Peptides >Liraglutide

Liraglutide (GLP-1 Analogue)

Liraglutide is derived from GLP-1, a natural peptide with known blood sugar-lowering and insulin secretion-enhancing properties. Studies indicate that Liraglutide, a GLP-1 analogue, could potentially enhance heart, liver, and lung functions, as well as mitigate the progression of Alzheimer’s disease. One of its notable effects is the substantial reduction of appetite by slowing gastric emptying and decreasing intestinal motility. Additionally, modifications to Liraglutide have extended its half-life and improved its pharmacokinetics.

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. Liraglutide and Glucagon-Like Peptide-1 Overview


2. Molecular Structure of Liraglutide


3. Research on Liraglutide & GLP-1

Liraglutide and Glucagon-Like Peptide-1 Overview

GLP-1 is a naturally occurring peptide hormone consisting of approximately 30-31 amino acids. Its primary function is to lower blood sugar levels by enhancing insulin secretion. Additionally, GLP-1 promotes insulin gene transcription, protects beta cell insulin stores, and has demonstrated neurotrophic effects in the brain and central nervous system. In the gastrointestinal system, GLP-1 reduces appetite by delaying gastric emptying and decreasing intestinal motility. Research has also highlighted its potential impact on the heart, fat, muscles, bones, liver, lungs, and kidneys.

Research on GLP-1 has primarily focused on its applications in diabetes treatment and appetite suppression. Secondary research has explored its potential cardiovascular benefits. More recent studies have delved into GLP-1’s potential in preventing neurodegenerative diseases, particularly Alzheimer’s disease, where it has shown promise in slowing or preventing the accumulation of amyloid beta plaques. 

Molecular Structure of Liraglutide

Molecular Formula: C172H265N43O51
Molecular Weight: 3751.24 g/mol
PubChem CID: 16134956
CAS Number: 204656-20-2
Synonyms: Liraglutide, Victoza, Saxenda, Liraglutidea, NN2211, Liraglultidum

Research on Liraglutide & GLP-1

The Incretin Effect of GLP-1

Dr. Holst emphasizes the pivotal role of GLP-1 in the “incretin effect,” a phenomenon driven by metabolic hormones released by the gastrointestinal tract. These hormones, known as incretins, work to lower blood glucose levels. In rodent models, GLP-1, alongside GIP, emerges as one of the key hormones responsible for stimulating the incretin effect, despite GIP circulating at levels approximately ten times higher than GLP-1. Notably, when blood glucose levels are elevated, GLP-1 exhibits greater potency.

Furthermore, researchers have identified a GLP-1 receptor on the surface of pancreatic beta cells, indicating that GLP-1 directly triggers insulin release from the pancreas. When combined with sulfonylurea drugs, GLP-1 demonstrates the ability to enhance insulin secretion, resulting in mild hypoglycemia in up to 40% of subjects. This increased insulin secretion carries several beneficial effects, including heightened protein synthesis, reduced protein breakdown, and greater amino acid uptake by skeletal muscles.

GLP-1 and Beta Cell Protection

Studies conducted in animal models suggest that GLP-1 fosters the growth and proliferation of pancreatic beta cells. Additionally, it appears to promote the differentiation of new beta cells from progenitors residing in the pancreatic duct epithelium. Notably, GLP-1 also inhibits beta cell apoptosis, tilting the balance between beta cell growth and death in favor of growth. These findings suggest the potential utility of GLP-1 in treating diabetes and safeguarding pancreatic beta cells from harm.

In a compelling trial, GLP-1 was found to counteract the death of beta cells induced by elevated levels of inflammatory cytokines. In mouse models of type 1 diabetes, GLP-1 protects islet cells from destruction, offering promise as a preventive measure against the onset of type 1 diabetes.

GLP-1 and Appetite

In mouse models, administering GLP-1, along with its close relative GLP-1, directly into the brains of mice has shown the ability to reduce the drive to eat and suppress food intake. This effect stems from GLP-1’s potential to enhance feelings of satiety, leading to a sense of fullness and a reduction in hunger. Recent clinical studies in mice have demonstrated that twice-daily administration of GLP-1 receptor agonists results in gradual, consistent weight loss. Over time, this weight loss correlates with significant improvements in cardiovascular risk factors and reduced hemoglobin A1C levels, indicating improved diabetes management.

Potential Cardiovascular Benefits of GLP-1

Research has unveiled the presence of GLP-1 receptors throughout the heart, enhancing cardiac function under specific circumstances by increasing heart rate and decreasing left ventricular end-diastolic pressure. This latter effect, although seemingly modest, plays a critical role in countering left ventricular hypertrophy, cardiac remodeling, and eventual heart failure.

Emerging evidence suggests that GLP-1 may contribute to limiting damage caused by heart attacks. GLP-1 appears to enhance glucose uptake in cardiac muscle cells, providing essential nutrition to ischemic heart muscle cells, which can stave off programmed cell death. Importantly, this increase in glucose uptake occurs independently of insulin.

Large infusions of GLP-1 in dogs have shown improvements in left ventricular performance and a reduction in systemic vascular resistance. This reduction in vascular resistance helps lower blood pressure, easing the strain on the heart. Consequently, this can mitigate the long-term consequences of high blood pressure, such as left ventricular remodeling, vascular thickening, and heart failure. Dr. Holst notes that administering GLP-1 following cardiac injury consistently enhances myocardial performance in both experimental animal models and patients.

GLP-1 and the Brain

Evidence suggests that GLP-1 may enhance learning and protect neurons against neurodegenerative diseases like Alzheimer’s. Studies have shown that GLP-1 can improve associative and spatial learning in mice, even mitigating learning deficits in mice with specific gene defects. In rats with overexpressed GLP-1 receptors in certain brain regions, both learning and memory significantly outperform normal controls.

Additionally, research in mice indicates that GLP-1 can protect against excitotoxic neuron damage, offering complete protection against glutamate-induced apoptosis in rat models of neurodegeneration. GLP-1 can also stimulate neurite outgrowth in cultured cells, raising hopes for its potential in halting or reversing neurodegenerative diseases.

Notably, GLP-1 and its analogue exendin-4 have demonstrated the ability to reduce amyloid-beta levels in the brain, as well as beta-amyloid precursor protein in neurons. These are key components of the plaques observed in Alzheimer’s disease, which, while not definitively causative, are associated with disease severity. While the prevention of amyloid-beta accumulation’s impact on Alzheimer’s disease remains to be determined, this research provides valuable insights into potential interventions for mild cognitive impairment progressing to full Alzheimer’s disease.

Please note that GLP-1 has minimal to moderate side effects, excellent subcutaneous bioavailability in mice, and dosage in mice does not scale to humans. It is available for research purposes only and not intended for human consumption.

Size of damage in heart in control mice (A), mice given standard vasopressin therapy (B), and mice give GLP-1 (C).

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.