Cagrilintide: A Long-Acting Amylin Analog for Weight Management Research

This content is provided by Superpower Health for educational and informational purposes only. Cagrilintide is an investigational compound that is not FDA-approved for any indication and is not available through Superpower. This page is not a substitute for medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider.

GLP-1 receptor agonists changed the clinical picture for weight management. They also raised a new question: what happens when you pair them with a hormone the body already uses to regulate appetite? Amylin has been co-secreted alongside insulin at every meal for your entire life. For decades it was clinically underappreciated. That is changing.

Cagrilintide is Novo Nordisk's long-acting amylin analog, designed for once-weekly dosing. Here is what it is, what the Phase 2 monotherapy data shows, and why its clinical future lies primarily in combination rather than solo use.

Key Takeaways

• Regulatory Status: As of April 2026, cagrilintide is not FDA-approved for any indication. It is an investigational compound under clinical development by Novo Nordisk and is not available through compounding pharmacies or by prescription outside of clinical trials.
• Research Stage: Phase 2 monotherapy data published in The Lancet in 2021; Phase 3 data for the CagriSema combination published in NEJM in 2025
• Availability: Not available through Superpower or through standard prescribing pathways; access limited to clinical trial enrollment
• Compound reference: PubChem CID 155142498
• How it works: Activates amylin receptors and the calcitonin receptor in the brain to slow gastric emptying, suppress glucagon, and reduce food intake.
• What the research shows: Phase 2 monotherapy produced approximately 10.8% weight loss at 26 weeks; the clinical focus has since shifted to the CagriSema combination, which achieved approximately 20.4% weight loss in the REDEFINE 1 Phase 3 trial.

Where Cagrilintide Comes From and How It Works

Amylin: the co-secreted appetite signal

Amylin is a 37-amino acid peptide hormone secreted by the pancreatic beta cells alongside insulin in response to food intake. It was first characterized in 1987 by Cooper and colleagues, published in the Proceedings of the National Academy of Sciences, when the team isolated it from the amyloid deposits in pancreases of type 2 diabetic patients and noted its structural similarity to calcitonin gene-related peptide. The hormone's three primary metabolic roles are well established: it slows gastric emptying (reducing the rate at which glucose reaches the bloodstream), suppresses postprandial glucagon secretion from the pancreatic alpha cells, and signals meal-ending satiation through the central nervous system. These effects are mediated primarily through the caudal hindbrain, with the area postrema and nucleus tractus solitarius serving as key relay sites for amylin's appetite-suppressing signal. Amylin was first isolated and characterized in 1987 by Cooper and colleagues in the Proceedings of the National Academy of Sciences, who purified the 37-amino-acid peptide from amyloid-rich pancreases of type 2 diabetic patients and established its structural relationship to calcitonin gene-related peptide. A canonical review of amylinergic control of food intake by Lutz in Physiology & Behavior in 2006 laid out the central role of the area postrema in amylin's satiety signaling, along with gastric emptying slowing and postprandial glucagon suppression. A 2022 review by Boyle, Zheng, and Lutz in the Journal of Clinical Medicine identifies amylin as a physiological satiation signal that functions synergistically with leptin, connecting meal-by-meal regulation to longer-term body weight control. A broader 2024 review by Eržen and colleagues in the International Journal of Molecular Sciences places amylin within the emerging landscape of neuroendocrine hormones being developed for "diabesity." Human pharmacology data support the central mechanism: a randomized crossover study by Chapman and colleagues in Diabetologia in 2005 demonstrated that pramlintide reduced food intake and increased satiety in obese and type 2 diabetic subjects, providing direct human evidence for amylin's appetite-suppressing effect. An earlier mechanistic study by Levetan and colleagues in Diabetes Care in 2003 showed that pramlintide added to insulin pump therapy reduced postprandial glucose, glucagon, and triglyceride excursions in type 1 diabetes, establishing what amylin does postprandially beyond central satiety.

Amylin receptor pharmacology

Amylin receptors are not single-protein structures. As established by Hay and colleagues in a 2004 paper in Biochemical Society Transactions, each amylin receptor is a heterodimer consisting of the calcitonin receptor (CTR) core plus one of three receptor activity-modifying proteins (RAMP1, RAMP2, or RAMP3), yielding AMY1, AMY2, and AMY3 receptor subtypes. A subsequent IUPHAR pharmacology review by Hay and colleagues in the British Journal of Pharmacology in 2018 positioned amylin receptors within the broader calcitonin/CGRP family and formalized the RAMP-dependent receptor phenotypes that distinguish amylin receptors from the calcitonin receptor alone. A 2022 cryo-electron microscopy paper by Cao and colleagues in Science established the structural basis for amylin receptor phenotype and showed how calcitonin-based ligands engage AMYR differently than amylin-based peptides, setting the stage for the cagrilintide-specific structural work that followed. This architecture explains why cagrilintide is described as a dual amylin/calcitonin receptor co-agonist: the molecule binds both the CTR component and the full RAMP-containing amylin receptor complexes, with AMY1 and AMY3 representing its primary functional targets in the brain. The preclinical work of Carvas and colleagues, published in EBioMedicine in 2025, confirmed this using receptor-knockout mice: weight loss effects from cagrilintide were eliminated when AMY1R and AMY3R receptors were absent in the hindbrain, while hindbrain neuronal activation was substantially diminished. This establishes central amylin receptor signaling as the mechanistic backbone of cagrilintide's weight-reducing effects.

From pramlintide to cagrilintide: the engineering difference

Pramlintide (Symlin), the only amylin-based therapy previously FDA-approved, requires three injections daily before meals because native amylin aggregates rapidly in solution and has a short half-life. The clinical burden of that dosing schedule limited its uptake and its usefulness outside of insulin-dependent diabetes. Cagrilintide was engineered to solve that problem. Structural studies by Cao and colleagues at Monash University and Novo Nordisk, published in Nature Communications in April 2025, used cryo-electron microscopy to characterize how cagrilintide engages AMY1, AMY2, AMY3, and CTR receptors in active, Gs-coupled conformations. The peptide's lipid modification and an ionic lock create distinctive interaction patterns at the receptor interface that confer stability in solution and support once-weekly subcutaneous dosing. That single pharmacokinetic advance makes the clinical comparison with pramlintide stark: the same amylinergic mechanism, now accessible without the pre-meal injection burden.

What the Human Evidence Looks Like

Phase 2 monotherapy: the Lau 2021 Lancet trial

The pivotal Phase 2 monotherapy dataset comes from Lau and colleagues, published in The Lancet in December 2021. The trial was a 26-week, multicentre, randomized, double-blind, placebo-controlled and active-controlled dose-finding study enrolling 706 adults with overweight or obesity (without type 2 diabetes) across 57 sites in ten countries. Participants were randomized to one of seven once-weekly cagrilintide doses (0.3 mg to 4.5 mg), placebo, or an active comparator arm receiving liraglutide 3.0 mg (the approved daily GLP-1 dose for obesity). At the top dose of 4.5 mg, mean weight loss was 10.8% (approximately 11.5 kg) versus 3.0% for placebo and 9.0% for liraglutide 3.0 mg. A clear dose-response relationship was observed across all cagrilintide arms, with weight losses ranging from approximately 6.0% at the lowest dose to 10.8% at the highest. Gastrointestinal side effects (nausea, constipation) were the most common adverse events, affecting 41% to 63% of cagrilintide-treated participants depending on dose, versus 32% in the placebo group.

The Phase 1b combination signal: Enebo 2021

Before the Phase 2 monotherapy results were published, a critical proof-of-concept study by Enebo and colleagues appeared in The Lancet in May 2021, testing cagrilintide co-administered with semaglutide 2.4 mg over 20 weeks in 95 adults with overweight. The trial showed that adding cagrilintide to semaglutide 2.4 mg produced additive weight loss: approximately 15.7% at the 1.2 mg cagrilintide dose and 17.1% at 2.4 mg, compared to 9.8% with semaglutide alone. The safety profile was acceptable and did not reveal unexpected signals from the combination. This was the first human evidence that amylin receptor co-agonism and GLP-1 receptor agonism operate through sufficiently distinct pathways to produce additive rather than merely overlapping effects. That finding directly shaped the subsequent development trajectory toward CagriSema.

The Phase 2 combination data in type 2 diabetes: Frias 2023

A Phase 2 trial by Frias and colleagues, published in The Lancet in August 2023, enrolled 92 adults with type 2 diabetes across 17 U.S. sites over 32 weeks. Participants received once-weekly cagrilintide 2.4 mg plus semaglutide 2.4 mg (CagriSema), cagrilintide monotherapy, or semaglutide monotherapy. CagriSema produced approximately 15.6% mean body weight reduction versus 5.1% for semaglutide alone, along with superior HbA1c reductions. No level 2 or 3 hypoglycemia events occurred. The combination's advantage over either monotherapy arm, including the already-approved semaglutide dose, supported advancing to Phase 3.

Monotherapy ceiling: the honest framing

Cagrilintide's monotherapy results deserve honest contextualization within the current landscape. The approximately 10.8% weight loss achieved at 4.5 mg over 26 weeks is clinically meaningful, exceeding both placebo and liraglutide 3.0 mg in the same trial. It also exceeds pramlintide's historical ceiling. A 16-week Phase 2 dose-escalation RCT in obese adults without diabetes by Aronne and colleagues in the Journal of Clinical Endocrinology and Metabolism in 2007 showed progressive, dose-dependent weight loss with pramlintide, and a 12-month RCT by Smith and colleagues in Diabetes Care in 2008 demonstrated that pramlintide combined with lifestyle intervention produced approximately 6 to 7 kg placebo-corrected weight loss at one year in obese adults. A subsequent 2010 RCT by Aronne and colleagues in Obesity tested pramlintide alone or combined with sibutramine or phentermine and observed additive weight loss with combination therapy, foreshadowing the logic that would later drive the cagrilintide-plus-semaglutide development program. But approximately 10.8% falls short of the benchmarks set by the current GLP-1 and dual-incretin standards. The STEP 1 trial of semaglutide 2.4 mg, reported by Wilding and colleagues in NEJM in 2021, showed approximately 14.9% mean weight loss over 68 weeks. The SURMOUNT-1 trial of tirzepatide 15 mg, reported by Jastreboff and colleagues in NEJM in 2022, showed approximately 20.9% at 72 weeks. Against these benchmarks, cagrilintide as a monotherapy represents a meaningful but second-tier efficacy profile. The clinical excitement about cagrilintide is about the combination, not the monotherapy.

Regulatory and Legal Status

FDA status: investigational only

As of April 2026, cagrilintide is not FDA-approved for any indication. It is an investigational compound under clinical development by Novo Nordisk and has not been submitted to the FDA as a standalone new drug application. Cagrilintide has never been approved for compounding under Section 503A or 503B. It has not appeared on any FDA bulk drug substance list (Category 1 or 2) because it was never pursued as a compounded product. Cagrilintide is available only within the context of clinical trials and is not obtainable through licensed compounding pharmacies or by standard prescription. Cross-trial comparisons cited in this article reflect data from published trials using Novo Nordisk's investigational formulation and are not applicable to any compounded or commercially available product.

The development pivot toward CagriSema

Novo Nordisk has not announced plans to seek FDA approval for cagrilintide as a monotherapy. The regulatory pathway being pursued is for CagriSema, a fixed co-administration regimen of cagrilintide 2.4 mg and semaglutide 2.4 mg, both given as once-weekly subcutaneous injections. Phase 3 data from the REDEFINE program underpin that NDA pathway. The REDEFINE 1 trial, reported by Garvey and colleagues in the New England Journal of Medicine in 2025, enrolled 3,417 adults with obesity and no type 2 diabetes over 68 weeks and reported approximately 20.4% weight loss versus approximately 3.0% for placebo. The companion REDEFINE 2 trial in adults with overweight or obesity and type 2 diabetes, reported by Davies and colleagues in the same journal in 2025, enrolled 1,206 participants over 68 weeks and reported approximately 13.7% weight loss with improved glycemic endpoints. Within that regulatory frame, cagrilintide functions as the amylin component of a two-drug regimen, not as a standalone agent. Readers seeking a full treatment of CagriSema's Phase 3 data and NDA status should consult the CagriSema article; this article is scoped to cagrilintide as an amylin analog in isolation.

Cardiovascular-outcomes data for cagrilintide, whether as a monotherapy or as part of CagriSema, are not yet available. The benchmark for this class is the SELECT trial of semaglutide, reported by Lincoff and colleagues in the New England Journal of Medicine in 2023, which showed a reduction in major adverse cardiovascular events in overweight or obese adults without diabetes. That trial evaluated semaglutide, not cagrilintide, and no cardiovascular benefit should be inferred for the amylin component. The REDEFINE-3 cardiovascular outcomes trial for CagriSema is ongoing and will be the next major readout relevant to this question.

Where Novo's amylin-mechanism strategy is heading beyond CagriSema

Two papers published in The Lancet in June 2025 describe the next iteration of Novo Nordisk's amylin-mechanism program. A Phase 1 first-in-human trial of amycretin, reported by Gasiorek and colleagues, characterized safety, tolerability, and pharmacokinetics of this novel unimolecular GLP-1 and amylin receptor co-agonist. A Phase 1b/2a subcutaneous amycretin trial by Dahl and colleagues reported up to approximately 24% body weight reduction at the highest dose versus approximately 1% for placebo at week 36. Amycretin achieves the same GLP-1 plus amylin receptor co-agonism as CagriSema in a single molecule. This distinction matters for understanding cagrilintide's commercial trajectory: it is unlikely to be developed as a standalone product when the combination it anchors is being superseded by a single-molecule successor within the same company's pipeline.

What this means practically

Cagrilintide is not prescribable through any standard pharmacy or compounding pathway in the United States. Products sold online claiming to be cagrilintide are not the investigational compound used in Novo Nordisk's trials, carry no manufacturing oversight, and have not been evaluated for safety, identity, potency, or purity by any regulatory authority. The only legitimate access pathway is enrollment in a clinical trial. Any product marketed under this name through gray-market or research chemical vendors should not be presumed to be what it claims to be.

Comparators and Alternatives

Cagrilintide is one of several long-acting amylin analogs in active clinical development. A high-impact review by Walker, Aitken, and colleagues, published in Nature Reviews Endocrinology in 2025, situates cagrilintide within the broader amylin pipeline alongside eloralintide (Lilly) and petrelintide (Zealand Pharma), noting that emerging amylin-based therapeutics are now on the cusp of clinical availability. A 2025 systematic review of emerging obesity pharmacotherapies by Kokkorakis and colleagues in Pharmacological Reviews places cagrilintide, CagriSema, and related amylin agents within the broader competitive landscape and current regulatory framework.

Eloralintide (LY3841136) is Lilly's once-weekly AMY1R-selective amylin analog, meaning it preferentially activates amylin receptor 1 rather than the broader AMY/CTR profile that characterizes cagrilintide. Discovery and preclinical proof-of-concept data were published by Briere and colleagues in Molecular Metabolism in 2025, showing 12-fold selectivity for AMY1R over CTR and noting reduced taste aversion compared to cagrilintide in rodent models. Phase 2 results from a 48-week RCT enrolling 263 adults with obesity, reported by Billings and colleagues in The Lancet in November 2025, showed dose-dependent weight reductions ranging from approximately 9% to 20% depending on dose and escalation schedule. The highest dose arms of eloralintide's Phase 2 trial approximately double cagrilintide's monotherapy ceiling from the Lau 2021 data. Whether selective AMY1R agonism (eloralintide's approach) ultimately outperforms dual AMY/CTR co-agonism (cagrilintide's approach) in humans at equivalent doses remains an open question in the field, and one that will be answered by Phase 3 head-to-head data that does not yet exist.

Zealand Pharma's petrelintide is a third long-acting amylin analog advancing through preclinical and early clinical development. A 2025 medicinal-chemistry paper by Fischer Munch and colleagues in the Journal of Medicinal Chemistry described the design and preclinical profile of petrelintide as a selective amylin-receptor agonist, offering a further contrast to cagrilintide's dual AMY/CT pharmacology. Across these programs, the amylin-mechanism space is becoming more crowded, with selective and non-selective receptor strategies advancing in parallel.

Pramlintide (Symlin) is the only approved amylin-class therapy and the historical reference point for this mechanism. It was FDA-approved in 2005 as an adjunct to mealtime insulin in type 1 and type 2 diabetes, not as a standalone obesity therapy. It requires pre-meal injections three times daily. A review by Panou and colleagues in Expert Reviews in Clinical Pharmacology in 2024 frames cagrilintide as a direct pharmacological successor to pramlintide: the same amylin-mimetic mechanism, with the engineering advances that address pramlintide's primary clinical limitations of injection frequency and modest weight-loss ceiling. This comparison is for scientific context only. Pramlintide and cagrilintide have fundamentally different regulatory statuses and evidence bases, and their clinical indications do not overlap.

Safety: What Is and Is Not Known

Clinical safety data from Phase 2 trials

The most comprehensive available safety data for cagrilintide comes from the Lau 2021 Phase 2 monotherapy trial (N = 706, 26 weeks) and the Enebo 2021 Phase 1b combination trial (N = 95, 20 weeks). Gastrointestinal adverse events, primarily nausea and constipation, were the dominant adverse effects, occurring in 41% to 63% of cagrilintide participants versus 32% in the placebo group in the Lau trial. This profile is consistent with the known pharmacology of amylin receptor activation, which includes slowing of gastric emptying. Cardiac safety was specifically evaluated in a thorough QT study by Gabe and colleagues, published in Diabetes, Obesity and Metabolism in 2024, enrolling 105 healthy participants (53 receiving cagrilintide 4.5 mg, 52 receiving placebo). No clinically relevant QTcF prolongation occurred at any measured timepoint after the last dose. The absence of QTc signal at supratherapeutic exposure is a meaningful cardiac safety data point for an investigational compound in this phase of development.

Risks from unregulated sources

Because cagrilintide is not available through any licensed pharmacy or prescribing pathway, any product sold online or through research-chemical vendors as cagrilintide falls entirely outside regulatory oversight. Independent testing of research peptides sold through unregulated online vendors has documented contamination with incorrect compounds, inaccurate dosing, sterility failures, and misidentification. These are not theoretical risks. The peptide in Novo Nordisk's clinical trials is a precisely engineered, lipid-modified, stability-tested compound manufactured under cGMP conditions. No gray-market vendor can replicate that manufacturing process, and no purchaser can verify what they are receiving.

Who Should Not Use Cagrilintide

Based on cagrilintide's mechanisms and the adverse event profiles observed in clinical trials, the following groups face elevated risk. No prescribing pathway exists outside clinical trials, so these are not screening criteria for prescription decisions but rather risk signals relevant to understanding the compound's biology.

• Individuals with a personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia type 2 (MEN2): calcitonin receptor co-agonism shares a receptor target with GLP-1 class compounds, which carry a boxed warning for this population; the relevance of CTR co-agonism to thyroid C-cell risk in humans is not yet established for cagrilintide specifically, but the mechanistic overlap warrants disclosure
• Individuals with a history of pancreatitis: amylin analogs affect gastrointestinal motility and may be contraindicated if pancreatitis history is present, consistent with the precautionary approach applied across incretin-class compounds
• Pregnancy and breastfeeding: safety has not been established in human pregnancy; weight loss therapy is generally not indicated during pregnancy
• Individuals with severe gastroparesis: because cagrilintide's mechanism includes slowing gastric emptying, further impairment of gastric motility in pre-existing gastroparesis represents a theoretical risk
• Individuals with hypersensitivity to cagrilintide or any component of its formulation

This is not an exhaustive list. A licensed provider would evaluate individual risk factors before prescribing any investigational compound within the framework of a clinical trial.

Which Biomarkers Are Relevant if You Are Exploring Metabolic Health?

Understanding your metabolic baseline is a reasonable step regardless of which weight management approaches are accessible or under investigation. The markers below are directly relevant to the biology cagrilintide acts on, and each is measurable through standard bloodwork.

• HbA1c (glycated hemoglobin): Reflects average blood glucose over approximately 90 days. Relevant because amylin's primary metabolic roles include postprandial glucagon suppression and glucose excursion control; baseline HbA1c establishes where glycemic status stands independently of any intervention.
• Fasting insulin: A sensitive marker of insulin resistance that often rises before glucose or HbA1c move outside the reference range. Amylin is co-secreted with insulin; insulin levels help characterize beta-cell demand and insulin sensitivity at baseline. Superpower's guide to blood sugar stability and insulin sensitivity biomarkers covers how fasting insulin fits into the broader metabolic picture.
• Fasting glucose: The primary screening marker for impaired fasting glucose and type 2 diabetes. Provides the immediate glucose context that HbA1c alone does not capture.
• Fasting lipid panel (total cholesterol, LDL, HDL, triglycerides): Obesity-related metabolic dysfunction often manifests in the lipid panel before glycemic markers become abnormal. Triglycerides and HDL in particular reflect insulin sensitivity and are relevant to assessing the full metabolic picture for anyone considering weight management interventions.
• Body weight and waist circumference: These are the primary endpoints of every cagrilintide and CagriSema trial. Establishing a measured baseline provides an objective reference point against which any intervention, lifestyle or pharmacological, can be tracked. The Superpower body composition biomarker guide covers the full set of relevant body composition markers.
• hs-CRP (high-sensitivity C-reactive protein): Low-grade inflammation is closely linked to insulin resistance and visceral adiposity. Baseline hs-CRP is useful for understanding the inflammatory context of metabolic dysfunction.
• Leptin (if available): Leptin resistance is closely linked to amylin signaling in the hypothalamus. Evidence from rodent models and human studies suggests that amylin and leptin co-agonism may produce synergistic appetite-suppressing effects. Leptin levels, in context, can help characterize the degree of leptin resistance that may be present alongside obesity.

A broader guide to metabolic health and weight management biomarkers covers how these markers combine to characterize metabolic risk more comprehensively than any single value.

The Bottom Line

Cagrilintide represents a meaningful pharmacological advance over pramlintide: the same amylin-mimetic mechanism with once-weekly dosing, Phase 2 monotherapy weight loss of approximately 10.8% at 26 weeks, and the structural characterization now available from cryo-EM studies. The clinical picture is genuinely interesting. It is also incomplete. Cagrilintide monotherapy is not being filed for approval as a standalone agent. Its regulatory future is tied to the CagriSema combination, and even that combination faces a successor in Novo Nordisk's own pipeline in the form of amycretin. Understanding what cagrilintide is and how its mechanism compares to other amylin-class approaches requires separating the compound itself from the broader combination strategy it is embedded in. For anyone interested in the amylin pathway, the relevant questions to bring to a provider are metabolic: what does your own baseline look like across glucose, insulin, and body composition, and what does the weight management evidence base tell us about the full range of available and investigational approaches.

That principle, understand the underlying biology first, then evaluate the clinical options in context, is central to Superpower's approach to preventive health. The compounds will continue to evolve. The value of knowing what your biomarkers show will not.

IMPORTANT SAFETY INFORMATION

Cagrilintide is not FDA-approved for any indication and is not available through Superpower or through standard prescribing or compounding pathways. It is an investigational compound under clinical development by Novo Nordisk. Cagrilintide has not been reviewed by the FDA for inclusion on either the 503A Category 1 (permitted) or Category 2 (prohibited) bulk drug substance list because it has never been pursued as a compounded product; it is not eligible for compounding under Section 503A or 503B. Access is limited to clinical trial enrollment. Superpower is a technology platform that facilitates connections between patients and licensed healthcare providers; Superpower does not prescribe or dispense medications.

Cagrilintide has not completed the FDA approval process. Its safety and efficacy for any use have not been established through adequate and well-controlled clinical trials sufficient for FDA approval. Data cited in this article are from Phase 1 and Phase 2 investigational trials and do not constitute an FDA-reviewed safety or efficacy determination.

Contraindications (based on proposed mechanism and available trial data): personal or family history of medullary thyroid carcinoma or MEN2 (CTR co-agonism mechanistic concern); history of pancreatitis; severe gastroparesis; pregnancy and breastfeeding; hypersensitivity to cagrilintide or any formulation component.

Warnings: gastrointestinal adverse events (nausea, constipation) occurred in 41% to 63% of participants in Phase 2 trials; a 2024 thorough QT study found no clinically relevant QTcF prolongation at therapeutic or supratherapeutic doses; long-term safety data beyond 26 weeks for cagrilintide monotherapy are limited.

Common adverse events reported in the Lau 2021 Phase 2 trial: nausea, constipation, decreased appetite, injection site reactions.

Products sold online or through unregulated research-chemical vendors as cagrilintide are not the investigational compound used in Novo Nordisk's clinical trials, carry no manufacturing oversight, and have not been evaluated for identity, potency, purity, or sterility. These products should not be presumed to be what they claim to be.

This is not a complete summary of all risks associated with cagrilintide. For information about active clinical trials, see clinicaltrials.gov.

Additional Questions

What are the side effects of cagrilintide?

In the Lau 2021 Phase 2 trial (N = 706), the most common adverse events were gastrointestinal: nausea and constipation affected 41% to 63% of cagrilintide-treated participants depending on dose, versus 32% in the placebo group. A thorough QT cardiac safety study by Gabe and colleagues, published in 2024, enrolled 105 healthy participants and found no clinically relevant QTcF prolongation at any dose or timepoint. Long-term safety data beyond 26 weeks for cagrilintide monotherapy is limited.

How does cagrilintide compare to eloralintide?

Eloralintide is Lilly's once-weekly AMY1R-selective amylin analog, meaning it preferentially activates amylin receptor 1 over the calcitonin receptor. The 48-week Phase 2 trial reported by Billings and colleagues in The Lancet in 2025 showed dose-dependent weight reductions ranging from approximately 9% to 20% depending on dose, with the highest dose arms approaching roughly double cagrilintide's monotherapy figure. Whether selective AMY1R agonism (eloralintide) outperforms dual AMY/CTR co-agonism (cagrilintide) in Phase 3 human trials remains an open question; no head-to-head data exists. This comparison is for scientific context only; these compounds have different regulatory statuses and evidence bases.

Will cagrilintide become available through compounding pharmacies?

There is no current indication that this will occur. Cagrilintide has never been part of the FDA's compounding bulk drug substance framework (Category 1 or 2) and has not been the subject of any FDA petition or review for compounding eligibility. It is a patented investigational compound by Novo Nordisk. The realistic access pathway is either through CagriSema if and when that combination receives FDA approval, or through amycretin as Novo Nordisk's next-generation single-molecule successor to the same mechanism.