Cagrilintide vs Adipotide
Comprehensive side-by-side comparison of mechanisms, dosing, side effects, and research
Also: AM833, NN9838
Cagrilintide (also called AM833) is a long-acting synthetic analog of amylin, the gut-brain satiety hormone co-secreted with insulin by pancreatic beta cells. It is an investigational once-weekly injectable being developed by Novo Nordisk for obesity, most prominently as the amylin half of CagriSema (cagrilintide plus semaglutide). It is not yet approved as a standalone drug, but it has cleared phase 2 trials and is in late-stage development.
Also: FTPP, Fat-Targeted Proapoptotic Peptide
Adipotide is an experimental peptide built to kill fat tissue by cutting off its blood supply. One half homes in on prohibitin, a protein on the blood vessels that feed white fat, and the other half is a cell-killing sequence that triggers those vessel cells to self-destruct. It produced striking weight loss in obese mice and monkeys, but it also caused kidney damage in every primate species tested, and its only human trial was terminated after enrolling 4 people with no results ever posted.
Key Comparison Insights
- Both peptides belong to the Weight Loss category, suggesting similar primary applications.
- Cagrilintide has stronger research evidence (Human Trials) compared to Adipotide (Animal Studies).
Detailed Comparison
| Attribute | Cagrilintide | Adipotide |
|---|---|---|
| Category | Weight Loss | Weight Loss |
| FDA Status | Not FDA Approved | Not FDA Approved |
| Clinical Status | Pre I II III IV FDA | Pre I II III IV FDA |
| Mechanism of Action | Cagrilintide is a non-selective agonist of the amylin and calcitonin receptor family. It activates amylin receptors (which are calcitonin receptors paired with RAMP accessory proteins) to signal satiety in the brain, slow gastric emptying, and blunt the post-meal glucagon rise. Mechanistic work in mice shows it reduces body weight mainly through amylin receptors AMY1R and AMY3R acting in the hindbrain, with the area postrema as a key entry point and downstream signaling through the nucleus of the solitary tract and parabrachial nucleus. Notably, weight loss in those studies persisted even after the acute appetite-suppressing effect faded, hinting at effects on energy balance beyond simple food-intake reduction. Chemically it is built on a pramlintide-like 37-amino-acid backbone with substitutions and a fatty-diacid chain attached to extend its half-life to roughly a week, enabling once-weekly dosing. | The molecule has two parts joined together. The targeting part, CKGGRAKDC, was found by screening peptides in living mice for ones that stick to fat-tissue blood vessels; it binds prohibitin on the endothelial cells lining white fat vasculature. The payload, D(KLAKLAK)2, is a known pro-apoptotic peptide that disrupts mitochondrial membranes once inside a cell, setting off programmed cell death. Kill the vessels and the fat tissue they supply is starved and resorbed. This is a destructive mechanism, not a metabolic nudge like GLP-1 drugs, and that matters for safety: prohibitin is not exclusive to fat vessels, and the kidney's proximal tubule cells turned out to be a clear off-target casualty in monkeys. |
| Common Dosing | 2.4 mg weekly Once weekly | No established human dose Once daily in animal studies |
| Administration | Subcutaneous injection once weekly | Subcutaneous injection |
| Typical Duration | Long-term / chronic use expected | 28 days in the main monkey efficacy study; up to 63 days in dose-escalation |
| Best Time to Take | Any consistent time weekly | No evidence-based timing |
Possible Side Effects May vary by individual |
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| Research Summary | Cagrilintide has real human data, which sets it apart from most peptides in this category. In a 2021 Lancet phase 2 dose-finding trial (Lau et al.), once-weekly cagrilintide at 4.5 mg produced about 10.8% mean body weight loss over 26 weeks, beating both placebo (around 3%) and liraglutide 3.0 mg (around 9%), establishing that amylin agonism alone can drive clinically meaningful weight loss. Its bigger story is combination therapy: paired with semaglutide as CagriSema, it advanced into phase 3 REDEFINE trials for obesity and type 2 diabetes, with reported weight loss in the low 20% range, though final results came in somewhat below the most optimistic expectations. Side effects are dominated by the expected gastrointestinal effects (nausea, vomiting) common to gut-hormone drugs. As of 2026 cagrilintide is investigational and not FDA-approved on its own. The evidence is genuinely human and well-controlled here, which is rare, but it is still a drug under regulatory review rather than an approved therapy. | The concept came from Kolonin and colleagues (Nature Medicine, 2004), who reported that ablating fat vasculature reversed obesity in mice. The key primate study is Barnhart et al. (Science Translational Medicine, 2011) from MD Anderson. Obese rhesus monkeys given 0.43 mg/kg/day subcutaneously for 28 days lost 7.4% to 14.7% of body weight (average 10.6%) while controls stayed roughly flat, with MRI and DEXA confirming fat loss and clear improvements in insulin resistance. Lean monkeys at the same dose did not lose weight. The cost: serum creatinine rose in a dose-dependent way above 0.25 mg/kg, and the authors documented kidney tubule injury with glucose and protein in the urine, dehydration at higher doses, and low phosphorus and potassium. Most of it reversed within 28 days, but one treated monkey in each study still had residual changes. A first-in-human phase I trial at MD Anderson in obese men with metastatic prostate cancer (NCT01262664) started in 2012, enrolled only 4 patients, and was terminated at the investigator's request in 2019 with no results posted. That is the whole human record. Nobody knows the safe human dose, and the kidney signal is the opposite of reassuring. |
Frequently Asked Questions: Cagrilintide vs Adipotide
What is the difference between Cagrilintide and Adipotide?
Cagrilintide is a weight loss peptide that cagrilintide (also called am833) is a long-acting synthetic analog of amylin, the gut-brain satiety hormone co-secreted with insulin by pancreatic beta cells. it is an investigational once-weekly injectable being developed by novo nordisk for obesity, most prominently as the amylin half of cagrisema (cagrilintide plus semaglutide). it is not yet approved as a standalone drug, but it has cleared phase 2 trials and is in late-stage development. Adipotide is a weight loss peptide that adipotide is an experimental peptide built to kill fat tissue by cutting off its blood supply. one half homes in on prohibitin, a protein on the blood vessels that feed white fat, and the other half is a cell-killing sequence that triggers those vessel cells to self-destruct. it produced striking weight loss in obese mice and monkeys, but it also caused kidney damage in every primate species tested, and its only human trial was terminated after enrolling 4 people with no results ever posted. The main differences lie in their mechanisms of action and clinical applications.
Which is better, Cagrilintide or Adipotide?
Neither is universally "better" - the choice depends on your specific goals. Cagrilintide is typically used for weight loss purposes, while Adipotide is used for weight loss. Always consult with a healthcare provider to determine which may be appropriate for your situation.
Can Cagrilintide and Adipotide be used together?
Some peptide protocols combine multiple compounds for synergistic effects. However, using Cagrilintide and Adipotide together should only be considered under medical supervision, as both compounds have their own side effect profiles and potential interactions. Research on their combined use may be limited.