Cagrilintide in Canada: A Research Guide to the Long-Acting Amylin Analogue

Why cagrilintide deserves a dedicated research guide#

Cagrilintide Canada searches are rising because the peptide represents a genuine mechanistic departure from the GLP-1 receptor agonists that currently dominate weight-management research. Unlike Semaglutide, Tirzepatide, or Retatrutide, which act through incretin receptors, cagrilintide targets the amylin receptor axis—a separate hormonal system with distinct peripheral and central actions. For researchers designing comparative or combination studies, that mechanistic independence matters.

Northern Compound places cagrilintide in the weight-management archive because the dominant search intent is metabolic: researchers want to understand how this peptide influences appetite, energy balance, glucagon secretion, and body composition. But the responsible framing is broader. Amylin biology intersects with pancreatic islet physiology, gastric motility, central satiety neurocircuitry, and leptin signalling. A rigorous guide should explain the full mechanistic picture, the strength of the clinical evidence, the regulatory landscape, and the practical sourcing considerations that apply to a peptide with this specific research identity.

This article treats Cagrilintide as research-use-only material. It does not provide dosing instructions, injection guidance, obesity-treatment advice, or personal-use recommendations. The purpose is to map the evidence, clarify the mechanism, distinguish cagrilintide from GLP-1-based compounds, and set sourcing standards that match its actual clinical development history.

What cagrilintide is at the molecular level#

Cagrilintide is a synthetic, long-acting analogue of human amylin (islet amyloid polypeptide, IAPP). Its development code is AM833. The peptide was engineered by Novo Nordisk to overcome the two principal limitations of pramlintide (Symlin), the first amylin analogue approved by the FDA in 2005: a very short plasma half-life requiring two or three daily subcutaneous injections, and modest efficacy that limited its standalone use for obesity.

Structural modifications#

Human amylin is a 37-amino-acid peptide. Cagrilintide retains the core amylin sequence but incorporates three amino-acid substitutions and an N-terminal acylation:

• N14E (asparagine → glutamic acid at position 14)
• V17R (valine → arginine at position 17)
• P37Y (proline → tyrosine at position 37)
• N-terminal acylation with a C16 fatty-acid side chain (palmitoyl) via a γ-glutamyl linker

The acylation enables reversible albumin binding, which slows renal clearance and extends the half-life to approximately 7–9 days—sufficient for once-weekly dosing. The amino-acid substitutions increase solubility, reduce fibrillogenic aggregation propensity, and enhance receptor-binding affinity relative to native amylin. Amylin's well-known tendency to form toxic β-sheet fibrils is a major barrier to therapeutic development; cagrilintide's structural modifications were selected specifically to mitigate this biophysical liability.

Receptor pharmacology#

Cagrilintide is a non-selective agonist at amylin receptors (AMYRs) and calcitonin receptors (CTRs). Amylin receptors are heterodimers formed by the calcitonin receptor (CTR) and one of three receptor activity-modifying proteins (RAMP1, RAMP2, or RAMP3). The RAMP subunit determines ligand selectivity and signalling bias:

• AMY1 (CTR + RAMP1): abundant in the central nervous system, particularly the area postrema and hypothalamus
• AMY2 (CTR + RAMP2): expressed in pancreatic islets and gastrointestinal tract
• AMY3 (CTR + RAMP3): widely distributed in peripheral tissues including kidney, lung, and skeletal muscle

Cagrilintide activates all three receptor subtypes with high affinity. This broad receptor profile distinguishes it from more selective calcitonin receptor agonists or dual amylin/calcitonin receptor agonists (DACRAs) such as eloralintide, which are being developed by other companies. The non-selective profile may contribute to cagrilintide's robust efficacy but also to its side-effect profile, which overlaps with both amylin-like gastrointestinal symptoms and calcitonin-like effects.

Analytical identity#

For research-grade sourcing, the peptide should be verified as the exact 37-residue sequence with N-terminal palmitoyl-γ-glutamyl modification. The molecular weight is approximately 4,900 Da, though the exact mass depends on counter-ions and formulation. A rigorous certificate of analysis should include:

1. Batch-specific HPLC purity with peak integration, gradient method, and lot number. Reversed-phase chromatography with acidic mobile phase is standard for amylin analogues.
2. Mass spectrometry identity confirmation showing the expected molecular ion. ESI-MS is preferred; MALDI-TOF may struggle with the hydrophobic acylated peptide.
3. Sequence verification by tandem MS (MS/MS) or orthogonal methods, confirming the three substitutions and the N-terminal acylation.
4. Fill amount documentation stating net peptide content per vial, not merely total lyophilisate mass.
5. Endotoxin testing with a stated limit, typically < 5 EU/g or lower.
6. Sterility confirmation where claimed, with method and acceptance criteria.
7. Storage and stability guidance appropriate for an acylated peptide: lyophilised, protected from light, stored at -20 °C or below.

Researchers should not accept material labelled only "amylin analogue" without sequence specification. The amylin analogue class now includes pramlintide, cagrilintide, eloralintide, and multiple DACRAs in development. Cross-contamination or mislabelling between related sequences is a documented risk in unregulated supply chains.

Mechanism: amylin biology and the satiety axis#

Understanding cagrilintide requires understanding amylin physiology. Amylin is not a metabolic afterthought; it is a co-hormone secreted with insulin from pancreatic β-cells in response to nutrient intake. Its actions are complementary to insulin and, in the context of obesity research, potentially additive to GLP-1 receptor agonism.

Peripheral actions#

After a meal, amylin is released in a biphasic pattern that mirrors insulin secretion. Its peripheral effects include:

• Glucagon suppression: Amylin suppresses postprandial glucagon secretion from pancreatic α-cells, reducing hepatic glucose output. This effect is particularly important after meals, when excessive glucagon can cause postprandial hyperglycaemia even in insulin-treated patients.
• Gastric emptying delay: Amylin slows gastric motility and pyloric relaxation, increasing stomach distension and prolonging nutrient delivery to the small intestine. This mechanistic overlap with GLP-1 receptor agonists may explain why nausea and vomiting are common to both drug classes.
• Glycaemic stabilisation: By coordinating insulin-mediated glucose disposal with glucagon suppression and gastric emptying modulation, amylin contributes to postprandial glycaemic stability.

Central actions#

Amylin's most therapeutically relevant action for obesity research is central appetite suppression. The peptide crosses the blood–brain barrier poorly, but it does not need to. The area postrema (AP) and the adjacent nucleus tractus solitarius (NTS) in the brainstem lie outside the blood–brain barrier and are directly accessible to circulating peptides. Amylin binds to AMY1 receptors in the AP, activating satiety signals that project to the hypothalamus (particularly the lateral hypothalamic area and ventromedial nucleus) and to mesolimbic reward circuits.

The result is a reduction in meal size and, in chronic administration models, a sustained decrease in food intake. Unlike anorectic drugs that act through monoaminergic pathways (e.g., amphetamine-like compounds), amylin's appetite suppression is specific to meal termination rather than generalized arousal or aversion. In preclinical studies, amylin analogues reduce the size of individual meals without changing meal frequency—a pattern consistent with enhanced satiation rather than malaise.

Leptin synergy#

A critical feature of amylin biology is its interaction with leptin signalling. Leptin resistance is a hallmark of human obesity: despite high circulating leptin levels, the brain fails to respond with reduced appetite and increased energy expenditure. Amylin analogues appear to restore leptin sensitivity, at least in rodent models. Pramlintide plus metreleptin achieved 12.7% body-weight reduction versus 8.4% with pramlintide alone in a 24-week randomised trial. The mechanism is thought to involve amylin-mediated sensitisation of leptin-responsive neurons in the ventromedial hypothalamus.

Cagrilintide's long half-life makes it more suitable than pramlintide for chronic leptin-sensitisation studies. Whether this synergy translates into human research models is an active area of investigation.

Distinction from GLP-1 mechanism#

Both amylin and GLP-1 delay gastric emptying and suppress appetite, but their primary receptors, signalling pathways, and physiological contexts differ:

• Receptor: Amylin acts through CTR/RAMP heterodimers; GLP-1 acts through the GLP-1 receptor, a class B GPCR.
• Secretion: Amylin is co-secreted with insulin from β-cells; GLP-1 is secreted from intestinal L-cells in response to nutrient contact.
• Glucagon effect: Amylin suppresses glucagon directly; GLP-1 suppresses glucagon in a glucose-dependent manner.
• Gastric emptying: Both delay emptying, but through different enteric neuronal pathways.
• Cardiovascular: GLP-1 receptor agonists have well-documented cardiovascular outcome data; amylin analogues do not yet have comparable large-scale cardiovascular trial results.

For researchers comparing peptide approaches, these distinctions are more important than the surface similarity of "both cause weight loss." Cagrilintide is relevant for islet co-hormone biology, central satiety neurocircuitry, and gastric motility research. GLP-1 agonists are relevant for incretin physiology, gut–brain axis signalling, and cardiovascular metabolic outcomes.

Clinical evidence: from Phase 1 to REDEFINE 1#

The clinical development programme for cagrilintide is substantial and unusually well-documented in the peer-reviewed literature for an early-stage metabolic peptide. Researchers can draw on published Phase 1, Phase 2, and Phase 3a data, as well as ongoing Phase 3 trials in diabetes.

Phase 1: pharmacokinetics and tolerability#

The Phase 1 programme established cagrilintide's pharmacokinetic profile and safety in healthy volunteers and in people with overweight or obesity. Key findings include:

• Half-life: Approximately 7–9 days, supporting once-weekly dosing.
• Titration: A standard 4-week titration schedule (starting at a low dose and escalating to 2.4 mg) reduced gastrointestinal side effects.
• Immunogenicity: Low incidence of anti-drug antibodies, consistent with the structural similarity to human amylin.
• Gastrointestinal effects: Nausea, vomiting, diarrhoea, and constipation were the most common adverse events, occurring in a dose-dependent manner and generally resolving during continued treatment.

Phase 2: monotherapy and combination dose-ranging#

The Phase 2 programme included multiple randomised controlled trials evaluating cagrilintide monotherapy, cagrilintide dose-ranging, and the CagriSema combination.

Lau et al. (2021) randomised 302 adults with overweight or obesity to cagrilintide (0.3, 0.6, 1.2, 2.4, or 4.5 mg), liraglutide 3 mg, or placebo for 26 weeks. Key results:

• Cagrilintide 2.4 mg produced a 7.8% mean weight reduction versus 3.0% with placebo.
• Cagrilintide 4.5 mg produced a 9.7% mean weight reduction.
• Weight loss was dose-dependent across the range tested.
• Gastrointestinal adverse events were the primary dose-limiting factor.

Enebo et al. (2021) evaluated the CagriSema combination in a 20-week Phase 1b/2a trial. Participants received cagrilintide 2.4 mg plus semaglutide 2.4 mg, semaglutide 2.4 mg alone, or placebo. The combination produced greater weight loss than semaglutide alone, with a tolerability profile consistent with the individual components.

Frias et al. (2023) randomised 92 adults with type 2 diabetes and obesity to cagrilintide 2.4 mg, CagriSema 2.4/2.4 mg, semaglutide 2.4 mg, or placebo for 32 weeks. Results:

• CagriSema produced superior weight loss and HbA1c reduction versus both monotherapies.
• Cagrilintide monotherapy produced weight loss comparable to semaglutide monotherapy in this population.
• The combination's efficacy supported progression to Phase 3.

Meta-analysis of early-phase data#

A 2024 systematic review and meta-analysis (PMCID: PMC11642503) pooled three RCTs (n = 430) and provided the most rigorous quantitative summary of early-phase cagrilintide efficacy:

The meta-analysis also found that cagrilintide monotherapy had a significantly lower incidence of vomiting than semaglutide 2.4 mg or liraglutide 3 mg, despite comparable weight-loss efficacy. This differential side-effect profile is mechanistically interesting and may reflect amylin's distinct receptor distribution in the brainstem vomiting centre versus GLP-1 receptor expression in the same regions.

REDEFINE 1: the pivotal Phase 3a trial#

REDEFINE 1 (NCT05567796) is the largest and most definitive cagrilintide trial published to date. The results were published in the New England Journal of Medicine in August 2025.

Design:

• 68-week, multicentre, double-blind, placebo-controlled and active-controlled trial
• 3,417 adults without diabetes; BMI ≥30, or BMI ≥27 with at least one obesity-related complication
• Randomised 21:3:3:7 to CagriSema (n=2,108), semaglutide 2.4 mg (n=302), cagrilintide 2.4 mg (n=302), or placebo (n=705)
• All participants received lifestyle interventions

Primary endpoints:

1. Relative change in body weight from baseline to week 68
2. Achievement of ≥5% body-weight reduction (CagriSema vs. placebo)

Key results:

• CagriSema: −20.4% mean body-weight change
• Semaglutide: −14.2% mean body-weight change
• Cagrilintide: −11.5% mean body-weight change (estimated from supplementary data)
• Placebo: −3.0% mean body-weight change

The estimated treatment difference between CagriSema and placebo was −17.3 percentage points (95% CI, −18.1 to −16.6; P < 0.001). CagriSema also achieved significantly higher proportions of participants reaching ≥20%, ≥25%, and ≥30% weight-loss thresholds versus placebo (P < 0.001 for all).

Safety:

• Gastrointestinal adverse events affected 79.6% of the CagriSema group versus 39.9% of the placebo group.
• Events were primarily nausea, vomiting, diarrhoea, constipation, and abdominal pain.
• Most events were transient and mild-to-moderate in severity.
• Discontinuation rates due to adverse events were higher in the active-treatment arms than placebo but within the range expected for intensive incretin-based therapy.

Interpretation for researchers:

REDEFINE 1 establishes that amylin receptor agonism, when combined with GLP-1 receptor agonism, produces additive or synergistic weight loss that exceeds either mechanism alone. The magnitude of effect (20.4% mean weight loss) approaches the lower bound of metabolic surgery outcomes and sets a new efficacy benchmark for pharmacological obesity research. For Canadian labs studying peptide combinations, this trial provides the strongest evidence to date that mechanistically orthogonal pathways can be successfully integrated.

REIMAGINE programme: diabetes and insulin-treated populations#

While REDEFINE 1 studied adults without diabetes, the REIMAGINE programme evaluates CagriSema in type 2 diabetes across three trials:

• REIMAGINE 1: Drug-naïve T2D patients, including a 12-week treatment-free period at study end to assess diabetes remission criteria
• REIMAGINE 2: T2D on metformin ± SGLT2 inhibitor; CagriSema vs. components vs. placebo
• REIMAGINE 3: T2D on basal insulin ± metformin

Top-line results released in early 2026 indicated that CagriSema achieved superior HbA1c and weight reductions versus both monotherapies across all three populations. Detailed data are scheduled for presentation at the June 2026 ADA Scientific Sessions. REIMAGINE 3 is particularly notable because adding GLP-1 receptor agonists to basal insulin is already an established strategy; the combination with amylin agonism appears to produce stronger A1C reductions to below-target levels with very robust weight loss, addressing the long-standing challenge of insulin-associated weight gain.

Comparison with other weight-management peptides#

Cagrilintide occupies a unique position in the peptide weight-management landscape. The table below clarifies its research positioning relative to the major compounds already covered by Northern Compound.

For Canadian researchers, the choice between these peptides should be driven by the experimental question. Cagrilintide is the correct tool for amylin receptor pharmacology, islet co-hormone biology, and combination studies with GLP-1 agonists. It is not a substitute for GLP-1 receptor studies, mitochondrial metabolic studies, or adipose-specific lipolysis research.

Regulatory status and compliance framing#

As of April 2026, cagrilintide has no regulatory approval for human therapeutic use in any jurisdiction, including Canada, the United States, the European Union, or the United Kingdom. Novo Nordisk submitted CagriSema to the FDA for weight-loss indication in late 2025; a regulatory decision is pending. Health Canada has not issued a Notice of Compliance for cagrilintide or CagriSema.

Canadian regulatory context#

In Canada, cagrilintide is classified as a research chemical or investigational compound, depending on the specific formulation and intended use. It is not listed in the Health Canada Drug Product Database. Researchers importing cagrilintide for laboratory use should ensure that:

• The material is labelled clearly as research-use-only (RUO) or not for human consumption.
• The importation quantity and documentation are consistent with bona fide research purposes.
• The supplier provides batch documentation that supports identity and purity claims.

Health Canada and the Canada Border Services Agency have broad authority to detain or refuse shipments of unapproved pharmaceutical substances. Researchers should maintain records of intended experimental use, institutional affiliations, and ethical approvals where applicable.

WADA and anti-doping considerations#

Cagrilintide is not explicitly named on the 2026 WADA Prohibited List. However, as a peptide hormone analogue with metabolic and appetite-modulating activity, it would likely fall within Section S2 (Peptide hormones, growth factors, related substances, and mimetics), which prohibits all peptide hormones and their analogues at all times (in- and out-of-competition). Researchers working with athlete populations or sport-science models should treat cagrilintide as a prohibited substance for anti-doping purposes and should document its use accordingly in any research involving competitive athletes.

Practically, WADA's monitoring programme and the scientific literature review process may lead to explicit inclusion of cagrilintide in future list updates, particularly if CagriSema receives regulatory approval and becomes widely available.

Sourcing standards for Canadian researchers#

Cagrilintide is a complex peptide: 37 amino acids, acylated, prone to aggregation if improperly handled. The sourcing bar should be correspondingly high.

What a rigorous COA should include#

1. HPLC purity: ≥ 95% is the minimum acceptable standard for research-grade material; ≥ 98% is preferable for mechanistic studies where impurities could confound results. The chromatogram should show a single dominant peak with integrated area percentage.
2. Mass spectrometry: ESI-MS confirmation of the expected molecular weight. The acylated peptide may show adducts or multimers; the monoisotopic mass should match theoretical prediction.
3. Sequence confirmation: MS/MS fragmentation or Edman degradation confirming the full 37-residue sequence, including the N14E, V17R, and P37Y substitutions.
4. Acylation verification: Specific detection of the C16 palmitoyl-γ-glutamyl modification, either by MS shift or by orthogonal hydrolysis/derivatisation assay.
5. Net peptide content: Stated in milligrams per vial, distinct from total lyophilisate mass.
6. Endotoxin: < 5 EU/g, preferably < 0.5 EU/vial for cell-culture or in vivo work.
7. Sterility: Where claimed, documented by membrane filtration or comparable method.
8. Aggregation state: Optional but valuable: dynamic light scattering (DLS) or thioflavin T fluorescence to confirm the absence of amyloid fibril formation, given amylin's known fibrillogenicity.
9. Storage and handling: Clear guidance on reconstitution solvent (typically bacteriostatic water or sterile water for injection), recommended concentration, and stability at 2–8 °C post-reconstitution.

Supplier red flags#

• A product labelled only "amylin analogue" or "weight-loss peptide" without sequence specification.
• A COA that reports only total powder mass, not net peptide content.
• Absence of mass spectrometry, especially for an acylated peptide where identity verification is critical.
• Claims about therapeutic efficacy, regulatory approval, or human dosing on the product page.
• Pricing or packaging oriented toward consumer rather than laboratory use.
• Confusion with pramlintide, eloralintide, or unrelated metabolic peptides.

Lynx Labs lists Cagrilintide in the weight-management category and is the domestic supplier Northern Compound currently points readers toward for Canadian research-source evaluation. That recommendation is based on the same criteria applied elsewhere: batch documentation, domestic fulfilment, product-category clarity, and attribution-transparent outbound links. Researchers should still verify the current lot's COA before using any material in an experiment.

Designing better cagrilintide studies#

Because cagrilintide is still in Phase 3 development, there is no approved therapeutic indication to align with, and researchers have considerable latitude to explore mechanistic questions. A well-designed cagrilintide study should exploit the compound's specific pharmacological features.

Amylin receptor pharmacology studies#

The CTR/RAMP heterodimer system is understudied relative to other GPCR families. A strong cagrilintide study should measure:

• Receptor binding affinity (Ki) at AMY1, AMY2, and AMY3 receptors expressed in recombinant cell lines.
• cAMP accumulation and calcium mobilisation as proximal signalling readouts.
• Receptor internalisation and desensitisation kinetics after chronic exposure.
• Comparison with pramlintide and native amylin to quantify the effect of the acylated modifications.

Central satiety neurocircuitry studies#

Cagrilintide's appetite-suppressing effects are mediated through the area postrema and NTS. A neurobiological study should include:

• c-Fos immunohistochemistry in the AP, NTS, and downstream hypothalamic nuclei after acute and chronic dosing.
• Meal-pattern analysis (meal size, meal frequency, inter-meal interval) using automated feeding monitors.
• Comparison with GLP-1 receptor agonists to determine whether the two pathways produce additive or redundant satiety signals.
• Leptin-sensitisation endpoints: pSTAT3 signalling in the ventromedial hypothalamus, leptin receptor expression, and functional response to exogenous leptin challenge.

Gastric motility and gastrointestinal studies#

Because amylin and GLP-1 both delay gastric emptying, combination studies must disentangle additive from synergistic GI effects. Endpoints should include:

• Gastric emptying half-time (T½) measured by scintigraphy, acetaminophen absorption, or stable-isotope breath testing.
• Small-bowel transit time and colonic motility.
• Nausea and vomiting behavioural markers in appropriate animal models.
• Enteric neuronal activity, including vagal afferent firing rate.

Combination and synergy studies#

The REDEFINE 1 trial established clinical synergy between cagrilintide and semaglutide, but the molecular basis remains unclear. Preclinical combination studies should:

• Include single-agent arms for both cagrilintide and semaglutide at the doses used in combination.
• Measure body weight, food intake, glucose tolerance, and insulin sensitivity in parallel.
• Use isobolographic analysis or Bliss independence models to classify the interaction as additive, synergistic, or antagonistic.
• Examine receptor cross-talk: does chronic GLP-1 receptor activation alter amylin receptor expression, or vice versa?

Metabolic safety monitoring#

Any study involving a peptide that suppresses appetite, delays gastric emptying, and influences glucagon secretion should include comprehensive safety monitoring:

• Fasting and postprandial glucose, insulin, C-peptide, and glucagon.
• Lipid panels, liver enzymes, and renal function.
• Body composition (DEXA or NMR) to distinguish fat mass from lean mass changes.
• Bone turnover markers, because calcitonin receptor activation can influence osteoclast activity.
• Pancreatic enzyme levels and histology, given the peptide's pancreatic origin and the precedent of GLP-1-related pancreatitis concerns.

Common mistakes in cagrilintide interpretation#

The first mistake is conflating cagrilintide with GLP-1 receptor agonists because both produce weight loss and GI side effects. The receptor systems, physiological contexts, and clinical development paths are entirely distinct. A researcher who treats cagrilintide as "another semaglutide" will design studies that miss the amylin-specific biology.

The second mistake is assuming that CagriSema's 20.4% weight loss means cagrilintide is individually responsible for the additional 6–7% beyond semaglutide alone. The interaction may be synergistic rather than purely additive; the individual contribution of cagrilintide in the combination cannot be calculated by simple subtraction. Mechanistic studies are needed to determine whether the synergy occurs at the receptor level, the neuronal circuit level, or the behavioural level.

The third mistake is extrapolating from pramlintide's modest efficacy to cagrilintide's potential. Pramlintide's limitations—short half-life, multiple daily injections, and high nausea burden—are pharmacokinetic and formulation problems, not intrinsic limitations of amylin receptor agonism. Cagrilintide was engineered specifically to overcome these problems, and the clinical data show that it succeeds.

The fourth mistake is ignoring the calcitonin receptor component of cagrilintide's pharmacology. Because cagrilintide activates CTR as well as AMYR, it may produce calcitonin-like effects on bone metabolism, renal calcium handling, and vascular tone. Studies that measure only weight and glucose may miss important off-target biology.

The fifth mistake is using product-page copy or secondary blog sources as primary literature. The REDEFINE 1 trial, the Lau et al. Phase 2 trial, and the Frias et al. diabetes trial are all published in peer-reviewed journals. Researchers should read the original papers, examine the supplementary data, and monitor ClinicalTrials.gov for REIMAGINE updates rather than relying on supplier marketing materials.

The sixth mistake is accepting material labelled only "amylin analogue" without sequence confirmation. The amylin analogue class includes multiple distinct compounds, and mislabelling or cross-contamination is a known risk in non-pharmaceutical supply chains.

References and further reading#

• Garvey W.T. et al. "Coadministered Cagrilintide and Semaglutide in Adults with Overweight or Obesity." New England Journal of Medicine (2025). DOI: 10.1056/NEJMoa2502081.
• Lau D.C.W. et al. "Once-weekly cagrilintide for weight management in people with overweight and obesity: a multicentre, randomised, double-blind, placebo-controlled and active-controlled, dose-finding phase 2 trial." The Lancet (2021). DOI: 10.1016/S0140-6736(21)01751-7.
• Frias J.P. et al. "Cagrilintide and semaglutide in combination for the treatment of type 2 diabetes: a randomised, controlled, phase 2 trial." The Lancet (2023). DOI: 10.1016/S0140-6736(23)01308-2.
• Enebo L.B. et al. "Safety and efficacy of once-weekly cagrilintide in combination with once-weekly semaglutide in adults with overweight or obesity: a multicentre, randomised, double-blind, active-controlled and placebo-controlled, phase 1b/2a trial." The Lancet (2021). DOI: 10.1016/S0140-6736(21)02030-0.
• Chung C.W., Kim J. "Amylin Revisited: A 5-Year Perspective on Its Emerging Role in the Treatment of Diabesity." Journal of Obesity & Metabolic Syndrome (2026). DOI: 10.7570/jomes25085.
• "Efficacy and Safety of Cagrilintide Alone and in Combination with Semaglutide (Cagrisema) as Anti-Obesity Medications: A Systematic Review and Meta-Analysis." Indian Journal of Endocrinology and Metabolism (2024). PMCID: PMC11642503.
• ClinicalTrials.gov. "NCT05567796: A Research Study to See How Well Cagrilintide and Semaglutide Work Together in People With Overweight or Obesity." ClinicalTrials.gov.
• ClinicalTrials.gov. "NCT07220759: A Study to Evaluate the Effect of Cagrilintide in People With Overweight or Obesity and Type 2 Diabetes." ClinicalTrials.gov.
• World Anti-Doping Agency. 2026 Prohibited List. WADA.
• Health Canada. Drug Product Database. Health Canada.