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Weight Loss · Emerging Treatments
Cagrilintide: What It Is, How It Works, and Why It Could Change Weight Loss Medicine
Everything you need to know about the next generation of obesity treatment, and what happens when it is combined with a GLP-1.
Updated September 2026 · Medically reviewed · 12 min read
Important: This guide is for information only and does not replace medical advice. Cagrilintide and the combination drug CagriSema are investigational treatments under regulatory review. They are not approved for use in the UK, EU or USA at the time of publication. Always speak to a qualified healthcare professional before making decisions about weight loss treatment.
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Cagrilintide is not yet available anywhere. Two clinically proven weight loss injections are, through our regulated online clinic: Wegovy and Mounjaro. Both need a clinical assessment first. See our weight loss treatments
Cagrilintide is not yet available anywhere. Two clinically proven weight loss injections are, through our regulated online clinic: Wegovy and Mounjaro. Both need a clinical assessment first. See our weight loss treatments
What this guide covers
What is cagrilintide?
Cagrilintide is a long acting analogue of amylin, a hormone produced naturally by the pancreas. It was developed by the Danish pharmaceutical company Novo Nordisk. It is given once a week by injection under the skin, and its purpose is the treatment of obesity and overweight.
Unlike GLP-1 receptor agonists such as semaglutide (Wegovy) or tirzepatide (Mounjaro), which target hormones released from the gut, cagrilintide works through a completely different pathway. It mimics amylin, a hormone with a distinct but complementary role in appetite control and energy regulation. That difference is exactly why researchers became so interested in combining cagrilintide with GLP-1 therapy.
On its own, cagrilintide produced meaningful weight loss in Phase 2 trials. Its real promise emerged when it was paired with semaglutide, producing results neither drug could achieve alone. That combination, known as CagriSema, became one of the most closely watched developments in obesity medicine.
Key fact
Cagrilintide is not a GLP-1 agonist. It works on a different receptor system, the amylin receptor, so it addresses appetite and weight through a biological pathway that GLP-1 medicines do not directly target. That is the foundation of its complementary value.
Cagrilintide is not a GLP-1 agonist. It works on a different receptor system, the amylin receptor, so it addresses appetite and weight through a biological pathway that GLP-1 medicines do not directly target. That is the foundation of its complementary value.
The hormone behind it: what is amylin?
To understand cagrilintide, you first need to understand amylin, the hormone it is designed to mimic.
Amylin (also called islet amyloid polypeptide, or IAPP) is a 37 amino acid peptide hormone released by the beta cells of the pancreas alongside insulin, typically in response to meals. It was identified in the late 1980s and first attracted attention because deposits of it are found in the pancreases of people with type 2 diabetes. Over time, researchers came to understand that amylin has an important set of functions of its own in regulating metabolism and food intake.
Natural amylin acts across several key systems. It slows gastric emptying, the rate at which food leaves the stomach, which moderates the rise in blood glucose after a meal. It suppresses the release of glucagon, the hormone that tells the liver to release glucose into the bloodstream. And, critically for obesity research, it acts centrally: amylin binds to receptors in the area postrema and the brainstem, generating satiety signals that tell the brain the body has had enough to eat.
The problem with natural amylin as a medicine is its short half life. It breaks down rapidly in the bloodstream, which makes it impractical without significant modification. The existing amylin analogue pramlintide (sold as Symlin in the US for diabetes) needs several injections a day. Cagrilintide solves that. Through chemical modifications to the amylin molecule, Novo Nordisk’s scientists created a compound with a half life of around seven days, long enough for once weekly dosing.
Natural amylin
- 37 amino acid peptide hormone
- Released with insulin by pancreatic beta cells
- Half life: minutes
- Needs several injections a day if used as a medicine
- Reduced or absent in type 1 diabetes; impaired in type 2
Cagrilintide
- Long acting amylin analogue (engineered copy)
- Binds to amylin and calcitonin receptors
- Half life: about 7 days
- Once weekly injection under the skin
- Designed specifically for long term weight management
How cagrilintide works in the body
Cagrilintide works by binding to amylin receptors, specifically the calcitonin receptor combined with receptor activity modifying proteins (RAMP1 and RAMP3). These receptor complexes are found in several key locations, including the brain, stomach and kidney. Activating them produces a coordinated set of responses that together reduce body weight.
1
Appetite suppression via the brain
Cagrilintide acts on the area postrema and hypothalamus, key brain centres for hunger and fullness. By activating amylin receptors there, it creates a sustained feeling of fullness that reduces overall calorie intake, independently of GLP-1 signalling.
2
Slowing of gastric emptying
By slowing how quickly food moves from the stomach into the small intestine, cagrilintide extends the sense of fullness after meals and moderates how fast glucose enters the blood. That also reduces how much you eat at the next meal.
3
Glucagon suppression
Cagrilintide reduces glucagon release after meals. Glucagon normally tells the liver to release stored glucose, so suppressing it after eating helps prevent unnecessary rises in blood sugar. That is particularly useful in people with insulin resistance or type 2 diabetes.
4
Complementary action in the nervous system
Amylin receptor signalling in the brain uses different neural circuits from GLP-1 receptor signalling. Cagrilintide and GLP-1 agonists are not competing for the same mechanism. They engage the appetite system through separate, reinforcing pathways, which is the rationale for combining them.
One further point of interest: cagrilintide appears to produce a preferential loss of fat mass rather than lean mass, a finding seen in preclinical and clinical studies. Preserving muscle while losing fat is a major goal in obesity medicine, because losing muscle can worsen metabolic function and long term outcomes.
GLP-1 agonists: a quick recap
To appreciate why combining cagrilintide with a GLP-1 agonist matters, it helps to understand what GLP-1 drugs do, and what they do not do.
GLP-1 (glucagon like peptide 1) is an incretin hormone released by L cells in the gut wall in response to food. It plays a central role in the body’s response to a meal: it stimulates insulin release from the pancreas, suppresses glucagon, slows gastric emptying and sends fullness signals to the brain. GLP-1 receptor agonists such as semaglutide (the active ingredient in Ozempic and Wegovy) are synthetic molecules that mimic those actions with a much longer half life than the natural hormone.
In clinical trials, GLP-1 receptor agonists have produced substantial, clinically meaningful weight loss. In the STEP 1 trial, semaglutide 2.4mg produced an average body weight reduction of around 14.9% at 68 weeks in people with obesity. Those results beat virtually every previous drug approach to weight management.
Yet GLP-1 agonists have a ceiling. Not every patient reaches the weight loss they hoped for, and a meaningful proportion, even on maximum doses, do not reach the 15 to 20% body weight reduction that guidelines increasingly use as a benchmark for real metabolic benefit. There is also the question of what happens when GLP-1 therapy stops: weight tends to return, suggesting the underlying biology of obesity has not been fundamentally changed.
The GLP-1 ceiling problem
Even with the most effective GLP-1 therapies available, a significant proportion of patients do not reach clinically optimal weight loss. The appetite and energy systems that drive obesity are regulated by multiple overlapping hormonal pathways, and targeting just one has limits. That is the scientific case for combination therapy.
Even with the most effective GLP-1 therapies available, a significant proportion of patients do not reach clinically optimal weight loss. The appetite and energy systems that drive obesity are regulated by multiple overlapping hormonal pathways, and targeting just one has limits. That is the scientific case for combination therapy.
Already on a GLP-1 and not seeing the results you hoped for?
Dose, timing, side effects and the support around you all affect how well treatment works. Our prescribers can review where you are, whether a dose change or a switch between Wegovy and Mounjaro makes sense, and what monitoring you need. No pressure to change anything.
Dose, timing, side effects and the support around you all affect how well treatment works. Our prescribers can review where you are, whether a dose change or a switch between Wegovy and Mounjaro makes sense, and what monitoring you need. No pressure to change anything.
The combination: CagriSema explained
CagriSema is Novo Nordisk’s fixed dose combination of cagrilintide 2.4mg and semaglutide 2.4mg, delivered as a single once weekly injection under the skin. The case for combining them rests on the complementary biology described above.
Semaglutide acts mainly through GLP-1 receptors in the gut and brain. Cagrilintide acts through amylin receptors, which are anatomically and mechanistically separate. Together they engage two distinct hormonal systems that both regulate body weight, creating an additive and potentially synergistic effect on appetite and calorie intake.
Think of it this way. If GLP-1 therapy turns down one volume knob on the brain’s hunger signal, cagrilintide turns down a second, parallel knob. Neither alone can reduce the signal as much as both together. This is not duplication. It is complementary pharmacology acting on different receptors in different neural circuits.
Why combination therapy makes sense
Obesity is regulated by at least six distinct appetite controlling hormonal systems. GLP-1 therapies address one of them very well. Cagrilintide addresses a second, independent system. Targeting both at once has the potential to produce weight loss that neither drug could achieve alone, without simply doubling the side effects.
Beyond appetite, the combination offers metabolic breadth. Semaglutide improves insulin sensitivity and has shown cardiovascular benefit in people with type 2 diabetes. Cagrilintide adds glucagon suppression and its own favourable effects on glucose regulation. Together, CagriSema addresses obesity not just as body weight but as a wider disorder of metabolic function.
What the clinical evidence shows
Phase 2: cagrilintide alone
The Phase 2 trial of cagrilintide on its own was published in The Lancet in 2021. This randomised, double blind, placebo controlled trial enrolled 706 adults with overweight or obesity (BMI 27 or above) across several dose groups over 26 weeks.
Participants on the highest dose (4.5mg weekly) lost around 10.8% of body weight from baseline, against around 3% on placebo. Crucially, the weight loss had not plateaued at 26 weeks, suggesting longer treatment would produce further reductions. These results established cagrilintide as a meaningful agent in its own right and confirmed its mechanism was distinct enough from existing therapies to justify combination trials.
Phase 2 cagrilintide alone
~10.8%
body weight reduction at 26 weeks (4.5mg)
Phase 2 CagriSema combination
~15.6%
body weight reduction at 32 weeks
Phase 3 REDEFINE 1
~22.7%
body weight reduction at 68 weeks
Phase 2: the CagriSema combination
The Phase 2 CagriSema trial was published in The Lancet in 2023 and drew immediate attention. Adults with overweight or obesity were randomised to CagriSema, cagrilintide alone, semaglutide alone or placebo for 32 weeks.
The combination clearly beat both single agents. Participants on CagriSema lost around 15.6% of body weight from baseline, substantially more than semaglutide or cagrilintide alone. That was notable because semaglutide 2.4mg on its own is already one of the most effective weight loss drugs available. Adding cagrilintide and getting meaningfully more weight loss in just 32 weeks confirmed the additive effect of the dual mechanism.
The trial also showed dose dependent, sustained weight loss without any worrying extra adverse effects. The side effect profile was broadly what you would expect from each agent individually.
Phase 3: the REDEFINE trials
The Phase 3 programme for CagriSema runs under the name REDEFINE, a series of large randomised controlled trials designed to confirm efficacy and establish the safety profile needed for regulatory approval.
| Trial | Population | Duration | Primary endpoint |
|---|---|---|---|
| REDEFINE 1 | Adults with obesity (no diabetes) | 68 weeks | % body weight change from baseline |
| REDEFINE 2 | Adults with overweight or obesity and type 2 diabetes | 68 weeks | % body weight change plus HbA1c reduction |
| REDEFINE 3 | Adults with cardiovascular disease and overweight or obesity | Multi year outcome trial | Major adverse cardiovascular events |
REDEFINE Phase 3 programme overview. A fourth trial, REDEFINE 4, compared CagriSema directly with tirzepatide.
REDEFINE 1, the pivotal trial in adults with obesity without diabetes, reported results in early 2025. CagriSema 2.4/2.4mg produced a mean body weight reduction of around 22.7% at 68 weeks in participants who stayed on treatment, against around 2 to 3% with placebo. That is in the same territory as tirzepatide (Mounjaro), which showed around 20.9% at 72 weeks in SURMOUNT-1, and well above the roughly 14.9% achieved by semaglutide alone in STEP 1.
REDEFINE 1 also showed a significant proportion of participants losing 25% or more of their body weight, a level previously achievable only through bariatric surgery.
One caution for UK readers. In REDEFINE 4, the head to head trial against tirzepatide, tirzepatide produced slightly more weight loss than CagriSema. Mounjaro is already available in the UK. CagriSema is not.
Putting the numbers in context
A 22.7% mean weight reduction in a 100kg person is around 22.7kg. At that level, weight loss starts to produce meaningful improvements in joint health, sleep apnoea, blood pressure, blood glucose and cardiovascular risk, changes that can significantly alter someone’s long term health.
A 22.7% mean weight reduction in a 100kg person is around 22.7kg. At that level, weight loss starts to produce meaningful improvements in joint health, sleep apnoea, blood pressure, blood glucose and cardiovascular risk, changes that can significantly alter someone’s long term health.
You do not have to wait for CagriSema
Mounjaro delivered around 20.9% average weight loss in its pivotal trial and is available in the UK now, through GPhC registered pharmacies like ours, after a clinical assessment. Wegovy is available too. Find out whether either is right for you.
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Side effects and safety profile
CagriSema’s side effects largely reflect what is already known about its two components, with gut effects the most common. That fits the mechanism: slowing gastric emptying affects digestion, and central appetite suppression can cause nausea, particularly early on and during dose increases.
In REDEFINE 1, the most common adverse events were nausea, vomiting, diarrhoea and constipation. They were generally mild to moderate, most frequent during dose escalation, and became less common once participants settled on a maintenance dose. The rate of people stopping because of side effects was comparable to GLP-1 trials.
Injection site reactions occurred in a minority, as with other injectable weight loss medicines. No new or unexpected safety signals emerged in Phase 3 that had not already been seen in Phase 2.
| Side effect | Frequency | When most common | Management |
|---|---|---|---|
| Nausea | Very common | During dose escalation | Small meals, slow titration |
| Vomiting | Common | Early treatment | Dietary adjustments; usually settles |
| Diarrhoea | Common | Variable | Hydration; usually self limiting |
| Constipation | Common | Maintenance phase | More fluid and fibre |
| Injection site reaction | Uncommon | Any time | Rotate injection sites |
| Decreased appetite | Very common | Throughout treatment | Expected; this is the therapeutic effect |
Important safety note
Like GLP-1 receptor agonists, CagriSema is expected to be contraindicated in people with a personal or family history of medullary thyroid carcinoma (MTC) or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2), and should not be used in pregnancy. These are standard precautions for this class. Regulatory review will set the full list of contraindications and warnings before any authorisation.
Like GLP-1 receptor agonists, CagriSema is expected to be contraindicated in people with a personal or family history of medullary thyroid carcinoma (MTC) or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2), and should not be used in pregnancy. These are standard precautions for this class. Regulatory review will set the full list of contraindications and warnings before any authorisation.
Regulatory status and what comes next
At the time of publication, CagriSema has not been approved by any major regulator, including the MHRA (UK), EMA (Europe) or FDA (United States). It remains an investigational medicine. It is not available through any legitimate pharmacy, in the UK or anywhere else, outside a clinical trial.
Novo Nordisk submitted a New Drug Application to the FDA on 18 December 2025, based on REDEFINE 1, and the FDA is expected to review it during 2026. No submission to the MHRA or the EMA had been publicly confirmed at the time of our last check. The REDEFINE 3 cardiovascular outcomes trial will take several more years and is not a prerequisite for initial approval, but its results will matter for later label expansion, as they did for tirzepatide and semaglutide.
For the UK, that means a realistic private launch is not before 2027, and only if Novo Nordisk files with the MHRA and the review goes smoothly. NHS access would then depend on a separate NICE appraisal, the same route Wegovy and Mounjaro took, which historically has added a year or more.
Where things stand (September 2026)
Phase 3 results reported. FDA application filed December 2025 and under review. No UK or EU filing publicly confirmed. No approval anywhere. CagriSema is not legally available to buy. Any website or individual offering CagriSema or cagrilintide outside a clinical trial is acting unlawfully and putting patients at serious risk.
Phase 3 results reported. FDA application filed December 2025 and under review. No UK or EU filing publicly confirmed. No approval anywhere. CagriSema is not legally available to buy. Any website or individual offering CagriSema or cagrilintide outside a clinical trial is acting unlawfully and putting patients at serious risk.
For people managing obesity who are not yet on treatment, or who are on a GLP-1 and not getting the outcome they want, the right next step is a conversation with a qualified prescriber, not a wait for a drug that has no approval date. Wegovy and Mounjaro are approved, evidenced and available now through regulated channels.
Frequently asked questions
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ML
Medically reviewed by a UK Superintendent Pharmacist
Mohammed Ismail Lakhi MPharm, Superintendent Pharmacist at The Care Pharmacy
GPhC Registration Number: 2072815
All clinical content published by The Care Pharmacy is reviewed by a UK registered pharmacist for accuracy and alignment with current UK medical guidance. Last reviewed: 28 September 2026
Medical disclaimer: This article provides general information only and is not a substitute for personalised medical advice. Cagrilintide and CagriSema are investigational treatments that have not been approved in the UK, EU or USA. Nothing in this article is an endorsement or recommendation to seek out unapproved medicines. Always speak to your GP, pharmacist prescriber or clinician about weight loss treatment options. Report side effects from approved medicines through the Yellow Card Scheme.
Last updated: 28 September 2026. Information reflects data available at the time of publication. Spot an error? Contact us.
Sources
Lau DCW et al. (2021). Lancet. Phase 2 cagrilintide monotherapy trial (PMID 34480864) · Enebo LB et al. (2021). Lancet Diabetes Endocrinol · Frias JP et al. (2023). Phase 2 CagriSema combination, Lancet · Novo Nordisk REDEFINE 1 Phase 3 results (2025) · Novo Nordisk FDA submission announcement, 18 December 2025 · European Medicines Agency · MHRA
Medically reviewed by
Mohammed Lakhi
Superintendent Pharmacist
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