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Peptides for Diabetes Management

More than 537 million adults worldwide live with diabetes, and that number is projected to hit 783 million by 2045. Type 2 diabetes accounts for over 95% of cases and causes roughly 1.66 million deaths annually.

More than 537 million adults worldwide live with diabetes, and that number is projected to hit 783 million by 2045. Type 2 diabetes accounts for over 95% of cases and causes roughly 1.66 million deaths annually. In the United States alone, the direct and indirect costs of diagnosed diabetes reached $413 billion in 2022.

Against this backdrop, peptide-based therapies have fundamentally changed how diabetes is treated. GLP-1 receptor agonists --- a class of drugs built on naturally occurring peptide hormones --- now deliver HbA1c reductions of 1.5-2.0%, weight loss of 7-24%, and cardiovascular risk reductions of 14-20%. And the science is moving fast. Dual agonists, triple agonists, oral formulations, and combination therapies are expanding what's possible.

This guide covers the full range of peptide-based diabetes treatments: what's available now, what's in the pipeline, and what the clinical evidence actually shows.

Table of Contents

How Peptide Hormones Regulate Blood Sugar {#how-peptide-hormones-regulate-blood-sugar}

Your body uses several peptide hormones to keep blood sugar in a tight range. Understanding these systems explains why peptide-based drugs work so well --- and why researchers keep building on them.

The Incretin System

When food hits your small intestine, specialized cells release two key peptide hormones:

GLP-1 (glucagon-like peptide-1): Released from L-cells in the intestine, GLP-1 does several things at once. It tells your pancreatic beta cells to release insulin. It tells your alpha cells to stop releasing glucagon (the hormone that raises blood sugar). It slows gastric emptying so glucose enters the bloodstream more gradually. And it acts on the brain to reduce appetite [1].

GIP (glucose-dependent insulinotropic polypeptide): Released from K-cells, GIP also stimulates insulin secretion. It has additional effects on fat metabolism and bone health. For years, researchers thought GIP was less useful than GLP-1 for diabetes treatment. The success of tirzepatide proved them wrong.

Here's the problem: natural GLP-1 has a half-life of about two minutes. The enzyme DPP-4 (dipeptidyl peptidase-4) chews it up almost immediately. So the biological signal is powerful, but fleeting. Every GLP-1-based drug is essentially an engineered version of this peptide designed to resist DPP-4 and last much longer [2].

Other Peptide Regulators

Amylin: Co-secreted with insulin from beta cells, amylin slows gastric emptying, suppresses glucagon, and acts on the brain to promote satiety. In type 2 diabetes, amylin secretion is reduced. In type 1, it's essentially absent.

Glucagon: The counter-regulatory hormone to insulin. It raises blood sugar by triggering glucose release from the liver. Too much glucagon after meals is a hallmark of type 2 diabetes. But at the right dose, glucagon also increases energy expenditure and fat burning --- which is why the triple agonist retatrutide includes glucagon receptor activation.

Insulin: The most famous peptide hormone. Discovered in 1921, it remains essential for type 1 diabetes and advanced type 2 diabetes. Modern insulin analogs are themselves products of peptide engineering.

GLP-1 Receptor Agonists: The Foundation {#glp-1-receptor-agonists-the-foundation}

GLP-1 receptor agonists (GLP-1 RAs) are now prescribed to millions of people worldwide for type 2 diabetes, obesity, and increasingly for cardiovascular and kidney protection. They work by mimicking or amplifying the natural GLP-1 signal.

How They Differ from DPP-4 Inhibitors

DPP-4 inhibitors (sitagliptin, saxagliptin, etc.) work by blocking the enzyme that degrades natural GLP-1, modestly increasing its levels. GLP-1 RAs bypass this entirely by providing pharmacological concentrations of GLP-1 receptor activation --- far higher than what DPP-4 inhibitors achieve. The result: GLP-1 RAs produce much larger reductions in HbA1c and body weight.

The Evolution of GLP-1 Drugs

The field has evolved through three generations:

First generation: Exenatide (Byetta, 2005) --- derived from Gila monster saliva, dosed twice daily. Modest efficacy but proved the concept.

Second generation: Liraglutide (Victoza, 2010) --- once-daily injection with improved efficacy. First GLP-1 RA to demonstrate cardiovascular benefit (LEADER trial). Dulaglutide (Trulicity, 2014) --- once-weekly injection that simplified dosing.

Third generation: Semaglutide (Ozempic, 2017 injectable; Rybelsus, 2019 oral) --- the most potent single GLP-1 RA, available in both injectable and oral forms. Demonstrated cardiovascular, kidney, and metabolic benefits across multiple landmark trials.

Each generation improved on potency, dosing convenience, and clinical outcomes.

Semaglutide: The Most Studied GLP-1 Agonist {#semaglutide-the-most-studied-glp-1-agonist}

Semaglutide has become the most extensively studied GLP-1 receptor agonist in history, with data from dozens of clinical trials encompassing tens of thousands of patients across diabetes, obesity, cardiovascular disease, and kidney disease.

How It Works

Semaglutide is a modified human GLP-1 analog with 94% structural similarity to native GLP-1. Key engineering changes --- including an amino acid substitution at position 8 and a C-18 fatty acid chain --- make it resistant to DPP-4 degradation and allow it to bind to albumin in the blood, extending its half-life to approximately 7 days [3]. This enables once-weekly dosing.

Diabetes Efficacy: The SUSTAIN Program

The SUSTAIN trial program established semaglutide's diabetes credentials:

  • SUSTAIN 1-5: Across multiple comparator trials, subcutaneous semaglutide (0.5 mg and 1.0 mg weekly) consistently reduced HbA1c by 1.5-1.8% and body weight by 4-6 kg over 30-56 weeks.
  • SUSTAIN 7: Head-to-head against dulaglutide, semaglutide produced significantly greater HbA1c reduction and weight loss at both dose levels.

In the SUSTAIN program, 66-79% of patients achieved HbA1c below 7.0% with semaglutide, compared to 37-48% with comparator drugs [4].

Cardiovascular Protection: SUSTAIN 6 and SELECT

SUSTAIN 6 (2016): In 3,297 patients with type 2 diabetes at high cardiovascular risk, semaglutide reduced MACE by 26% (hazard ratio 0.74), driven by reductions in nonfatal stroke (39%) and nonfatal heart attack (26%) [5].

SELECT (2023): In 17,604 patients with obesity and cardiovascular disease but without diabetes, semaglutide 2.4 mg weekly reduced MACE by 20% (hazard ratio 0.80, P < 0.001). Weight loss averaged 9.4% versus 0.9% with placebo. The cardiovascular benefits were consistent regardless of baseline HbA1c, BMI, or weight lost --- suggesting mechanisms beyond glucose and weight control [6].

The SOUL Trial: Oral Semaglutide's Cardiovascular Proof

Published in the New England Journal of Medicine in 2025, the SOUL trial tested oral semaglutide (14 mg daily) in 9,650 patients with type 2 diabetes and established cardiovascular or kidney disease. The results:

  • 14% reduction in MACE (hazard ratio 0.86, P = 0.006)
  • 26% reduction in nonfatal heart attacks
  • 12% reduction in nonfatal stroke
  • 7% reduction in cardiovascular death

This made oral semaglutide the first and only oral GLP-1 receptor agonist to demonstrate cardiovascular benefit --- a significant development for patients who prefer pills over injections [7].

Tirzepatide: The Dual GIP/GLP-1 Agonist {#tirzepatide-the-dual-agonist}

Tirzepatide (Mounjaro for diabetes, Zepbound for obesity) changed the game by activating two incretin receptors simultaneously: GLP-1 and GIP. This dual mechanism produces greater metabolic effects than GLP-1 activation alone.

Clinical Evidence: SURPASS and SURMOUNT

SURPASS-2 (Head-to-Head vs. Semaglutide): This was the trial that established tirzepatide's superiority. In patients with type 2 diabetes inadequately controlled on metformin, tirzepatide at all three doses (5 mg, 10 mg, 15 mg) was noninferior and superior to semaglutide 1.0 mg for HbA1c reduction:

  • Tirzepatide 15 mg: -2.30% HbA1c reduction
  • Tirzepatide 10 mg: -2.20%
  • Tirzepatide 5 mg: -2.01%
  • Semaglutide 1.0 mg: -1.86%

Weight loss was also significantly greater with tirzepatide across all doses [8].

SURMOUNT-1 (3-Year Data, NEJM 2025): In 2,539 people with obesity (including 1,032 with prediabetes), three years of tirzepatide treatment produced sustained weight loss and a markedly lower rate of progression from prediabetes to type 2 diabetes compared to placebo. This is one of the first trials to demonstrate that a peptide-based drug can actually prevent diabetes onset [9].

Why Dual Agonism Works

GIP receptor activation adds additional insulin secretion through a separate pathway, improves beta-cell function, produces greater appetite suppression through distinct brain circuits, and may improve fat metabolism. Cardiovascular outcome trials (SURPASS-CVOT in T2D, expected 2025; SURMOUNT-MMO without diabetes, expected 2027) will determine whether tirzepatide's cardiovascular protection matches semaglutide's.

Other Approved GLP-1 Receptor Agonists {#other-approved-glp-1-receptor-agonists}

While semaglutide and tirzepatide dominate current prescribing, other GLP-1 RAs remain in clinical use:

  • Liraglutide (Victoza/Saxenda): Once-daily injection. The LEADER trial showed a 13% MACE reduction. Less potent than semaglutide or tirzepatide, but well-established safety profile [10].
  • Dulaglutide (Trulicity): Once-weekly injection. The REWIND trial demonstrated cardiovascular benefit in a broad type 2 diabetes population. HbA1c reductions of 1.1-1.5% [11].
  • Exenatide (Byetta/Bydureon): The first approved GLP-1 RA. The EXSCEL cardiovascular trial did not show statistically significant MACE reduction. Generally considered less effective than newer agents.

Retatrutide: The Triple Agonist {#retatrutide-the-triple-agonist}

If tirzepatide proved that two receptor targets are better than one, Eli Lilly's retatrutide is testing whether three targets are better than two. Retatrutide activates GLP-1, GIP, and glucagon receptors simultaneously.

Why Add Glucagon?

On the surface, activating glucagon receptors in diabetes seems counterintuitive --- glucagon raises blood sugar. But at carefully calibrated doses, glucagon receptor activation increases energy expenditure, promotes fat oxidation, and reduces liver fat. When combined with the insulin-promoting effects of GLP-1 and GIP activation, the net result is better metabolic outcomes than dual agonism alone [12].

Phase 2 Results

In the phase 2 trial published in the New England Journal of Medicine:

  • People with obesity achieved up to 24.2% weight loss after 48 weeks
  • People with type 2 diabetes achieved 16.9% weight loss and 2.2% HbA1c improvement after 36 weeks
  • 82% of T2D participants reached HbA1c of 6.5% or lower
  • Lipid improvements were substantial: total cholesterol dropped 15-18%, LDL fell 12-22%, and triglycerides decreased 35-40% --- surpassing dulaglutide

Phase 3: TRIUMPH Program

In December 2025, Lilly announced results from TRIUMPH-4:

  • Retatrutide achieved up to 28.7% weight loss at the efficacy estimand (23.7% at the treatment-regimen estimand for the 12 mg dose)
  • Significant improvements in osteoarthritis pain and physical function
  • Side effects were predominantly gastrointestinal (nausea, diarrhea, constipation, vomiting) with no major safety signals [13]

Seven additional Phase 3 trials are studying retatrutide across type 2 diabetes, knee osteoarthritis, obstructive sleep apnea, chronic low back pain, cardiovascular outcomes, kidney outcomes, and liver disease. Results are expected throughout 2026.

Body Composition Data

A body composition substudy showed retatrutide reduced total body fat mass by up to 26.1%. The proportion of lean mass to total weight loss was similar to other obesity treatments, providing reassurance that the drug preferentially targets fat rather than muscle [14].

Amylin Analogs and CagriSema {#amylin-analogs-and-cagrisema}

Amylin is co-secreted with insulin and complements its action by slowing gastric emptying, suppressing post-meal glucagon, and reducing appetite through brain signaling. In type 2 diabetes, amylin secretion declines alongside insulin. Targeting the amylin pathway adds a distinct mechanism to GLP-1-based treatment.

From Pramlintide to Cagrilintide

Pramlintide (Symlin), available since 2005, requires three-times-daily injection and produces modest HbA1c reductions (0.3-0.6%). Cagrilintide is Novo Nordisk's next-generation amylin analog, engineered for once-weekly injection through amino acid substitutions (preventing fibril formation) and a fatty acid chain (enabling albumin binding) [15].

In the REDEFINE 1 Phase 3 trial:

  • Cagrilintide monotherapy (2.4 mg weekly): 11.8% weight loss over 68 weeks
  • Semaglutide monotherapy (2.4 mg weekly): 16.1% weight loss
  • CagriSema combination (cagrilintide 2.4 mg + semaglutide 2.4 mg): 22.7% weight loss

The combination outperformed either drug alone, confirming that GLP-1 and amylin pathways produce additive effects [16].

CagriSema and the Pipeline

In mid-2025, Novo Nordisk submitted CagriSema to the FDA. If approved, it would be the first combination GLP-1 and amylin analog treatment. The pipeline also includes eloralintide (a selective amylin receptor agonist in phase 2), amycretin (a chimeric GLP-1/amylin peptide), and ACCG-2671 (an oral dual amylin/calcitonin receptor agonist in preclinical development).

Oral Peptide Formulations {#oral-peptide-formulations}

Peptides are notoriously difficult to deliver orally. Stomach acid destroys them, and their large molecular size makes intestinal absorption poor. But for diabetes management, the convenience of a pill versus an injection is a major factor in patient adherence.

Oral Semaglutide (Rybelsus)

Oral semaglutide uses SNAC (sodium N-[8-(2-hydroxybenzoyl)amino] caprylate) to boost peptide absorption through the gastric mucosa. Patients must take it on an empty stomach with minimal water, then wait 30 minutes before eating. At 14 mg, it reduces HbA1c by 1.2-1.4% with the SOUL trial proving its cardiovascular benefit [7].

What's Next: Orforglipron and Higher Doses

Orforglipron (Eli Lilly) is a non-peptide small molecule that activates the GLP-1 receptor, making oral formulation much simpler. Phase 3 trials are ongoing [17]. Novo Nordisk is also developing higher-dose oral semaglutide (25 mg and 50 mg) that may match injectable efficacy.

Kidney Protection: The FLOW Trial {#kidney-protection-the-flow-trial}

Diabetic kidney disease (diabetic nephropathy) is the leading cause of kidney failure worldwide. The FLOW trial established semaglutide as the first GLP-1 receptor agonist with dedicated kidney outcome evidence --- and the results were strong enough that the trial was stopped early.

Key Results

The FLOW trial enrolled 3,533 patients with type 2 diabetes and chronic kidney disease (eGFR 25-75 mL/min/1.73 m2 with significant albuminuria). Over a median 3.4 years on semaglutide 1.0 mg weekly versus placebo [18]:

  • 24% reduction in the primary composite outcome (kidney failure, 50% eGFR decline, or kidney/cardiovascular death) --- hazard ratio 0.76, P = 0.0003
  • 29% reduction in cardiovascular death
  • Slower kidney decline: Annual eGFR loss was 1.16 mL/min/1.73 m2 less steep with semaglutide

This positions GLP-1 RAs as a "fourth pillar" of diabetic kidney disease treatment, alongside RAS inhibitors, SGLT2 inhibitors, and finerenone. Modeling suggests combining all four classes could extend event-free survival by 5.5 years for kidney disease progression compared to RAS inhibitor monotherapy [19].

Cardiovascular Benefits {#cardiovascular-benefits}

The cardiovascular evidence for GLP-1 receptor agonists is now extensive and consistent across multiple drugs and trials.

The Evidence Base

TrialDrugPopulationMACE ReductionP-value
LEADERLiraglutideT2D, high CV risk13%0.01
SUSTAIN 6Semaglutide (SC)T2D, high CV risk26%<0.001 (non-inferiority)
SELECTSemaglutide (SC)Obesity + CVD, no diabetes20%<0.001
SOULSemaglutide (oral)T2D, CVD/CKD14%0.006
REWINDDulaglutideBroad T2D12%0.026

How GLP-1 RAs Protect the Heart

Multiple mechanisms likely contribute to cardiovascular protection beyond glucose and weight control: reduced inflammation (lower C-reactive protein), blood pressure reduction (3-5 mmHg systolic), improved lipid profiles, direct protective effects on blood vessels via vascular GLP-1 receptors, and reduced liver fat leading to less atherogenic lipoprotein production.

Head-to-Head Comparison Table {#head-to-head-comparison-table}

FeatureSemaglutide (SC)Semaglutide (Oral)TirzepatideLiraglutideDulaglutideRetatrutide*
Receptor TargetsGLP-1GLP-1GLP-1 + GIPGLP-1GLP-1GLP-1 + GIP + Glucagon
DosingWeekly injectionDaily oralWeekly injectionDaily injectionWeekly injectionWeekly injection
HbA1c Reduction1.5-1.8%1.2-1.4%2.0-2.3%1.1-1.5%1.1-1.5%~2.2%
Weight Loss (T2D)4-6 kg3-5 kg7-12 kg2-4 kg2-4 kg~16.9% of body weight
CV Outcome DataYes (SUSTAIN 6, SELECT)Yes (SOUL)Pending (2025/2027)Yes (LEADER)Yes (REWIND)Not yet
Kidney Outcome DataYes (FLOW)PendingNoNoNoNot yet
FDA Approved (Diabetes)YesYesYesYesYesNo (Phase 3)

*Retatrutide data from Phase 2/3 trials; not yet approved.

Beyond Blood Sugar: Expanding Indications {#beyond-blood-sugar-expanding-indications}

The scope of peptide-based therapies now extends far beyond glucose control. Here's where the research is heading:

Liver disease (MASLD): Formerly called NAFLD, metabolic-associated steatotic liver disease affects up to 70% of people with type 2 diabetes. Semaglutide and tirzepatide both reduce liver fat significantly. Retatrutide's glucagon component may be particularly effective, as glucagon receptor activation directly promotes hepatic fat oxidation.

Diabetes prevention: The SURMOUNT-1 three-year data showed tirzepatide dramatically reduced progression from prediabetes to type 2 diabetes, positioning peptide therapies as prevention tools [9].

Heart failure: The STEP-HFpEF trial demonstrated semaglutide improved heart failure symptoms, physical function, and quality of life in patients with HFpEF and obesity.

Sleep apnea: Tirzepatide significantly reduced sleep apnea severity in the SURMOUNT-OSA trial, with some patients eliminating the need for CPAP therapy.

Type 1 diabetes: Early research is exploring GLP-1 RAs as adjuncts to insulin in type 1 diabetes. By reducing glucagon secretion and slowing gastric emptying, these peptides may smooth post-meal glucose spikes. However, hypoglycemia and diabetic ketoacidosis risks require careful study [20].

Side Effects and Safety Profiles {#side-effects-and-safety-profiles}

GLP-1 receptor agonists and related peptide drugs share a common side effect profile, primarily gastrointestinal.

Common Side Effects

Side EffectFrequency (approximate)Management
Nausea15-45%Usually temporary; slow dose escalation helps
Diarrhea10-35%Often resolves within weeks
Vomiting5-25%More common during dose escalation
Constipation10-25%Adequate hydration, fiber intake
Injection site reactions1-5%Rotate injection sites
Decreased appetiteVery commonExpected pharmacological effect

Gastrointestinal side effects are most common during dose escalation and typically improve over 4-8 weeks. Slow dose titration is the standard approach to minimize these effects.

Serious but Rare Risks

Pancreatitis: A small increased risk of acute pancreatitis has been observed with GLP-1 RAs. Patients with a history of pancreatitis should use these drugs cautiously. Monitoring for persistent severe abdominal pain is recommended.

Thyroid concerns: In rodent studies, GLP-1 RAs caused thyroid C-cell tumors. This has not been seen in humans, but GLP-1 RAs carry a boxed warning and are contraindicated in patients with a personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia syndrome type 2 (MEN2).

Gallbladder disease: Rapid weight loss increases gallstone risk. This applies to all weight-loss interventions, not just peptide drugs.

Gastroparesis risk: GLP-1 RAs slow gastric emptying, which can be problematic for patients with pre-existing gastroparesis or severe gastrointestinal motility disorders.

Hypoglycemia: GLP-1 RAs alone rarely cause hypoglycemia because their insulin-stimulating effect is glucose-dependent. However, when combined with insulin or sulfonylureas, hypoglycemia risk increases and dose adjustments are often needed.

Muscle mass loss: Significant weight loss from any cause results in some lean mass loss. The retatrutide body composition data suggests roughly 25-30% of weight lost is lean mass [14]. Exercise and adequate protein intake are important adjuncts to any peptide-based weight loss therapy.

Frequently Asked Questions {#frequently-asked-questions}

What is the most effective peptide drug for type 2 diabetes?

Based on current evidence, tirzepatide produces the greatest HbA1c reduction (up to 2.3%) and weight loss among approved medications. Retatrutide may surpass it but is not yet approved. For patients who also need cardiovascular or kidney protection, semaglutide has the broadest evidence base across outcome trials.

Can GLP-1 drugs cure diabetes?

No current medication cures type 2 diabetes. However, GLP-1 RAs and dual agonists can produce diabetes remission (HbA1c below 6.5% without diabetes medication) in some patients, particularly those who achieve significant weight loss. Stopping the medication typically leads to weight regain and glucose deterioration.

Are oral GLP-1 drugs as effective as injections?

Currently, oral semaglutide at 14 mg is somewhat less effective than injectable semaglutide. Higher-dose oral formulations (25 mg, 50 mg) in development may close this gap. The SOUL trial proved oral semaglutide has cardiovascular benefit.

How do GLP-1 drugs protect the kidneys?

The FLOW trial showed semaglutide slowed kidney function decline by reducing the annual rate of eGFR loss. Proposed mechanisms include reduced intrarenal inflammation, lower blood pressure, improved glucose control, and direct protective effects on kidney GLP-1 receptors. The benefit was seen on top of standard kidney-protective medications.

What is the difference between semaglutide and tirzepatide?

Semaglutide activates only the GLP-1 receptor. Tirzepatide activates both GLP-1 and GIP receptors. In the head-to-head SURPASS-2 trial, tirzepatide produced greater HbA1c reduction and weight loss. However, semaglutide has more cardiovascular and kidney outcome data from completed trials. See our dedicated guides on semaglutide and tirzepatide for full comparisons.

What is retatrutide and when will it be available?

Retatrutide is an investigational once-weekly injectable that activates three receptors: GLP-1, GIP, and glucagon. Phase 3 trials are underway with results expected throughout 2026. If approved, it could be available by 2027-2028 at the earliest. Phase 2 data showed up to 24.2% weight loss and robust glucose control.

What about peptides for fat loss without diabetes?

Several peptides studied for diabetes also work for obesity. AOD-9604 is a growth hormone fragment studied for fat loss. GLP-1 RAs like semaglutide are FDA-approved for obesity management. See our guide on best peptides for fat loss.

Will semaglutide become cheaper?

In 2026, Novo Nordisk's semaglutide patent expires in several countries including India and China, allowing generic production. U.S. patents extend until 2032, though generic manufacturers are already positioning for earlier market entry.

Can peptide drugs be combined with other diabetes medications?

Yes. GLP-1 RAs are commonly used alongside metformin, SGLT2 inhibitors, and sometimes insulin. The semaglutide + SGLT2 inhibitor combination is particularly powerful, providing complementary cardiovascular and kidney protection. Combining GLP-1 RAs with sulfonylureas increases hypoglycemia risk and typically requires dose reduction.

The Bottom Line {#the-bottom-line}

Peptide-based therapies have transformed diabetes management over the past decade, and the pace of innovation is accelerating. GLP-1 receptor agonists like semaglutide have moved from "diabetes drug" to multi-organ protection agents with proven cardiovascular and kidney benefits. Tirzepatide showed that dual receptor targeting improves outcomes further. Retatrutide's triple agonism and CagriSema's amylin + GLP-1 combination are pushing the boundaries of what's metabolically achievable.

For people with type 2 diabetes, the practical implications are clear. These drugs don't just lower blood sugar --- they reduce heart attacks, slow kidney disease, promote meaningful weight loss, and may prevent diabetes in those at risk. Oral formulations with cardiovascular benefit (oral semaglutide in the SOUL trial) remove the injection barrier for many patients.

Open questions remain: long-term safety beyond 3-5 years, cardiovascular outcome data for tirzepatide and retatrutide, optimal combination strategies with SGLT2 inhibitors, and global access to what remain expensive medications. But the direction is set. Peptide engineering has given us tools that address the root metabolic dysfunction of type 2 diabetes more effectively than anything before. For the 537 million people living with diabetes worldwide, that matters.

References {#references}

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  2. Muller TD, et al. "The expanding landscape of GLP-1 medicines." Nature Medicine. 2025. https://www.nature.com/articles/s41591-025-04124-5

  3. Knudsen LB, Lau J. "The Discovery and Development of Liraglutide and Semaglutide." Frontiers in Endocrinology. 2019.

  4. Aroda VR, et al. "Comparative efficacy, safety, and cardiovascular outcomes with once-weekly subcutaneous semaglutide in the treatment of type 2 diabetes: Insights from the SUSTAIN 1-7 trials." Diabetes & Metabolism. 2019. https://pubmed.ncbi.nlm.nih.gov/30615985/

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  10. Marso SP, et al. "Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes." New England Journal of Medicine. 2016;375:311-322.

  11. Gerstein HC, et al. "Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND)." Lancet. 2019;394:121-130.

  12. "Triple Agonism Based Therapies for Obesity." PMC. 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC12304053/

  13. "Lilly's triple agonist, retatrutide, delivered weight loss of up to an average of 71.2 lbs." Eli Lilly and Company. December 2025. https://investor.lilly.com/news-releases/news-release-details/lillys-triple-agonist-retatrutide-delivered-weight-loss-average

  14. "Effects of retatrutide on body composition in people with type 2 diabetes." Lancet Diabetes & Endocrinology. 2025. https://www.thelancet.com/journals/landia/article/PIIS2213-8587(25)00092-0/abstract

  15. Lau DCW, et al. "Development of Cagrilintide, a Long-Acting Amylin Analogue." Journal of Medicinal Chemistry. 2022. https://pubs.acs.org/doi/10.1021/acs.jmedchem.1c00565

  16. Frias JP, et al. "Coadministered Cagrilintide and Semaglutide in Adults with Overweight or Obesity." New England Journal of Medicine. 2025. https://www.nejm.org/doi/full/10.1056/NEJMoa2502081

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  21. Amylin: From Mode of Action to Future Clinical Potential in Diabetes and Obesity. PMC. 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC12085449/

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