Cagrilintide (5mg)

What is Cagrilintide?

Cagrilintide is a synthetic research peptide designed to mimic and enhance the effects of amylin, a naturally occurring hormone involved in appetite regulation and energy balance. Structurally, it is an amylin analog modified for increased half-life, receptor activity, and stability in experimental models.

In research settings, Cagrilintide is studied for its potential to modulate satiety signals, slow gastric emptying, and influence weight-related metabolic pathways. Its enhanced formulation offers high water solubility and resistance to enzymatic degradation, making it well-suited for long-term and repeatable studies.

Note: Cagrilintide is for research use only. Not for human or veterinary consumption.

Cagrilintide Mechanism of Action (Based on Research)

Cagrilintide (AM833) is a synthetic, long‑acting analog of amylin, engineered to activate both amylin receptors (AMYRs) and to a lesser extent calcitonin receptors (CTR).

Activation of AMYRs and CTRs

Cagrilintide is a long-acting, synthetic analog of the human hormone amylin, which is co-secreted with insulin by pancreatic beta cells.

While native amylin plays a role in regulating appetite, slowing gastric emptying, and modulating glucagon release, it is rapidly degraded in the body. Cagrilintide was engineered for enhanced receptor selectivity and prolonged half-life, making it a promising compound in preclinical studies on appetite regulation and weight management.

It also engages calcitonin receptors, contributing to modulation of energy balance and potentially enhancing metabolic effects

Effects on Satiety and Appetite

Cagrilintide’s primary mechanism involves acting on key regions of the brainstem involved in energy balance and appetite control, specifically the area postrema and the nucleus tractus solitarius (NTS).

These centers are critical in processing satiety signals, and their activation is associated with reduced food intake and altered feeding behavior. Studies suggest that Cagrilintide not only diminishes hunger but also shifts food preference, indicating potential effects on both homeostatic and hedonic pathways of appetite control.

That’s because cagrilintide stimulates neurons in the area postrema (AP) and nucleus tractus solitarius (NTS), which are key brainstem sites involved in regulating fullness and eating behavior and leading to reduced food intake and shifts in food preference [1].

Cagrilintide also influences both homeostatic (hunger-signaling) and hedonic (reward-related) pathways, supporting changes in eating behavior and feeding motivation.

Gastric Emptying & Glucagon Modulation

In addition to suppressing appetite, Cagrilintide has been shown to delay gastric emptying, which prolongs the feeling of fullness after eating.

This effect is consistent with the actions of native amylin and is thought to contribute significantly to its weight-reducing potential. Moreover, Cagrilintide may also suppress postprandial glucagon secretion, thereby helping regulate blood glucose levels. It does this indirectly, through amylin receptor-mediated pathways, rather than by binding to glucagon receptors themselves [2].

Cagrilintide Research Applications

Cagrilintide is gaining attention in metabolic research for its promising effects on weight loss, appetite regulation, and glycemic control. By mimicking the hormone amylin, Cagrilintide enhances satiety, slows gastric emptying, and reduces food intake, making it a valuable candidate in the treatment of obesity and type 2 diabetes.

Weight Loss and Appetite Regulation in Pre‑clinical Models

In rodent studies, cagrilintide demonstrated robust appetite suppression and body weight reduction that significantly exceeded placebo. In diet‑induced obese rats receiving 10 nmol/kg/week, researchers observed a 20–25 % reduction in food intake and around 15 % weight loss over just four weeks.

One study reported an 18 % reduction in visceral fat and improved glucose tolerance in mice, where body weight declined by 12–15 % and AUC glucose responses improved by about 20 % over six weeks [3][4][5].

These preclinical findings highlight the strong metabolic effects of Cagrilintide in animal models, particularly its ability to reduce food intake, body weight, and visceral fat while enhancing glucose regulation.

Emerging Cardiometabolic and Other Research Directions

Although much of the current data focus on weight regulation and glycemic control, emerging avenues include potential effects on lipid metabolism, inflammatory markers, and cardiovascular risk parameters.

Pre‑clinical literature suggests amylin analogs like cagrilintide may modulate lipid profiles and inflammatory signaling, prompting interest in broader metabolic research applications [7].

There is also exploratory discussion around its possible relevance in neurodegenerative models, cachexia, and gastrointestinal motility disorders—though these areas remain at an early research phase.

Cagrilintide Peptide Characteristics

• • Molecular Formula: C₁₉₄H₃₁₂N₅₄O₅₉S₂
  • Molar Mass: ~4409.0 g/mol
  • CAS Number: 1415456‑99‑3
  • Amino Acid Sequence:
    • {Eicosanedioic‑acid‑γ‑Glu}‑Lys‑Cys‑Asn‑Thr‑Ala‑Thr‑Cys‑Ala‑Thr‑Gln‑Arg‑Leu‑Ala‑Glu‑Phe‑Leu‑Arg‑His‑Ser‑Ser‑Asn‑Asn‑Phe‑Gly‑Pro‑Ile‑Leu‑Pro‑Pro‑Thr‑Asn‑Val‑Gly‑Ser‑Asn‑Thr‑Pro‑NH₂ (with a disulfide bridge between Cys‑3 and Cys‑8)
  • Synonyms: Cagrilintide, AM833, AT42613, GLXC‑26801, NN9838
  • Solubility: Water-soluble; solubility can be enhanced via mild heating (37 °C) or ultrasonic bath to aid dissolution in aqueous buffers

• Storage Recommendations:

• • Lyophilized Powder: Stored at –4 °F (–20 °C) or lower, protected from light and moisture.
  • Reconstituted Solution: Use promptly or store at 35–46 °F (2–8 °C) for up to 1 week. 
  • For long-term use, aliquot and freeze at –112 °F (–80 °C) to minimize freeze-thaw cycles.

Cagrilintide Safety and Side Effects in Studies

In both preclinical animal models and early human trials, cagrilintide has demonstrated a generally favorable tolerability profile at research doses.

Legal Disclaimer

This product is intended for laboratory research purposes only and is not approved for human or veterinary use. It is not for resale, diagnostic, or therapeutic applications.

Evolve Peptides provides products strictly for research purposes; they are not intended for human consumption, medical, or therapeutic uses. None of the products should be mistaken for or substituted as prescription drugs.

The U.S. Food and Drug Administration has not evaluated any claims made on this site, and these products are not designed to diagnose, treat, cure, or prevent any disease.

By purchasing and using this product, the customer acknowledges responsibility for ensuring compliance with all applicable laws and regulations.

Certificate of Analysis (COA)

Each vial of Cagrilintide (and all peptides from Evolve Peptides) is linked to a specific batch’s Certificate of Analysis (COA) issued by independent third-party laboratories. These COAs confirm high purity (>99%) and verify product identity through rigorous testing methods such as HPLC and mass spectrometry.

A typical COA provides:

• Batch/Lot Information: Identifies the specific peptide lot you received
• Purity & Potency Results: Listing the percent purity confirmed via HPLC, as well as net peptide content versus impurities
• Contaminant Screen: Confirms absence of heavy metals, microbial contamination, and residual solvents
• Analytical Methods & Lab Accreditation: Specifies testing techniques used (e.g., HPLC‑UV, MS) and accreditation status of the testing lab

Evolve Peptides conveniently provides a download link or embedded PDF of the COA associated with each batch. This ensures full transparency and allows you to independently verify key quality metrics like purity, identity, and absence of contaminants.

Scientific References

1. Kruse, T., Hansen, J. L., Dahl, K., Schäffer, L., Sensfuss, U., Lau, D. C. W., Erichsen, L., Francisco, A. M., Satylganova, A., Le Roux, C. W., McGowan, B., Pedersen, S. D., Pietiläinen, K. H., Rubino, D., & Batterham, R. L. (2022). Development of cagrilintide, a long‑acting amylin analogue. Current Opinion in Endocrinology, Diabetes and Obesity, 29(2), 183–190. https://www.sciencedirect.com/org/science/article/pii/S1520480421005482 
2. Hankir, M. K., & Le Foll, C. (2025). Central nervous system pathways targeted by amylin in the regulation of food intake. Biochimie, 229, 95–104. https://www.sciencedirect.com/science/article/pii/S0300908424002384 
3. Çetin E, Pedersen B, Burak MF. Paradigm shift in obesity treatment: an extensive review of current pipeline agents. Turk J Med Sci. 2025 Jan 15;55(1):1-16. https://pmc.ncbi.nlm.nih.gov/articles/PMC11913498/
4. Muhammad T, Pastore SF, Good K, Yu WH, Vincent JB. The role of amylin, a gut-brain axis hormone, in metabolic and neurological disorders. FASEB Bioadv. 2025 Jan 20;7(3):e1480. . https://pmc.ncbi.nlm.nih.gov/articles/PMC11886606/