Sema 2 mg

Buy Semaglutide 2mg from Adapt Peptides with confidence in our quality and reliability. Each vial of Sema 2mg for sale is verified through independent third-party testing to confirm identity, purity, and consistency, with typical purity levels exceeding 99%.

Manufactured to the highest research standards, our Semaglutide peptides are trusted by researchers who value accuracy and reproducibility. Adapt Peptides also provides fast U.S. shipping, secure packaging, and responsive customer support, ensuring your order arrives safely and on time.

What is Semaglutide?

Semaglutide is a synthetic peptide analog of the incretin hormone glucagon-like peptide-1 (GLP-1).

Incretins are gut-derived peptides released after food intake, particularly in response to glucose and dietary fats. Their primary function is to regulate glucose metabolism by stimulating insulin secretion when blood sugar is elevated, without causing excessive insulin release when levels are low.

Among incretin hormones, GLP-1 and GIP (glucose-dependent insulinotropic polypeptide) play the largest roles. GLP-1 activity includes:

• Enhancing insulin secretion in a glucose-dependent manner
• Suppressing glucagon release, which would otherwise raise blood sugar
• Slowing gastric emptying to better regulate digestion
• Promoting satiety, which can reduce food intake

Semaglutide in Research

In laboratory research, semaglutide is investigated for its ability to influence glucose homeostasis, appetite regulation, and energy balance.

Unlike native GLP-1, semaglutide has been structurally modified with amino acid substitutions and a fatty acid side chain, which promotes albumin binding. This significantly extends its half-life, improves stability, and enhances resistance to enzymatic breakdown in vitro and in vivo.

Thus, researchers value semaglutide because it offers:

• High stability under standard storage and handling conditions
• Strong GLP-1 receptor agonism, ensuring consistent receptor activation in models
• Extended activity compared to natural GLP-1, enabling long-duration experiments
• Reliable solubility in common research diluents for ease of use

These qualities make semaglutide a key peptide in studies related to obesity, diabetes, and metabolic research.

Important Notice: The peptide form of semaglutide is provided strictly for laboratory research use only. It is not approved by the FDA for human or veterinary use and must not be used for clinical or diagnostic purposes.

Semaglutide Mechanism of Action (Based on Research)

Semaglutide is a GLP-1 receptor agonist, meaning it binds to and activates the same receptor as the natural incretin hormone GLP-1.

Unlike endogenous GLP-1, which is rapidly degraded in the body, semaglutide has been structurally modified to resist enzymatic breakdown and remain active for longer durations.

In research, semaglutide both mimics and amplifies GLP-1’s physiological effects, making it highly relevant in studies exploring:

• Glucose regulation
• Appetite control and energy balance
• Obesity and metabolic disorders

Appetite Regulation

Semaglutide influences appetite control centers in the brain, particularly the hypothalamus, which plays a key role in regulating hunger and satiety[1]. It does this by slowing gastric emptying and enhancing signals of fullness, making it easier to feel satisfied with smaller portions.

In animal studies, this drug not only directly activates GLP-1 receptors in the hypothalamus and brainstem but also indirectly modulates neuronal circuits in other regions involved in eating behavior, such as the lateral parabrachial nucleus. By doing so, semaglutide reduces cravings, suppresses food intake, and supports weight loss without affecting energy expenditure[2].

In another study, chronic semaglutide treatment in rodent models produced sustained weight loss, primarily by shrinking meal size rather than reducing the number of meals. In two separate rat studies, semaglutide-treated rats consistently consumed less food and thus lost weight[3].

Notably, this suggests the drug enhances the mechanisms that signal fullness, rather than suppressing hunger. fMRI data also showed altered activation in brain regions tied to food reward and cravings (insula, putamen, orbitofrontal cortex).

Blood Sugar Modulation

Semaglutide stimulates insulin secretion in a glucose-dependent manner while suppressing glucagon release, contributing to improved postprandial glucose control[4].

Importantly, it does not typically drive insulin release under low-glucose conditions, reducing hypoglycemia risk in research settings.

Experimental data indicate semaglutide enhances peripheral glucose uptake, lowers hepatic glucose output, and slows gastric emptying. These mechanisms help stabilize fasting and post-meal glucose levels.

These properties make semaglutide a key research tool in models of insulin resistance, beta-cell function, and type 2 diabetes[5].

Hormonal Pathways

GLP-1 receptor activation affects gut-brain signaling by slowing gastric emptying and modulating nutrient absorption[6].

These actions influence gut-derived hormones that regulate insulin dynamics, satiety, and energy balance.

Emerging evidence suggests semaglutide may also interact with the hypothalamic-pituitary-adrenal (HPA) axis, potentially influencing cortisol regulation, stress-related feeding, and central energy-sensing pathways.

While still under investigation, these findings highlight semaglutide’s broader research potential beyond glycemic control alone.

Note: All findings described are from preclinical and non-clinical research. Semaglutide from Adapt Peptides is provided strictly for laboratory research use and is not FDA-approved for human or veterinary use.

Semaglutide Research Applications (Benefits)

Semaglutide has become a central focus of preclinical and non-clinical investigations due to its wide-ranging influence on metabolism, appetite, and endocrine pathways.

As a GLP-1 receptor agonist with structural modifications that enhance stability and bioavailability, semaglutide provides researchers with a consistent and versatile compound for controlled experimental settings.

Weight Management

A large body of research has examined semaglutide’s role in regulating body weight. In both animal models and human studies, the peptide has demonstrated an ability to lower food intake and reduce caloric consumption by acting on central satiety pathways and altering food-motivated behaviors[7].

One of the most notable investigations, the STEP 1 trial published in The New England Journal of Medicine, reported that participants receiving weekly semaglutide alongside lifestyle interventions experienced an average 14.9% decrease in body weight across 68 weeks[7][8].

This reduction was significantly greater than that seen in the placebo group. Importantly, the weight loss was attributed to enhanced satiety, fewer cravings, and reduced energy intake, which is consistent with earlier preclinical data.

Complementary evidence shows that semaglutide influences not only basic hunger circuits but also hedonic pathways linked to reward-based eating[9].

Imaging studies revealed diminished activation in brain regions such as the insula, putamen, and orbitofrontal cortex when exposed to high-calorie food cues, suggesting that semaglutide reshapes both physiological hunger responses and the motivational aspects of eating.

Taken together, these studies highlight semaglutide’s potential as a valuable research tool for exploring the neuroendocrine regulation of appetite and long-term body weight control.

Metabolic Studies

Semaglutide’s influence extends into glucose metabolism and insulin regulation, where it is frequently employed in research examining type 2 diabetes and metabolic dysfunction. Its mechanism of action includes stimulating insulin secretion in a glucose-dependent manner, suppressing glucagon release, and slowing gastric emptying—all of which contribute to improved glycemic profiles in experimental systems.

Investigators have reported significant improvements in postprandial glucose control, reductions in fasting glucose, and enhanced glucose disposal in peripheral tissues[10]. In controlled trials, subjects treated with semaglutide displayed lower glucose area under the curve (AUC) during standardized meal tests, pointing to coordinated effects on pancreatic, hepatic, and gastrointestinal functions.

These findings reinforce the peptide’s relevance for studies of insulin resistance, beta-cell dynamics, and the broader mechanisms underlying metabolic disease progression.

Hormonal Research

Beyond appetite and glucose regulation, semaglutide has attracted attention for its potential effects on wider endocrine systems. Preclinical models indicate that GLP-1 receptor activation can influence the gut-brain axis as well as the hypothalamic-pituitary-adrenal (HPA) axis, with possible implications for stress regulation and energy homeostasis[11].

Emerging studies also suggest that semaglutide may interact with thyroid hormone signaling. In rodent experiments, GLP-1 receptor activity within the hypothalamus was associated with changes in TSH (thyroid-stimulating hormone) secretion and downstream thyroid hormone regulation.

Although these findings remain early, they point to semaglutide’s expanding role as a research agent in neuroendocrine studies that go beyond traditional metabolic endpoints.

Remember: Semaglutide peptides are intended strictly for laboratory research use only. It is not approved for human or veterinary applications and must not be used for diagnostic or therapeutic purposes.

Semaglutide Peptide Characteristics

• • Molecular Formula: C₁₈₇H₂₉₁N₄₅O₅₉
  • Molar Mass: ~4113.58 g/mol
  • CAS Number: 910463-68-2
  • Amino Acid Sequence: HAEGTFTSDVSSYLEGQAAKEFIAWLVRGRG
    • Note: this sequence includes modifications that contribute to improved receptor affinity and metabolic stability
  • Synonyms: GLP-1(7-37) analog, NN9535

• Storage and Handling:

• • Long term storage: store semaglutide powder at –20 °C or below.
  • Store reconstituted solutions at 2–8 °C for 30–60 days.
  • Avoid repeated freeze–thaw cycles

Semaglutide vs. Tirzepatide vs. Retatrutide

Semaglutide Safety and Side Effects in Research

In controlled studies, semaglutide has generally been well-tolerated, though gastrointestinal events are among the most common findings. Nausea, vomiting, diarrhea, and constipation are frequently reported, especially during initial dose escalation phases.

These effects are often transient and may diminish with continued exposure.

More serious adverse events, though rare, have been noted in research. These include cases of pancreatitis and a potential association with thyroid C-cell tumors in rodent models. 

Please note that such risks have not been conclusively established in humans and appear consistent with other GLP-1 receptor agonists.

On the positive side, semaglutide has demonstrated cardiovascular benefits in large outcome trials, with evidence suggesting a reduction in the risk of major adverse cardiovascular events in participants with type 2 diabetes.

While these findings are significant, ongoing studies continue to investigate the underlying mechanisms. Note that any discussion of safety findings relates solely to published research. We only offer peptides for laboratory research use and sema is not approved for human or veterinary applications.

Certificate of Analysis (COA)

Every batch of semaglutide supplied by Adapt Peptides is subject to independent third-party analysis to confirm identity, purity, and consistency. A Certificate of Analysis (COA) is issued for each lot, with detailed results covering:

• Purity verification via high-performance liquid chromatography (HPLC)
• Mass spectrometry to confirm molecular weight and sequence integrity
• Microbial testing to rule out contamination

Researchers may download COAs on the product page or request one from our expert customer service team by referencing the batch number on your request order.

Legal Disclaimer

At Adapt Peptides, semaglutide peptide is offered exclusively for laboratory research purposes.

It is not approved for human consumption, diagnostic use, therapeutic application, or veterinary use.

Not for resale or use outside of controlled research settings.

Scientific References

1. Karlijn L. Kooij, Derek IJsbrand Koster, Emma Eeltink, Mieneke Luijendijk, Lisa Drost, Fabien Ducrocq, Roger A.H. Adan, GLP-1 receptor agonist semaglutide reduces appetite while increasing dopamine reward signaling, Neuroscience Applied, Volume 3, 2024, 103925, ISSN 2772-4085. https://www.sciencedirect.com/science/article/pii/S2772408523029071

2. Friedrichsen M, Breitschaft A, Tadayon S, Wizert A, Skovgaard D. The effect of semaglutide 2.4 mg once weekly on energy intake, appetite, control of eating, and gastric emptying in adults with obesity. Diabetes Obes Metab. 2021 Mar;23(3):754-762. https://pmc.ncbi.nlm.nih.gov/articles/PMC7898914/

3. Cawthon CR, Blonde GD, Nisi AV, Bloomston HM, Krubitski B, le Roux CW, Spector AC. Chronic Semaglutide Treatment in Rats Leads to Daily Excessive Concentration-Dependent Sucrose Intake. J Endocr Soc. 2023 Jun 7;7(7):bvad074. https://pmc.ncbi.nlm.nih.gov/articles/PMC10306276/

4. Hjerpsted JB, Flint A, Brooks A, Axelsen MB, Kvist T, Blundell J. Semaglutide improves postprandial glucose and lipid metabolism, and delays first-hour gastric emptying in subjects with obesity. Diabetes Obes Metab. 2018 Mar;20(3):610-619.

https://pmc.ncbi.nlm.nih.gov/articles/PMC5836914/ 

5. Eliaschewitz FG, Canani LH. Advances in GLP-1 treatment: focus on oral semaglutide. Diabetol Metab Syndr. 2021 Sep 15;13(1):99.

https://pmc.ncbi.nlm.nih.gov/articles/PMC8442336/ 

6. Cabou C, Burcelin R. GLP-1, the gut-brain, and brain-periphery axes. Rev Diabet Stud. 2011 Fall;8(3):418-31.

https://pmc.ncbi.nlm.nih.gov/articles/PMC3280675/                                                                                              

7. Fornes A, Huff J, Pritchard RI, Godfrey M. Once-Weekly Semaglutide for Weight Management: A Clinical Review. J Pharm Technol. 2022 Aug;38(4):239-246.

https://pmc.ncbi.nlm.nih.gov/articles/PMC9272494/ 

8. Wilding, J. P. H., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., McGowan, B. M., Rosenstock, J., Tran, M. T. D., Wadden, T. A., Wharton, S., Yokote, K., Zeuthen, N., & Kushner, R. F. (2021). Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine, 384(11), 989–1002. https://www.nejm.org/doi/full/10.1056/NEJMoa2032183

9. Matthew R Hayes, Heath D Schmidt, GLP-1 influences food and drug reward, Current Opinion in Behavioral Sciences, Volume 9, 2016, Pages 66-70, ISSN 2352-1546

https://www.sciencedirect.com/science/article/abs/pii/S2352154616300274 

10. Hjerpsted JB, Flint A, Brooks A, Axelsen MB, Kvist T, Blundell J. Semaglutide improves postprandial glucose and lipid metabolism, and delays first-hour gastric emptying in subjects with obesity. Diabetes Obes Metab. 2018 Mar;20(3):610-619. https://pubmed.ncbi.nlm.nih.gov/28941314/

11. Diz-Chaves Y, Herrera-Pérez S, González-Matías LC, Lamas JA, Mallo F. Glucagon-Like Peptide-1 (GLP-1) in the Integration of Neural and Endocrine Responses to Stress. Nutrients. 2020 Oct 28;12(11):3304.

https://pmc.ncbi.nlm.nih.gov/articles/PMC7692797/ 

12. Capuccio S, Scilletta S, La Rocca F, Miano N, Di Marco M, Bosco G, Di Giacomo Barbagallo F, Scicali R, Piro S, Di Pino A. Implications of GLP-1 Receptor Agonist on Thyroid Function: A Literature Review of Its Effects on Thyroid Volume, Risk of Cancer, Functionality and TSH Levels. Biomolecules. 2024 Jun 13;14(6):687.

https://pmc.ncbi.nlm.nih.gov/articles/PMC11202033/