expert commentary on amylin biology, therapeutic positioning and the emerging clinical evidence.
Which statement best reflects the current understanding of amylin in weight management?
How confident were you in the answer you selected for the previous question?
Foundations of amylin biology
Amylin is a 37‑amino‑acid peptide co‑secreted with insulin from pancreatic β‑cells in response to nutrient intake [Hay 2015; Secher 2026]. It acts both as a satiation signal, promoting meal termination, and as a glucoregulatory hormone, slowing gastric emptying and suppressing postprandial glucagon [Hay 2015; Chung 2026].
What separates amylin from incretin biology is where it acts. Amylin signals through calcitonin receptors complexed with receptor activity‑modifying proteins, densely expressed in the area postrema and nucleus tractus solitarius – hindbrain regions outside the blood–brain barrier [Walker 2025; Secher 2026]. Amylin and GLP‑1 recruit largely separate area postrema neuronal populations [Züger 2013; Secher 2026], and cagrilintide's weight‑lowering effect is mediated through brain amylin receptors AMY1 and AMY3 [Oliveira Carvas 2025]. Amylin receptor components are co‑expressed with leptin receptors on individual area postrema neurons, a mechanistic basis for amylin's capacity to restore leptin responsiveness [Trevaskis 2008; Roth 2008; Ravussin 2009; Liberini, 2016; Secher 2026].
Beyond appetite, part of the rationale for targeting amylin with pharmacotherapy is that it lowers postprandial glucose, and in preclinical models it reduces adiposity preferentially [Chung 2026; Walker 2025] – supporting the potential to alleviate fears of disproportionate loss of muscle mass or function when on weight loss medications [Langer 2026]. However, clear comparative human data is still awaited.
Progress to impactful pharmacotherapies has been slow. Pramlintide, the only approved amylin analog, is indicated solely as an adjunct to mealtime insulin in diabetes, requires multiple daily injections and produces modest weight and HbA1c reductions [Hay 2015; Chung 2026]. Native amylin's tendency to form amyloid fibrils further discouraged development [Chung 2026; Secher 2026]. However, the development of long‑acting, non‑aggregating analogs has now removed both constraints.
In the following video, Prof. Carel le Roux explains why targeting amylin is now becoming therapeutically viable.
Time to watch: 2 mins 59 secs
Video highlights
- Amylin and GLP-1 activate both overlapping and distinct areas of the brain, helping to explain why the two treatments can work synergistically.
- Amylin may have both weight loss-dependent and weight loss-independent effects on glucose regulation, including through slowing gastric emptying, although their relative contributions require further evaluation.
- Unlike pramlintide, which has been available for more than two decades, longer-acting amylin compounds now enable weekly administration, improving convenience and allowing more sustained effects.
After responding to the questions below, you will unlock the next part of the activity which builds on the contents of the animation, including expert commentary on amylin biology, therapeutic positioning and the emerging clinical evidence.
Why can non-GLP-1 pathways such as amylin contribute to appetite regulation and energy balance alongside GLP-1?
How confident were you in the answer you selected for the previous question?
Beyond GLP-1: the multi-pathway landscape
Energy homeostasis is defended by overlapping, partly redundant signals, so engaging one receptor system leaves compensatory pathways intact [Kusminski 2024; Müller 2022].
Among newer, high‑efficacy anti‑obesity medications, every widely available option is incretin‑based: subcutaneous semaglutide 2.4 mg and 7.2 mg, oral semaglutide 25 mg, subcutaneous liraglutide 3.0 mg, subcutaneous tirzepatide, and 17.2 mg oral orforglipron [Wilding 2021; Wharton 2025a; Jastreboff 2022; Wharton 2025b]. Supporting other metabolic outcomes than weight loss and type 2 diabetes Semaglutide 2.4 mg also carries an approved indication in metabolic dysfunction‑associated steatohepatitis with the caveat that the patient cannot have cirrhosis [Sanyal 2025].
Three key challenges related to current obesity medications persist. Between one third and one half of patients discontinue within a year [Rodriguez 2025]; around 60% of lost weight returns by 52 weeks after cessation [Budini 2026]; and reported higher muscle atrophy during use of newer high‑efficacy GLP‑1‑targeting agents semaglutide and tirzepatide vs older agents such as exenatide and liraglutide [Kwan 2026].
Investigational agents other than maridebart cafraglutide (once‑monthly GLP‑1 receptor agonist) add or change target mechanisms rather than dose, including triple GLP‑1, GIP and glucagon receptor agonism (retatrutide), glucagon and GLP‑1 receptor dual agonism (survodutide), dual amylin and GLP‑1 receptor agonism (zenagamtide), and cagrilintide‑semaglutide combines semaglutide’s GLP‑1 receptor agonist with the long‑acting amylin analog cagrilintide [Garvey 2025; Davies 2025; Buse 2026; Yamauchi 2026; Ravussin 2026; Scheen 2026]. Cagrilintide is also being investigated alone alongside other investigational amyloid receptor agonist agents eloralintide and the long‑acting amylin analog petrelentide [Billings 2025; Buse 2026; Garvey 2025, 2026; Ravussin 2026].
Amylin sits apart mechanistically by being in a different receptor family and by stimulating a different first‑order brain region to make it additive to incretin signaling rather than a variation on it [Secher 2026]. Its metabolic evidence to date is glycemic rather than hepatic, since published liver outcomes belong to incretin‑ and glucagon‑based agents [Sanyal 2025; Kaplan 2026].
Here, Prof. Carel le Roux considers the potential role of amylin-based therapy in obesity, including the importance of tolerability, treatment persistence, and health outcomes beyond weight loss.
Time to watch: 2 mins 1 secs
Video highlights
- Viewing obesity as a multi-pathway, multi-hormonal disease focuses attention on the brain pathways that regulate adipose mass.
- Tolerability and persistence are critical to achieving long-term health gains, making these important outcomes to assess in real-world studies of amylin-based treatment.
- Beyond weight loss, evidence that treatment improves obesity-related complications such as type 2 diabetes and MASLD will be important to supporting the long-term use of amylin-based treatments.
Clinical evidence
Amylin‑based evidence now spans monotherapy, co‑administered combination and unimolecular co‑agonism. Tables 1 and 2 summarize it alongside the wider landscape.
How those figures read depends on who was enrolled, and entry criteria vary more than they appear. For example, REDEFINE 1, SURMOUNT‑1 and the eloralintide trial required a body mass index (BMI) of at least 30, or 27 with a weight‑related complication, and excluded diabetes. Where diabetes was required the threshold falls: 27 in REDEFINE 2 and SURMOUNT‑2, 25 in REIMAGINE 2 and 23 in the zenagamtide trial [Garvey 2025; Davies 2025; Garvey 2023; Buse 2026; Mora 2026; Billings 2025]. Patient eligibility criteria were also different in REDEFINE 5. Conducted in Japan and Taiwan, it applied Japanese criteria of a BMI of at least 27 with two complications, or at least 35 with one complication, so its participants are not directly comparable with those in the global trials [Yamauchi 2026].
Duration of trials ranges from 36 to 84 weeks, and trials report their results in different ways, so the tables are a map of the evidence rather than a ranking. Only one comparison has been head‑to‑head: in REDEFINE 4 headline results, 2.4 mg cagrilintide‑semaglutide did not meet non‑inferiority against 15 mg tirzepatide, despite substantial weight reduction (23.0% and 25.5% over 84 weeks, respectively) in both arms [Scheen 2026].
With regards to metabolic outcomes other than weight loss, cagrilintide alone lowered HbA1c far less than semaglutide, yet the combination outperformed semaglutide (Table 1) [Buse 2026]. No amylin analog or GLP‑1/amylin co‑agonist has yet to report liver histology, hepatic fat or fibrosis in a peer‑reviewed publication, whereas semaglutide, tirzepatide, survodutide and retatrutide all have (Table 2) [Sanyal 2025; Loomba 2024; Kaplan 2026; Sanyal 2024].
Body composition impact of amylin currently rests on one imaging substudy (Table 1), in which the proportion of weight lost as fat was similar across arms [Ravussin 2026]. A lean‑mass advantage for amylin is as such not yet established [Ravussin 2026].
Amylin-targeting agent clinical trial data
| Agent | Status, August 2026 | Current weight data | Other current metabolic outcomes |
|---|---|---|---|
| Pramlintide Amylin receptor agonist SC, up to three times daily [Hay 2015; Chung 2026] |
Approved – adjunct to mealtime insulin in type 1 and type 2 diabetes Not approved for obesity |
Modest reductions as an insulin adjunct (approx. 2–4%) | Glycemic: HbA1c reduction by 0.3–0.6 pp, placebo‑adjusted,
in
both
type 1 and type 2 diabetes Hepatic: none reported Body composition: none reported |
| Cagrilintide Long‑acting amylin analog SC, once‑weekly [Garvey 2025; Buse 2026; Ravussin 2026] |
Investigational Phase 3 (ongoing in RENEW program) |
−11.5%, 68 weeks (REDEFINE 1, all participants) −8.4%, 68 weeks (REIMAGINE 2, full adherence) |
Glycemic: HbA1c −0.80 pp vs −1.75 pp for semaglutide 2.4 mg
(REIMAGINE 2, full adherence) Hepatic: none reported Body composition: 63% of weight loss was fat mass (REDEFINE 1 substudy) |
| Cagrilintide‑semaglutide Amylin + GLP‑1, co‑administered SC, once‑weekly [Garvey 2025; Davies 2025; Buse 2026; Yamauchi 2026; Scheen 2026; Ravussin 2026] |
Investigational (ongoing in phase 3 REDEFINE program) Under FDA review; submitted December 2025 |
−20.4%, 68 weeks (REDEFINE 1, all participants) −13.7%, 68 weeks (REIMAGINE 2, all participants) −14.2%, 68 weeks (REIMAGINE 2, full adherence) −18.4%, 68 weeks (REIMAGINE 5, full adherence) −23.0% with full adherence, 20.2% counting all participants, 84 weeks (REDEFINE 4) |
Glycemic: HbA1c −1.8 pp vs −0.4 pp placebo, and 73.5%
reached
≤6.5% (REDEFINE 2, all participants); −1.91 pp, superior to semaglutide 2.4 mg
(REIMAGINE
2, full adherence) Hepatic: none reported Body composition: 67% of weight loss was fat mass (REDEFINE 1 substudy) Other: systolic BP −6.5 vs −2.4 mmHg; waist −11.9 vs −3.6 cm (REDEFINE 2) |
| Zenagamtide Unimolecular GLP‑1 + amylin receptor agonist SC, once‑weekly and oral, once‑daily [Dahl 2025; Mora 2026] |
Investigational Phase 3 (ongoing in phase 3 AMAZE program) |
−24.3%, 36 weeks (phase 1b/2a, obesity, full adherence) −14.6%, 36 weeks (phase 2, type 2 diabetes, all participants) |
Glycemic: HbA1c −1.71 pp vs −0.14 pp placebo, and 76.2%
reached
≤6.5% (phase 2, T2D) Hepatic: none reported Body composition: none reported Other: triglycerides and hsCRP reduced, HDL‑C increased; systolic BP change not significant (phase 2) |
| Eloralintide Selective amylin receptor agonist SC, once‑weekly [Billings 2025] |
Investigational Phase 3 (ongoing in phase 3 ENLIGHTEN program) |
−20% with highest 9 mg dose, 48 weeks −16% counting all participants (NCT06230523, phase 2, full adherence) |
Glycemic: none reported Hepatic: none reported Body composition: 62–72% of weight lost was fat mass Other: systolic BP up to −7.6 mmHg; triglycerides up to −27%; hsCRP up to −64% |
| Petrelintide Long‑acting amylin analog SC, once‑weekly [Garvey 2026] |
Investigational (ongoing in phase 2 ZUPREME program) |
−10.7%, 42 weeks (ZUPREME‑1, phase 2, primary endpoint met at 28 weeks. Weight reductions were retained through 42 weeks) | Glycemic: not assessable; HbA1c ≥6.5% excluded by
design Hepatic: none reported Body composition: imaging pre‑specified as exploratory; not yet reported Other: triglycerides and hsCRP reduced vs placebo |
Figures from separate placebo-controlled trials; populations, durations and analyses differ. Rows and columns do not represent a ranking. Regulatory status as of 13 August. Abbreviations: BP, blood pressure; FDA, US Food and Drug Administration; GLP-1, glucagon-like peptide-1; HbA1c, glycated hemoglobin; HDL-C, high-density lipoprotein cholesterol; hsCRP, high-sensitivity C-reactive protein; pp, percentage points; SC, subcutaneous; T2D, type 2 diabetes.
Clinical trial data of non-amylin comparators
| Agent | Status, August 2026 | Weight | Other current metabolic outcomes |
|---|---|---|---|
| Semaglutide 25 mg GLP‑1 receptor agonist Oral, once‑daily [Wilding 2023; Wharton 2025b] |
Approved – obesity, type 2 diabetes | −13.6%, 64 weeks (OASIS, counting all participants) −6.7 kg, 52 weeks (PIONEER PLUS, 25, type 2 diabetes trial) |
Glycemic: HbA1c −1.88 pp from baseline of 9.0% at 52 weeks
(PIONEER
PLUS, 25 mg); in obesity without diabetes, 71.1% vs 33.3% of those with prediabetes
returned to normal glucose levels at 64 weeks (OASIS 4) Hepatic: none reported Body composition: none reported Other: greater improvements in waist circumference, lipids, and C‑reactive protein vs placebo (OASIS 4) |
| Semaglutide 2.4 mg GLP‑1 receptor agonist SC, once‑weekly [Wilding 2021; Garvey 2025; Buse 2026; Sanyal 2025; Ravussin 2026] |
Approved – obesity, MASH with F2‑F3 fibrosis, select cardiovascular disease risk reduction in those overweight or have obesity | −14.9%, 68 weeks (REDEFINE 1, all participants) −10.2%, 68 weeks (REIMAGINE 2, full adherence) −10.5%, 72 weeks (ESSENCE, MASH) |
Glycemic: HbA1c −1.75 pp (REIMAGINE 2, full
adherence) Hepatic: steatohepatitis resolution 62.9% vs 34.3%; fibrosis improvement 36.8% vs 22.4% at 72 weeks (ESSENCE, phase 3) Body composition: 70% of weight loss was fat mass (REDEFINE 1 substudy) |
| Semaglutide 7.2 mg GLP‑1 receptor agonist SC, once‑weekly [Wharton 2025a; Lingvay 2025] |
Approved – obesity | −18.7%, 72 weeks (STEP UP, all participants; −20.7% with full
adherence) −13.2%, 72 weeks (STEP UP T2D, all participants) |
Glycemic: HbA1c −1.5 pp vs placebo at 72 weeks in obesity with
type
2
diabetes (STEP UP T2D) Hepatic: none reported Body composition: none reported |
| Tirzepatide 5 / 10 / 15 mg GIP + GLP‑1 receptor agonist SC, once‑weekly [Jastreboff 2022; Garvey 2023; Look 2025; Loomba 2024; Scheen 2026] |
Approved – obesity, type 2 diabetes, and, at 10 and 15 mg only, also obstructive sleep apnea | −20.9%, 72 weeks (SURMOUNT‑1, 15 mg, all participants) −14.7%, 72 weeks (SURMOUNT‑2, 15 mg, all participants) −25.5% with full adherence, −23.6% counting all participants, 84 weeks (REDEFINE 4 head‑to‑head with cagrilintide‑semaglutide) |
Glycemic: HbA1c approx. −2.1 pp from a baseline of 8.28% with 49%
reaching <5.7% (SURMOUNT‑2) Hepatic: steatohepatitis resolution up to 62% vs 10% at 52 weeks (SYNERGY‑NASH, phase 2; fibrosis endpoint not multiplicity‑controlled) Body composition: approx. 25% of lost weight was lean mass (SURMOUNT‑1 substudy) |
| Orforglipron 0.8 to 17.2 mg Small‑molecule GLP‑1 receptor agonist Oral, once daily [Wharton 2025b; Rosenstock 2026] |
Approved 2026 – obesity Type 2 diabetes filing submitted |
−8.4% and −11.2% with 36 mg at 72 weeks
(ATTAIN‑1) −8.2% with 36 mg at 52 weeks (ACHIEVE‑3, type 2 diabetes trial) |
Glycemic: HbA1c −1.91 pp vs −1.47 pp for oral semaglutide
14 mg at 52 weeks (ACHIEVE‑3, open‑label) Hepatic: no efficacy data; hepatic safety analysis published Body composition: none reported |
| Retatrutide GLP‑1 + GIP + glucagon receptor agonist SC, once‑weekly [Jastreboff 2023; Sanyal 2024; Bajaj 2026; Jastreboff 2026] |
Investigational (key phase 3 TRIUMPH programs data available) | −28.3% with highest 12 mg dose at 80 weeks (TRIUMPH‑1, phase
3) −24.2% with 12 mg, 48 weeks (NCT04881760, phase 2) −15.3% at 40 weeks in phase 3 type 2 diabetes TRANSCEND‑T2D‑1 trial with 12 mg dose |
Glycemic: HbA1c −1.94 pp vs −0.81 pp placebo at 40 weeks,
with
75–83% reaching ≤6.5% (TRANSCEND‑T2D‑1, phase
3) Hepatic: liver fat −82.4% at 24 weeks and 86% reaching normal liver fat (phase 2a, MASLD) Body composition: none reported |
| Survodutide Glucagon + GLP‑1 receptor agonist SC, once‑weekly [le Roux 2026; Kaplan 2026] |
Investigational (ongoing in phase 3 SYNCHRONIZE program) | −13.0%, 76 weeks (SYNCHRONIZE‑1, 6.0 mg, all
participants) −12.2%, 48 weeks (SYNCHRONIZE‑MASLD, full adherence) |
Glycemic: not reported; SYNCHRONIZE‑2 in obesity with type 2
diabetes
has not yet been reported Hepatic: ≥50% liver‑fat reduction in 84.2% vs 24.5%; liver fat normalised in 61.0%; ALT −36.8% (SYNCHRONIZE‑MASLD, phase 3, MRI endpoint not histology) Body composition: visceral fat −34.0%; liver fat −63.1% (SYNCHRONIZE‑1 imaging substudy) |
| Maridebart cafraglutide GIP receptor antagonist + GLP‑1 receptor agonist SC, once‑monthly [Jastreboff 2025] |
Investigational (ongoing in phase 3 MARITIME program)
No once‑monthly injectable is currently approved |
−16.2%, 52 weeks (phase 2, without diabetes, all participants)
−12.3%, 52 weeks (phase 2, with diabetes, all participants) |
Glycemic: HbA1c −1.43 pp counting all participants, or
−2.03
pp with full adherence, in the type 2 diabetes cohort at 52 weeks
Hepatic: phase 3 liver‑fat study ongoing; no results Body composition: none reported |
Figures from separate placebo-controlled trials; populations, durations and analyses differ. Rows and columns do not represent a ranking Regulatory status as of 13 August. Abbreviations: ALT, alanine aminotransferase; GIP, glucose-dependent insulinotropic polypeptide; GLP-1, glucagon-like peptide-1; HbA1c, glycated hemoglobin; MASH, metabolic dysfunction-associated steatohepatitis; MASLD, metabolic dysfunction-associated steatotic liver disease; MRI, magnetic resonance imaging; pp, percentage points; SC, subcutaneous; T2D, type 2 diabetes.
In the video below, Prof. Carel le Roux provides their perspective on the REDEFINE and REIMAGINE programs and the available zenagamtide data, addressing what the evidence does and does not yet support.
Time to watch: 3 mins 13 secs
Video highlights
- REDEFINE and REIMAGINE showed benefits with cagrilintide plus semaglutide, while cagrilintide monotherapy data helps clarify the contribution of amylin alone.
- In REDEFINE 4, cagrilintide plus semaglutide did not meet non-inferiority versus tirzepatide but still achieved 23% weight loss at 84 weeks, which remains clinically substantial and may translate into meaningful functional benefits for patients
- Early zenagamtide data efficacy signals are promising with 24% weight loss at 36 weeks and a 1.7% HbA1c reduction in patients with obesity and type 2 diabetes; phase 3 will provide further insight into weight-loss outcomes and tolerability.
Bringing it together
Amylin is a distinct regulatory axis with its own receptors, brain targets and physiological role, that may act effectively on its own and not just as an accessory to incretins [Secher 2026; Walker 2025]. The rationale for multi-pathway treatment rests on that distinctness, since combinations are designed to engage complementary signals rather than amplify one [Kusminski 2024; Müller 2022].
For practice, useful factors to consider when it comes to emerging uses of amylin-containing regimens include not only how much weight a therapy removes but also how much it removes in different populations, its impact across metabolic outcomes, the tolerability for the patient, and potential weight regain after stopping therapy.
References
Supporting content of the animation
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Boyle CN, Lutz TA, Le Foll, et al. Amylin – Its role in the homeostatic and hedonic control of eating and recent developments of amylin analogs to treat obesity. Mol Metab. 2017;8:203‑210.
Budini B, Luo S, Tam M, et al. Trajectory of weight regain after cessation of GLP-1 receptor agonists: a systematic review and nonlinear meta-regression. eClinicalMedicine. 2026;93.
Chung CW, Kim J. Amylin revisited: a 5-year perspective on its emerging role in the treatment of diabesity. J Obes Metab Syndr. 2026;35(1):38‑48.
Davies MJ, Bajaj HS, Broholm C, et al. Cagrilintide–semaglutide in adults with overweight or obesity and type 2 diabetes (REDEFINE 2). N Engl J Med. 2025;393(7):648‑659.
Garvey WT, Blüher M, Osorto Contreras CK, et al. Coadministered cagrilintide and semaglutide in adults with overweight or obesity (REDEFINE 1). N Engl J Med. 2025;393(7):635‑647.
Hamarsheh S, Jaber AR, Abu-Khazneh O, et al. Comparative effectiveness of CagriSema, semaglutide, cagrilintide and tirzepatide in overweight and obesity: a network meta-analysis of randomised clinical trials. Endocrinol Diabetes Metab. 2026;9(4):e70248.
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Jastreboff AM, Aronne LJ, Ahmad NN, et al. Tirzepatide once weekly for the treatment of obesity (SURMOUNT-1). N Engl J Med. 2022;387(3):205‑216.
Jastreboff AM, Kaplan LM, Frías JP, et al. Triple–hormone-receptor agonist retatrutide for obesity — a phase 2 trial. N Engl J Med. 2023;389(6):514‑526.
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Cited in the narrative text copy and evidence tables
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Bajaj HS, Welch M, Shah, P, et al. Efficacy and safety of retatrutide, a GIP, GLP-1, and glucagon receptor agonist, in people with type 2 diabetes and inadequate glycaemic control with diet and exercise (TRANSCEND-T2D-1): a double-blind, randomised, phase 3 trial. Lancet. 2026;407(10546):2402‑2413.
Billings LK, Hsia SH, Bays H, et al. Eloralintide, a selective amylin receptor agonist for the treatment of obesity: a 48-week phase 2, multicentre, double-blind, randomised, placebo-controlled trial. Lancet. 2025;406(10520):2631‑2643.
Budini B, Luo S, Tam M, et al. Trajectory of weight regain after cessation of GLP-1 receptor agonists: a systematic review and nonlinear meta-regression. eClinicalMedicine. 2026;93.
Buse JB, Bajaj HS, Dalskov S-M, et al; REIMAGINE 2 study group. Cagrilintide–semaglutide (CagriSema) versus semaglutide or cagrilintide in people with type 2 diabetes (REIMAGINE 2): a double-blind, randomised, controlled, phase 3 study. Lancet Diabetes Endocrinol. 2026;14(8):662‑677.
Chung CW, Kim J. Amylin revisited: a 5-year perspective on its emerging role in the treatment of diabesity. J Obes Metab Syndr. 2026;35(1):38‑48.
Dahl K, Toubro S, Dey S, et al. Amycretin, a novel, unimolecular GLP-1 and amylin receptor agonist administered subcutaneously: results from a phase 1b/2a randomised controlled study. Lancet. 2025;406(10499):149‑162. [published under the name amycretin; INN zenagamtide]
Davies MJ, Bajaj HS, Broholm C, et al. Cagrilintide–semaglutide in adults with overweight or obesity and type 2 diabetes (REDEFINE 2). N Engl J Med. 2025;393(7):648‑659.
Garvey WT, Blüher M, Osorto Contreras CK, et al. Coadministered cagrilintide and semaglutide in adults with overweight or obesity (REDEFINE 1). N Engl J Med. 2025;393(7):635‑647.
Garvey T, Connery L, Dinesen M, et al. Petrelintide, a Human Amylin Analog for the Treatment of Obesity: Efficacy and Safety from the Phase 2 Trial, ZUPREME 1. Abstract presented at the American Diabetes Association (ADA) Scientific Sessions 2026, New Orleans, LA. June 5-8, 2026.
Garvey WT, Frias JP, Jastreboff AM, et al. Tirzepatide once weekly for the treatment of obesity in people with type 2 diabetes (SURMOUNT-2): a double-blind, randomised, multicentre, placebo-controlled, phase 3 trial. Lancet. 2023;402(10402):613‑626.
Hay DL, Chen S, Lutz TA, et al. Amylin: pharmacology, physiology, and clinical potential. Pharmacol Rev. 2015;67(3):564‑600.
Jastreboff A. Results of First Phase 3 Study of Retatrutide, a GIP, GLP-1, and Glucagon Receptor Agonist in Patients with Obesity (TRIUMPH-1). Presented at the American Diabetes Association (ADA) Scientific Sessions 2026, New Orleans, LA. June 5-8, 2026.
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