Peptides > Semaglutide (GLP-1 Analogue)

Semaglutide (GLP-1 Analogue)

Semaglutide, derived from the naturally occurring GLP-1 peptide, has demonstrated the ability to lower blood sugar levels and boost insulin secretion. Beyond its glucose-regulating effects, research suggests that Semaglutide may have broader health benefits, including improvements in heart, liver, and lung function, and potential efficacy in slowing or preventing the onset of Alzheimer’s disease. One notable effect of Semaglutide is its significant reduction in appetite, achieved by delaying gastric emptying and reducing intestinal motility. This GLP-1 analog has also been shown to stimulate insulin production and inhibit glucagon secretion in a glucose-dependent manner.

This PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabled as a drug, food or cosmetic.


1. Semaglutide and GLP-1 Overview


2. Semaglutide Structure


3. Semaglutide and GLP-1 Research

Semaglutide and GLP-1 Overview

GLP-1, or glucagon-like peptide-1, is a concise peptide hormone composed of just 30-31 amino acids. Its primary physiological function revolves around the regulation of blood sugar levels by naturally enhancing insulin secretion. Moreover, it contributes to the protection of insulin stores in beta cells by promoting the transcription of insulin genes. Additionally, GLP-1 is associated with neurotrophic effects in the brain and central nervous system. In the gastrointestinal system, GLP-1 is known to have a significant appetite-reducing effect by slowing down gastric emptying and decreasing intestinal motility. Emerging research has also revealed potential impacts of GLP-1 in various organs, including the heart, fat tissue, muscles, bones, liver, lungs, and kidneys.

The predominant focus of GLP-1 research has been on its applications in the realm of diabetes treatment and prevention, as well as its ability to suppress appetite. Secondary areas of research explore the potential cardiovascular benefits of this peptide. More recent studies, though less extensive, have been concentrating on the potential of GLP-1 to mitigate neurodegenerative diseases. This particular area of research is gaining momentum, especially since GLP-1 has shown promise in slowing down or preventing the accumulation of amyloid beta plaques associated with Alzheimer’s disease.

Semaglutide Structure

Molecular Formula: C187H291N45O59
Molecular Weight: 4113.64 g/mol
PubChem CID: 56843331
CAS Number: 910463-68-2
Synonyms: Semaglutide, Oxempic, Rybelsus, NN9535

Semaglutide and GLP-1 Research

The Incretin Effect of GLP-1 One of the most significant effects of GLP-1, as highlighted by Dr. Holst, is its role in the “incretin effect.” Incretins are hormones released by the gastrointestinal (GI) tract that lower blood glucose levels. In rodent models, GLP-1 is one of the two key hormones (the other being GIP) responsible for stimulating the incretin effect. Despite GIP’s higher circulating levels, GLP-1 appears to be more potent, especially when blood glucose levels are elevated.

A GLP-1 receptor has been identified on pancreatic beta cells, indicating that GLP-1 directly triggers the release of insulin from the pancreas. When combined with sulfonylurea drugs, GLP-1 can enhance insulin secretion, leading to mild hypoglycemia in up to 40% of individuals. Increased insulin secretion has various positive effects, including promoting protein synthesis, reducing protein breakdown, and enhancing amino acid uptake by skeletal muscles.

GLP-1 and Beta Cell Protection Research conducted in animal models suggests that GLP-1 can stimulate the growth and proliferation of pancreatic beta cells. It may also encourage the differentiation of new beta cells from progenitor cells in the pancreatic duct epithelium. Additionally, GLP-1 has been shown to inhibit beta cell apoptosis. Cumulatively, these effects shift the balance of beta cell growth and death toward growth, suggesting that GLP-1 may have potential therapeutic value in treating diabetes and protecting the pancreas from damage that could harm beta cells.

In a notable trial, GLP-1 was found to prevent beta cell death caused by elevated levels of inflammatory cytokines. Mouse models of type 1 diabetes have also demonstrated that GLP-1 can safeguard islet cells from destruction and may serve as a preventive measure against the onset of type 1 diabetes.

GLP-1 and Appetite Studies conducted in mouse models indicate that administering GLP-1, along with its counterpart GLP-1, directly into the brains of mice can reduce the urge to eat and suppress food intake. It appears that GLP-1 may enhance feelings of fullness, indirectly reducing hunger. Recent clinical studies in mice have shown that twice-daily administration of GLP-1 receptor agonists leads to gradual and consistent weight loss. Over time, this weight loss is associated with significant improvements in cardiovascular risk factors and a reduction in hemoglobin A1C levels, which is a marker for diabetes severity and blood sugar control.

Potential Cardiovascular Benefits of GLP-1 GLP-1 receptors are distributed throughout the heart and can enhance cardiac function under specific conditions. They increase heart rate and reduce left ventricular end-diastolic pressure, which is significant in preventing left ventricular hypertrophy, cardiac remodeling, and eventual heart failure.

Recent evidence suggests that GLP-1 may help reduce damage caused by heart attacks. GLP-1 improves glucose uptake in cardiac muscle cells, aiding ischemic heart muscle cells in obtaining the nutrition they need to continue functioning and avoid programmed cell death. This increase in glucose uptake appears to be independent of insulin.

In dog studies, large infusions of GLP-1 have been shown to enhance left ventricular performance and decrease systemic vascular resistance. This reduction in blood pressure and relief on the heart can help mitigate the long-term consequences of high blood pressure, such as left ventricular remodeling, vascular thickening, and heart failure. According to Dr. Holst, administering GLP-1 following cardiac injury consistently improves myocardial performance in both experimental animal models and patients.

GLP-1 and Cognitive Function There is emerging evidence suggesting that GLP-1 may have a positive impact on learning and neuron protection, particularly in the context of neurodegenerative diseases like Alzheimer’s disease. In one study, GLP-1 was found to enhance associative and spatial learning in mice and even ameliorate learning deficits in mice with specific genetic abnormalities. Rats with an overexpression of the GLP-1 receptor in certain brain regions showed significantly improved learning and memory compared to normal controls.

Further research in mice has demonstrated that GLP-1 can protect against excitotoxic damage to neurons, effectively shielding rat models of neurodegeneration from apoptosis induced by glutamate. Moreover, GLP-1 can stimulate neurite outgrowth in cultured cells. Scientists are optimistic that continued research on GLP-1 may reveal its potential to slow down or reverse the progression of various neurodegenerative diseases.

Interestingly, in mouse models, both GLP-1 and its analog, exendin-4, have been shown to reduce levels of amyloid-beta and beta-amyloid precursor protein in the brain. Amyloid beta is the primary component of the plaques observed in Alzheimer’s disease, although it’s not yet confirmed whether preventing amyloid beta accumulation can effectively protect against Alzheimer’s disease. Nevertheless, this research provides intriguing insights into potential interventions for mitigating mild cognitive impairment’s progression to full-blown Alzheimer’s disease.

GLP-1 is associated with minimal to moderate side effects, excellent subcutaneous bioavailability in mice, and low oral bioavailability. It’s important to note that dosage per kilogram in mice does not directly correlate to human dosages. GLP-1 is available for research purposes only and should not be consumed by humans without the appropriate research licensing. If you wish to purchase GLP-1, ensure that you are a licensed researcher.


Article Author

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.


The product information featured on this website pertains exclusively to in-vitro studies. In-vitro studies, also known as ‘in glass’ studies, are conducted outside of living organisms. It’s important to emphasize that these products do not constitute medicines or drugs and have not received FDA approval for the prevention, treatment, or cure of any medical conditions, ailments, or diseases. It is crucial to note that the introduction of these products into the bodies of humans or animals is strictly prohibited by law.