Best Liraglutide 5mg and 10mg Peptides GMP Factory



Other names:Victoza, Saxenda

Liraglutide was approved by the US Food and Drug Administration (FDA) in 2014 and the European Medicines Agency (EMA) in 2015. It is designed to treat type 2 diabetes and obesity. It belongs to the class of medications known as GLP-1 receptor agonists or incretin mimetics. These medications work by mimicking the activities of the glucagon-like peptide-1 (GLP-1) hormone, which is routinely produced in the body in response to food consumption. Liraglutide is available as an injection beneath the skin and is marketed under the brand names Victoza and Saxenda.

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Referenced Citations

[1]Marso SP, Daniels GH, Brown-Frandsen K, Kristensen P, Mann JF, Nauck MA, et al. (July 2016). “Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes”. The New England Journal of Medicine. 375 (4): 311–322.

[2]“Liraglutide injection”. DailyMed. U.S. National Library of Medicine. Retrieved 23 March 2019. 

[3] Nathan DM, Lachin JM, Balasubramanyam A, Burch HB, Buse JB, Butera NM, et al. (September 2022). “Glycemia Reduction in Type 2 Diabetes – Glycemic Outcomes”. The New England Journal of Medicine. 387 (12): 1063–1074.

[4]Egan AG, Blind E, Dunder K, de Graeff PA, Hummer BT, Bourcier T, Rosebraugh C (February 2014). “Pancreatic safety of incretin-based drugs–FDA and EMA assessment”. The New England Journal of Medicine. 370 (9): 794–797.

[5]Shyangdan D, Cummins E, Royle P, Waugh N (May 2011). “Liraglutide for the treatment of type 2 diabetes”. Health Technology Assessment. 15 (Suppl 1): 77–86.

[6]Beglinger C, Degen L (November 2006). “Gastrointestinal satiety signals in humans–physiologic roles for GLP-1 and PYY?”. Physiology & Behavior. 89 (4): 460–464.

[7]Singh S, Chang HY, Richards TM, Weiner JP, Clark JM, Segal JB (April 2013). “Glucagonlike peptide 1-based therapies and risk of hospitalization for acute pancreatitis in type 2 diabetes mellitus: a population-based matched case-control study”. JAMA Internal Medicine. 173 (7): 534–539.

[8]“Victoza- liraglutide injection”. DailyMed. U.S. National Library of Medicine. Retrieved 5 June 2021.

[9]“FDA approves weight-management drug Saxenda”. U.S. Food and Drug Administration (Press release). 23 December 2014. Archived from the original on 26 April 2016. Retrieved 26 April 2016.

[10]American Diabetes Association (January 2022). “Introduction: Standards of Medical Care in Diabetes-2022”. Diabetes Care. 45 (Suppl 1): S1–S2.

[11]“Public Citizen to FDA: Pull Diabetes Drug Victoza From Market Immediately”. Public Citizen. Retrieved 2 April 2013.

[12]Goldstein BJ, Mueller-Wieland D (14 November 2007). Type 2 Diabetes: Principles and Practice (2nd ed.). CRC PressISBN 978-0-8493-7958-1. Retrieved 17 January 2015.

[13]“Victoza (liraglutide)”. May 2008.

[14]“Drug Approval Package: Saxenda Injection (Liraglutide [rDNA origin])”. U.S. Food and Drug Administration (FDA). 1 October 2015. Retrieved 5 June 2021.

[15]Singh S, Chang HY, Richards TM, Weiner JP, Clark JM, Segal JB (April 2013). “Glucagonlike peptide 1-based therapies and risk of hospitalization for acute pancreatitis in type 2 diabetes mellitus: a population-based matched case-control study”. JAMA Internal Medicine. 173 (7): 534–539.

Liraglutide and Glucagon-Like Peptide-1 Overview

GLP-1, which stands for glucagon-like peptide-1, is a naturally occurring peptide hormone that is relatively short, consisting of 30-31 amino acids. Its primary physiological function is to regulate blood sugar levels by enhancing insulin secretion. Additionally, it plays a role in protecting beta cell insulin stores by promoting insulin gene transcription and has been associated with neurotrophic effects in the brain and central nervous system. In the gastrointestinal system, GLP-1 has been shown to effectively reduce appetite by delaying gastric emptying and slowing intestinal motility. Moreover, preliminary research suggests that GLP-1 has potential impacts on various organs such as the heart, adipose tissue, muscles, bones, liver, lungs, and kidneys. [1][4][2][3]

The primary emphasis of GLP-1 research has been on its role in diabetes treatment and prevention, as well as its ability to suppress appetite. Secondary research has explored the potential cardiovascular advantages of this peptide. In more recent years, there has been a growing interest in investigating the potential of GLP-1 to mitigate neurodegenerative diseases. Although this field of research is relatively new, it is rapidly expanding due to the discovery that GLP-1 can slow down or prevent the buildup of amyloid beta plaques, a hallmark of Alzheimer’s disease.

Liraglutide Structure

Liraglutide Molecule

Authoritative source:PubChem

Molecular Formula: C172H265N43051
Molecular Weight: 3751.24 g/mol
PubChem CID: 16134956
CAS Number: 204656-20-2
Synonyms: Liraglutide, Victoza, Saxenda, Liraglutidea, NN2211, Liragultidum

Liraglutide and GLP-1 Research

The Incretin Effect of GLP-1

According to Dr. Holst, the “incretin effect” is considered the most significant impact of GLP-1. Incretins are a group of metabolic hormones released by the GI tract, which contribute to a decrease in blood glucose levels. In rodent models, GLP-1 has been identified as one of the two key hormones (the other being GIP) that stimulate the incretin effect. While GIP circulates at approximately 10 times higher levels than GLP-1, evidence suggests that GLP-1 is the more potent molecule, especially when blood glucose levels are elevated.[3][4][5]

A GLP-1 receptor has been discovered on the surface of pancreatic beta cells, indicating that GLP-1 directly stimulates the release of insulin from the pancreas. When combined with sulfonylurea drugs, GLP-1 has been found to enhance insulin secretion to the extent that it can cause mild hypoglycemia in up to 40% of individuals. Increased insulin secretion is associated with various beneficial effects, such as elevated protein synthesis, reduced protein breakdown, and enhanced uptake of amino acids by skeletal muscle.

GLP-1 and Beta Cell Protection

Research conducted on animal models indicates that GLP-1 has the potential to stimulate the growth and replication of pancreatic beta cells. Additionally, it has been found to promote the differentiation of new beta cells from progenitor cells in the epithelium of the pancreatic duct. Furthermore, studies have demonstrated that GLP-1 can inhibit apoptosis (cell death) of beta cells. Collectively, these effects shift the balance between beta cell growth and death towards growth, suggesting that the peptide could be beneficial in diabetes treatment and in safeguarding the pancreas against factors that harm beta cells.

In a particularly compelling trial, it was demonstrated that GLP-1 can prevent the death of beta cells induced by elevated levels of inflammatory cytokines. Mouse models of type 1 diabetes have shown that GLP-1 protects islet cells from destruction and may serve as a valuable approach to preventing the onset of type 1 diabetes.

GLP-1 and Appetite

Research conducted in mouse models indicates that the administration of GLP-1 and its similar counterpart, GLP-1, directly into the brains of mice can decrease the urge to eat and suppress food intake. It appears that GLP-1 may enhance the sensation of satiety, leading to a feeling of fullness and indirectly reducing hunger. Recent clinical studies in mice have demonstrated that twice-daily administration of GLP-1 receptor agonists results in gradual and consistent weight loss. Over an extended period, this weight loss is associated with significant improvements in cardiovascular risk factors and a decrease in hemoglobin A1C levels. The latter serves as a proxy marker for the severity of diabetes and the effectiveness of blood sugar control achieved through treatment.

Potential Cardiovascular Benefits of GLP-1

It is now known that GLP-1 receptors are distributed throughout the heart and contribute to the improvement of cardiac function in specific conditions. They achieve this by increasing heart rate and reducing left ventricular end-diastolic pressure.[2][3] Although the reduction in left ventricular end-diastolic pressure may not appear significant, it is associated with the prevention of left ventricular hypertrophy, cardiac remodeling, and ultimately heart failure.

Recent evidence has suggested that GLP-1 could play a role in reducing the overall damage caused by a heart attack. It seems that the peptide enhances the uptake of glucose by cardiac muscles, thereby assisting ischemic heart muscle cells in receiving the necessary nutrition to sustain their function and avoid programmed cell death. Interestingly, the increase in glucose uptake in these cells appears to occur independently of insulin.

Large infusions of GLP-1 in dogs have demonstrated improved left ventricular (LV) performance and reduced systemic vascular resistance. The latter effect can contribute to the reduction of blood pressure and alleviate strain on the heart. Consequently, this can help mitigate the long-term consequences associated with high blood pressure, such as LV remodeling, vascular thickening, and heart failure. According to Dr. Holst, the administration of GLP-1 following cardiac injury has consistently resulted in increased myocardial performance in both experimental animal models and patients.

glp 1 diagram

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

Authoritative source:Diabetes Journal

GLP-1 and the Brain

There is evidence suggesting that GLP-1 can enhance learning abilities and provide neuroprotection against neurodegenerative diseases like Alzheimer’s. One study demonstrated that GLP-1 improved associative and spatial learning in mice, and even ameliorated learning deficits in mice with specific gene defects. Rats that overexpress the GLP-1 receptor in specific brain regions also exhibit significantly improved learning and memory compared to normal controls.

Further studies in mice have demonstrated that GLP-1 can provide neuroprotection against excitotoxic damage to neurons, effectively preventing glutamate-induced apoptosis in rat models of neurodegeneration. Moreover, GLP-1 has been found to promote neurite outgrowth in cultured cells. Researchers are optimistic that continued investigation into GLP-1 will uncover its potential in halting or even reversing certain neurodegenerative conditions.

Interestingly, in mouse models, both GLP-1 and its analogue exendin-4 have demonstrated the ability to reduce the levels of amyloid-beta in the brain, as well as the beta-amyloid precursor protein present in neurons. Amyloid beta is the primary component of the plaques observed in Alzheimer’s disease, which, although not confirmed as a direct cause, is associated with the severity of the condition. While it remains to be determined if preventing the accumulation of amyloid beta can effectively protect against the effects of Alzheimer’s disease, this research provides a promising lead in understanding how scientists may potentially intervene in the progression from mild cognitive impairment to full-blown Alzheimer’s disease.

GLP-1 demonstrates minimal to moderate side effects and has low oral bioavailability, but it exhibits excellent subcutaneous bioavailability in mice.[1][7][2] It is important to note that the dosage per kilogram in mice does not directly translate to humans. GLP-1 available for purchase at Peptide Sciences is restricted to educational and scientific research purposes only and should not be consumed by humans. It is advised to purchase GLP-1 only if you are a licensed researcher.

Referenced Citations

[1] “The Physiology of Glucagon-like Peptide 1 | Physiological Reviews.” [Online].

[2] “Combined treatment with lisofylline and exendin-4 reverses autoimmune diabetes. – PubMed – NCBI.” [Online].

[3] “The proglucagon-derived peptide, glucagon-like peptide-2, is a neurotransmitter involved in the regulation of food intake. – PubMed – NCBI.” [Online].

[4] “Interim analysis of the effects of exenatide treatment on A1C, weight and cardiovascular risk factors over 82 weeks in 314 overweight patients with… – PubMed – NCBI.” [Online].

[5] “Cardiac function in mice lacking the glucagon-like peptide-1 receptor. – PubMed – NCBI.” [Online].

[6] “Glucagon-like Peptide 1 Can Directly Protect the Heart Against Ischemia/Reperfusion Injury | Diabetes.” [Online].

[7] Front Endocrinol (Lausanne). 2019;10:260. Published 2019 Apr 26. doi:10.3389/fendo.2019.00260 

Author of this article:

Dr. Jean Zeng graduated from king’s college london Faculty of Life Sciences & Medicine. 

Scientific Journal paper Author:

1.Jeongmin Lee 

Division of Endocrinology and Metabolism, Department of Internal Medicine, Eunpyeong St. Mary’s Hospital, College of Medicine, The Catholic University of Korea,the Republic of Korea

2.Joana Nicolau

Endocrinology and Nutrition Department, Hospital Universitario Son Llàtzer, Health Research Institute of the Balearic Islands (IdISBa), Palma de Mallorca, Baleares, Spain

3.Gehad Sharaf

Pharmacist at Nasr Hospital Health Insurance, Helwan, Cairo, Egypt

4.Mi Kyoung Seo

Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea

5.Martina Yaneva MD

Department of Dermatology and Venereology, Acibadem City Clinic Tokuda Hospital, Sofia, Bulgaria

6.Seokjae Park

Department of Brain Sciences, Daegu Gyeongbuk Institute of Science and Technology, Daegu, Republic of Korea

Author of this article:

Dr. Jean Zeng graduated from king's college london Faculty of Life Sciences & Medicine.

Scientific Journal paper Author:

Stephen C. Bain
Diabetes Research Group, Swansea University Medical School, Swansea, SA2 8PP, UK
Department of Diabetes and Endocrinology, Singleton Hospital, Swansea Bay University Health Board, Swansea, SA2 8QA, UK

In no way does this doctor/scientist endorse or advocate the purchase, sale, or use of this product for any reason. has no affiliation or relationship, implied or otherwise, with this physician. The purpose of citing this doctor is to acknowledge, acknowledge and commend the exhaustive research and development work done by the scientists working on this peptide.