Liraglutide (GLP-1) (3mg)


Liraglutide (GLP-1) peptides are Synthesized and Lyophilized in the USA.

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Quantity 5 - 910 +
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Price $42.75$40.50
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(Required for reconstitution)
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SKU: Liraglutide-GLP-1-3mg Category:


What is the Liraglutide (GLP-1) peptide?

Liraglutide (GLP-1) is a chemical peptide, otherwise known as Glucagon Like Peptide – 1. It is a peptide hormone that occurs naturally, containing roughly 30 -31 amino acids. It appears to function primarily in lowering blood glucose levels by naturally acting on beta cells of the Islet of Langerhans to produce insulin. Its apparent functions are not limited to blood glucose reduction, it may also act on the gastrointestinal system (GIT), cardiovascular system, and brain. It also has a potential function in fat tissues, muscle tissues, bone, liver, lungs, and kidneys.


Molecular Formula: C172H265N43O51

Molecular Weight: 3751.20 g/mol

PubChem: CID 16134956

Synonyms: GLP-1, proglucagon (72-108), Glucagon – peptide – 1, victoza, Liraglutida, Liraglutidum, NN2211

Reconstitution: Required


Liraglutide Peptide and Incretin
According to research by Dr. Holst on GLP-1, the most critical potential effect of the Liraglutide is the “Incretin Effect”.[1] The researcher explains that “The main actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions.” Incretin is a collection of hormones that function to decrease blood glucose levels. These hormones are the Glucose-dependent insulinotropic polypeptide (GIP) and the Glucagon-like peptide (GLP-1). According to this research, Liraglutide may be the most potent among the incretin hormones, particularly in conditions of severe hyperglycemia.[2] Traces of the Liraglutide have been reported to be found on the surface of the pancreatic beta cells (insulin producers). Thus, Liraglutide (GLP-1) may have the potential to directly accelerate insulin production from the pancreas. In cases where the Liraglutide was studied in combination with Sulfonylurea medicines, it appeared to accelerate insulin production to the extent where it can cause hypoglycemia, as seen in some subjects.[3] There are variations in other subjects. Increased insulin in the blood is associated with increased protein synthesis, increased uptake of amino acids by skeletal muscle, and the reduction in the breakdown of protein. Of course, all of these have significant effects on the human body.

Liraglutide Peptide and Appetite
Studies on mouse models administered the Liraglutide (GLP-1) peptide into the brains of the mice.[4] The peptide appeared to reduce the drive to eat, and enhance the feelings of satiety, thus, inhibiting hunger indirectly. The mouse models were administered with a significant Liraglutide twice daily. This administration appeared to cause gradual and linear weight loss. Administration of Liraglutide over a long period eventually appeared to exhibit a reduction in hemoglobin A1C levels, which is known to be a proxy marker for severe diabetes. Administration over a long period was reported to exhibit possible improvement in cardiovascular risk factors. A reduction in hemoglobin A1C levels, indicating severe diabetes, would be treated with quality control of the blood glucose level.

Liraglutide Peptide and the Brain
Studies have suggested that Liraglutide (GLP-1) peptides may improve learning and protect the brain neurons against neurodegenerative diseases such as Alzheimer’s disease.[5] Amyloid beta is the primary component found in Alzheimer’s disease. It is not known to be a causative agent yet, but it is associated with the severity of the disease. Researchers are still finding out if preventing the accumulation of amyloid-beta can protect hosts against Alzheimer’s.[6]

Liraglutide Peptide and the Cardiovascular System
Researchers have hypothesized that Liraglutide is distributed evenly across the heart, improving cardiac function by reducing the left ventricular end-diastolic pressure, and boosting the heart rate.[7] The researchers note that “The defective cardiovascular response to insulin was not attributable to a generalized defect in the stress response, because GLP-1R(-/-) mice responded appropriately to insulin with increased c-fos expression in the hypothalamus and increased circulating levels of glucagon and epinephrine.” Increased LV end-diastolic pressure is one of the causes of LV hypertrophy, cardiac remodeling, and eventual heart failure. Thus, Liraglutide may function to put all these to a halt. Researchers further suggest that Liraglutide may improve the uptake of glucose by cardiac muscles, thus helping heart muscles under the struggle of ischemia get the nutrition to aid their continuous function and avoid apoptosis. According to the research by Dr. Holst, the continuous administration of Liraglutude (GLP-1) following a cardiac injury may “constantly increase myocardial performance in both inpatients and experimental models.”

Liraglutide Peptide and Beta-Cell Protection
In this research, animal models were used.[8] Here, Liraglutide was reported to apparently accelerate the growth and proliferation of pancreatic beta cells. Also, Liraglutide (GLP-1) may increase the differentiation of new beta cells from beta-cell progenitors in the epithelium of the pancreatic duct. This potential effect elicited by the Liraglutide peptide has suggested it’s potential in future diabetes treatments. In one of the studies, Liraglutide appeared to halt the death of beta cells caused by increased levels of inflammatory cytokines. In another experimental mouse model, where the mice had type 1 diabetes, Liraglutide appeared to protect the cells of the Islets of Langerhans from death. This process could mean the prevention of the onset of type 1 diabetes.


The Liraglutide (GLP-1) peptide, a naturally occurring peptide, may hold a lot of significance in human health. Like every other hormone in the body, it appears to exhibit side effects if produced in excessive or deficient amounts. Liraglutide peptides in the commodity market is for educational purposes and for scientific research only, not for human consumption.


  1. Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007;87(4):1409-1439. doi:10.1152/physrev.00034.2006.
  2. Bose AK, Mocanu MM, Carr RD, Brand CL, Yellon DM. Glucagon-like peptide 1 can directly protect the heart against ischemia/reperfusion injury. Diabetes. 2005;54(1):146-151. doi:10.2337/diabetes.54.1.146
  3. Nikolaidis LA, Elahi D, Hentosz T, et al. Recombinant glucagon-like peptide-1 increases myocardial glucose uptake and improves left ventricular performance in conscious dogs with pacing-induced dilated cardiomyopathy. Circulation. 2004;110(8):955-961. doi:10.1161/01.CIR.0000139339.85840.DD
  4. Tang-Christensen M, Larsen PJ, Thulesen J, Rømer J, Vrang N. The proglucagon-derived peptide, glucagon-like peptide-2, is a neurotransmitter involved in the regulation of food intake. Nat Med. 2000;6(7):802-807. doi:10.1038/77535.
  5. During MJ, Cao L, Zuzga DS, et al. Glucagon-like peptide-1 receptor is involved in learning and neuroprotection. Nat Med. 2003;9(9):1173-1179. doi:10.1038/nm919.
  6. Perry T, Haughey NJ, Mattson MP, Egan JM, Greig NH. Protection and reversal of excitotoxic neuronal damage by glucagon-like peptide-1 and exendin-4. J Pharmacol Exp Ther. 2002;302(3):881-888. doi:10.1124/jpet.102.037481.
  7. Gros R, You X, Baggio LL, et al. Cardiac function in mice lacking the glucagon-like peptide-1 receptor. Endocrinology. 2003;144(6):2242-2252. doi:10.1210/en.2003-0007.
  8. Yang Z, Chen M, Carter JD, et al. Combined treatment with lisofylline and exendin-4 reverses autoimmune diabetes. Biochem Biophys Res Commun. 2006;344(3):1017-1022. doi:10.1016/j.bbrc.2006.03.177.
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