2,400+ researchers supplied
99+ COAs published
6-panel tested every lot
Processing within 1–3 business days
FREE SHIPFree U.S. shipping on orders over $150Free U.S. shipping on orders over $150
Free U.S. shipping on orders over $150Cagrilintide is a synthetic long-acting amylin analogue studied for its role in appetite regulation and metabolic coordination.
By enhancing amylin-mediated satiety signaling and slowing gastric emptying, it supports smaller meal size and smoother post-meal nutrient handling. Its complementary pathway has drawn interest alongside GLP-1 agonists for layered appetite and energy-balance signaling.
Cagrilintide is a 37-amino acid, long-acting synthetic analogue of amylin, a peptide hormone that is co-secreted with insulin by pancreatic β-cells and plays a key role in appetite regulation, gastric emptying, and post-meal metabolic signaling [1].
Endogenous amylin acts as a satiety signal, helping coordinate how the body interprets meal size and nutrient intake. Cagrilintide mimics these physiologic actions while exhibiting enhanced molecular stability and prolonged activity compared with endogenous amylin [2].
Cagrilintide’s association with weight regulation is rooted in its ability to amplify amylin-mediated satiety signaling, rather than by directly altering metabolic rate or energy expenditure.
A multicenter, randomized, double-blind phase 2 trial evaluated the dose response, safety, and tolerability of cagrilintide [3]. A total of 706 overweight or obese participants were randomized to once-weekly cagrilintide (0.3–4.5 mg), once-daily liraglutide 3.0 mg, or placebo for 26 weeks, followed by a 6-week off-treatment period.
Results showed that cagrilintide:
Cagrilintide was generally well tolerated, with the most common adverse events including nausea, constipation, and diarrhea, as well as injection-site reactions.
Cagrilintide leads to clinically meaningful, dose-dependent weight reduction with an acceptable safety profile.
Cagrilintide’s relevance to blood-sugar regulation is indirect and comes from its influence on meal timing, gastric emptying, and postprandial signaling.
A randomized phase 2 trial evaluated the efficacy and safety of combined semaglutide and cagrilintide (CagriSema) compared with either agent alone in adults with type 2 diabetes and overweight or obesity [4].
Ninety-two participants were treated for 32 weeks with once-weekly injections of CagriSema, semaglutide, or cagrilintide, escalated to a target dose of 2.4 mg. All participants were on metformin, with or without an SGLT2 inhibitor.
Results showed that CagriSema:
No severe hypoglycaemia or fatal adverse events were observed, indicating that combined amylin and GLP-1 receptor agonism offers additive benefits for weight loss and glycemic control.
Amylin receptors are highly expressed in brain regions involved in integrating sensory input, nutrient status, and fullness cues, particularly within the brainstem and hypothalamus [5].
By engaging these receptors in a sustained manner, cagrilintide reinforces the signals that indicate meal completion and energy sufficiency, affecting both meal size and eating frequency.
This can reduce reward-driven or habitual eating behaviors, especially those that occur independently of physiological hunger.
Because amylin influences gastric emptying and central appetite centers, some individuals on cagrilintide may experience nausea, early fullness, or reduced appetite, especially during initial exposure.
Observed effects are dose- and context-dependent, aligning with its role as a regulatory peptide rather than a forceful metabolic driver.
While GLP-1–based peptides primarily influence insulin and glucose secretion, amylin analogues like cagrilintide contribute distinct satiety and gastric-emptying signals.
Together, these pathways engage multiple, non-redundant nodes to influence appetite perception.
This layered signaling approach allows for enhanced appetite regulation without relying on a single pathway.
Like other peptides that influence gastrointestinal motility and appetite signaling, cagrilintide may not be appropriate in contexts where delayed gastric emptying or altered digestive rhythm could be problematic, like in patients with pre-existing gastroparesis or gastrectomies.
Cagrilintide should also be evaluated in the context of overall metabolic signaling balance, particularly when combined with other appetite-modulating compounds.
References
1 Edwards, B. J. and Morley, J. E. (1992) Amylin. Life Sci., Life Sci 51, 1899–1912
2 Cao, J., Belousoff, M. J., Johnson, R. M., Keov, P., Mariam, Z., Deganutti, G., et al. (2025) Structural and dynamic features of cagrilintide binding to calcitonin and amylin receptors. Nat. Commun., Springer Science and Business Media LLC 16, 3389
3 Lau, D. C. W., Erichsen, L., Francisco, A. M., Satylganova, A., le Roux, C. W., McGowan, B., et al. (2021) 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. Lancet, Elsevier BV 398, 2160–2172
4 Frias, J. P., Deenadayalan, S., Erichsen, L., Knop, F. K., Lingvay, I., Macura, S., et al. (2023) Efficacy and safety of co-administered once-weekly cagrilintide 2·4 mg with once-weekly semaglutide 2·4 mg in type 2 diabetes: a multicentre, randomised, double-blind, active-controlled, phase 2 trial. Lancet, Elsevier BV 402, 720–730
5 Fu, W., Patel, A., Kimura, R., Soudy, R. and Jhamandas, J. H. (2017) Amylin receptor: A potential therapeutic target for Alzheimer’s disease. Trends Mol. Med. 23, 709–720
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Cagrilintide is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
Orders are processed within 1–3 business days after payment confirmation. Orders placed after 3:00 PM Pacific time or on weekends and holidays will begin processing the next business day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
What Is Cardiogen Peptide? Cardiogen is a short tetrapeptide (H-Ala-Glu-Asp-Arg-OH, also abbreviated as ADER) derived from cardiac tissue and belongs to a class of peptides developed to support organ-specific regulation. Studied initially in Eastern Europe, Cardiogen is designed to interact with cardiomyocytes and the cardiac conduction system, where it may influence gene expression linked to cell survival, protein synthesis, and myocardial repair [1]. Its peptide sequence allows it to function as a signaling molecule, potentially modulating various cellular pathways involved in cardiac metabolism and structural integrity. As there is no clinical study on the Cardiogen peptide to date, it remains a research compound without approved therapeutic use. Cardiogen remains under investigation for its potential role in supporting heart cell homeostasis. Cardiogen Peptide Benefits Cell Protection and Apoptosis Regulation Cardiogen may support cardiomyocyte survival by maintaining structural and functional stability in cells exposed to stress. Although the precise molecular mechanisms remain under investigation, experimental reports suggest that Cardiogen may modulate pathways involved in apoptosis [2]. Rather than acting as a direct inhibitor, Cardiogen could influence cellular homeostasis, potentially helping reduce premature loss of cardiac cells. In a rat model of myocardial infarction (MI), administration of Cardiogen resulted in a three-fold reduction in mortality, reduced necrotic heart tissue, and preserved glycogen reserves [3]. These findings suggest that Cardiogen preserves and protects cardiac tissue by stabilizing mitochondrial integrity and modulating apoptosis. Cardiac Tissue Regeneration and Antifibrosis Cardiogen has been studied for its potential to stimulate cardiomyocyte proliferation and enhance reparative biosynthesis, including the upregulation of anti-apoptotic factors necessary for tissue recovery. An animal study extracted myocardial tissue explants from young (three-month-old) and aged (24-month-old) rats to evaluate the effect of Cardiogen and other amino acids on cell proliferation and apoptosis regulation [4]. After tissue exposure to 20 individual amino acids or to the synthetic tetrapeptide Cardiogen, all substances were tested at a concentration of 10⁻¹² M. Among the 20 amino acids tested, 7 stimulated cell proliferation in young rats, while only 2 amino acids had any proliferative effect in aged rats. However, Cardiogen demonstrated the strongest effect by: Significantly stimulating cardiomyocyte proliferation in both young and old rats Exceeding activity of any individual amino acid tested Significantly decreasing p53 expression This study demonstrates that Cardiogen exhibits pro-proliferative and anti-apoptotic effects in myocardial tissue from both young and aged rats at extremely low concentrations. One mechanism proposed for Cardiogen is its modulation of extracellular matrix (ECM) remodeling. Following cardiac injury, excessive deposition of collagen and matrix proteins can lead to fibrosis, reducing myocardial elasticity and impairing contractile function [5]. If Cardiogen can help regulate fibroblast activity by balancing collagen synthesis and degradation, this may help preserve normal heart function after cardiac injury. Anti-Cancer Benefits Beyond its relevance to cardiology research, Cardiogen has also been evaluated in experimental oncology for its potential effects on cell differentiation and gene regulation. A preclinical in vivo study evaluated the effect of Cardiogen peptide on tumor growth in 78 aged rats implanted with M-1 sarcoma, a fast-growing connective tissue tumor [2]. Rats were divided into five total groups: Group 1: Control (tumor only) Group 2: Cardiogen 0.5 μg (low dose), administered days 1–10 Group 3: Cardiogen 0.5 μg (low dose), administered days 12–21 Groups 4: Cardiogen 5 μg (high dose), administered days 1–10 Groups 5: Cardiogen 5 μg (high dose), administered days 12–21 Results showed: Significant inhibition of tumor growth with low-dose Cardiogen (0.5 μg), especially when administered early (days 1–10) (p < 0.05) Full tumor regression in 3 animals in the high-dose late administration group (Group 5) Increased apoptosis across all Cardiogen groups No significant effect on proliferation Cardiogen may help restore regulatory signals in dysplastic or malignant cells, potentially promoting a shift toward more normalized cellular behavior. Further research is needed to clarify the molecular mechanisms behind these observations. Energy Production and Storage Cardiogen’s structure suggests that it may help maintain metabolic stability in cardiac cells, particularly under conditions of stress or aging. Pro-proliferative effects may occur via DNA and RNA synthesis, a process essential for sustaining protein turnover and cellular maintenance. This activity may indirectly support mitochondrial function by promoting the renewal of metabolic enzymes and structural proteins required for cardiac energy metabolism. Although direct effects on ATP production have not been formally established, Cardiogen may contribute to overall energetic resilience in cardiomyocytes. Further research is needed to clarify whether Cardiogen directly influences mitochondrial activity, oxidative phosphorylation, or glycogen storage.
What is CJC 1295 without DAC? CJC-1295 without DAC (Drug Affinity Complex) is a synthetic peptide analogue of growth hormone–releasing hormone (GHRH) designed to enhance pulsatile growth hormone (GH) secretion [1]. CJC-1295 is a modified 30-amino-acid fragment of native GHRH that incorporates substitutions at positions 2, 8, 15, and 27, to increase stability. Because GH secretion is tightly rhythm-regulated, particularly during sleep, preserving this pulsatile pattern can support metabolic, muscular, and regenerative functions. CJC 1295 mechanism of actions and health benefits GH/IGF secretagogue Because GH secretion naturally occurs in rhythmic bursts, especially during deep sleep, CJC-1295 without DAC preserves this pattern rather than producing continuous elevation [2]. Once GH is released, it stimulates hepatic and peripheral production of insulin-like growth factor-1 (IGF-1). IGF-1 mediates many of GH’s downstream actions, including [3]: Muscle protein synthesis Connective tissue repair Metabolic regulation By amplifying both GH and IGF-1 signaling, CJC-1295 without DAC acts as a dual-phase secretagogue. Two randomized, double-blind, placebo-controlled dose ascending trials of healthy adults (over 28 and 49 days, respectively), characterized the profile of CJC-1295 [4]. In the first trial, participants received one of four ascending single subcutaneous doses of CJC-1295 or placebo. In the second trial, participants received two or three weekly or biweekly injections. Results showed that: A single-dose administration induced dose-dependent increases in mean plasma GH, ranging from 2 to 10-fold above baseline Mean plasma IGF-1 increased 1.5 to 3-fold after a single subcutaneous injection, lasting 9–11 days. With multiple dosing, IGF-1 remained consistently above baseline for up to 28 days No serious adverse events or trial withdrawal were reported across either study. Improved body composition CJC-1295 without DAC amplifies natural pulsatile GH release, creating a metabolic environment that supports gradual, physiologic recomposition. Key mechanisms underlying these effects include [5]: Increased Lipolysis Improved Lean Mass Retention Preservation of Metabolic Rate A GHRH gene–ablated (GHRHKO) mice was studied to determine whether CJC-1295 can normalize growth and body composition in the absence of endogenous GHRH [5]. Over 5 weeks, mice were split into the following treatment groups: CJC-1295 2 µg every 24 hours CJC-1295 2 µg every 48 hours CJC-1295 2 µg every 72 hours Placebo-treated GHRHKO mice (control) Heterozygous littermates (normal growth reference) Results showed that: Daily CJC-1295 (24h interval) fully normalized body weight and body length, matching heterozygous controls. 48h or 72h dosing significantly improved growth but did not fully normalize it. Femur and tibia lengths were normal with daily or 48h dosing. 72h dosing did not fully normalize skeletal measures. All regimens preserved normal relative lean mass and subcutaneous fat mass. Increased total pituitary RNA and elevated GH mRNA expression This study highlights the therapeutic potential of CJC-1295 in severe GHRH deficiency and underscores the importance of dosing frequency in achieving full physiologic restoration. Injury recovery CJC-1295 without DAC may support tissue repair and recovery from musculoskeletal injury through its influence on growth hormone–mediated regenerative pathways [6]. Because GH and IGF-1 play roles in: Collagen turnover Tendon integrity Cellular repair enhancing their natural pulsatile release can create a biochemical environment favorable for healing. Key mechanisms underlying these effects include: Enhanced collagen synthesis Improved soft-tissue repair Support for bone and cartilage health Reduced downtime after physical stress Currently, no robust studies exist that investigate these potential effects. Advantages and disadvantages of CJC 1295 without DAC CJC-1295 without DAC offers a distinct therapeutic profile shaped by its shorter half-life and physiologic mimicry of natural growth hormone secretion. Advantages Mimics Natural GH Physiology Because CJC-1295 without DAC delivers pulsatile GH stimulation, this can reduce the risk of GH receptor desensitization. Lower Risk of Side Effects Pulsatile secretagogues tend to cause fewer adverse effects such as: Fluid retention Numbness Insulin resistance The intermittent stimulation gives metabolic pathways time to normalize between pulses. Better Control Over Timing Users and clinicians can schedule injections around sleep cycles, fasting windows, or training sessions to optimize GH peaks. Disadvantages Requires More Frequent Injections Because the peptide is rapidly cleared, achieving meaningful GH pulses may require one to three injections daily. This can reduce convenience and adherence compared to once-weekly DAC formulations. Shorter Therapeutic Window Missed doses or inconsistent scheduling can significantly affect outcomes, as the peptide’s benefits depend on steady, rhythmic stimulation.
