Glucagon (1-29) – Human, Porcine (CAS: 16941-32-5)


SB-PEPTIDE offers glucagon 1-29 peptide HSQGTFTSDYSKYLDSRRAQDFVQWLMNT for research on diabetes, obesity, and non-alcoholic fatty liver disease (NAFLD).


G-Protein Coupled Receptor


Glucagon operates through the GPCR signaling pathway, which plays a pivotal role in cellular communication. This type of receptors are known as seven-transmembrane domain receptors, which possess a unique structure that enables them to detect external molecules and activate cellular responses. Their vital association with G proteins fuels a cascade of events, initiating a cellular symphony, orchestrated by two principal signal transduction pathways: the cAMP signal pathway and the phosphatidylinositol signal pathway.

Glucagon class B GPCR receptor - Glucagon peptide CAS: 16941-32-5

Glucagon class B GPCR 3D structure


Glucagon receptor/class B GPCR


GPCR superfamily is organized into three main classes, among which the secretin receptor family (class B) regulated by glucagon peptides.

Glucagon receptor is a 62 kDa plasma membrane protein activated upon binding to glucagon. When HSQGTFTSDYSKYLDSRRAQDFVQWLMNT binds to its receptor, conformational changes occur, which leads to the activation of G proteins. This activation sets off a cascade of events, including adenylate cyclase activation and subsequent cyclic AMP (cAMP) production. The cellular response is further orchestrated by protein kinase A, initiating series of biochemical reactions.

Thanks to previous studies, it is known that glucagon receptors are predominantly present in the liver and kidneys, with varying expressions in other vital organs. Interestingly, the way glucagon works in diabetes, obesity, and NAFLD has led to new areas of investigation, suggesting its potential use as therapeutic target.


Glucagon(1-29) glucoregulatory peptide hormone


Thanks to its ability to stimulate hepatic glucose production, modulate energy balance, and potentially influence appetite regulation, glucagon 1-29 glucoregulatory peptide (CAS: 16941-32-5) represents a new powerful and versatile tool in driving scientific progress. It’s implication in various realms, ranging from the treatment of severe insulin-induced hypoglycemia to potentially addressing obesity and NAFLD, opens doors to innovative therapeutic avenues.

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For research use only


Technical specifications

 MAGE-A p248V9 (multi-MAGE-A)  peptide synthesis MW : 3482,75 g/mol (C153H225N43O49S)
 MAGE-A p248V9 (multi-MAGE-A) price Purity : > 95%
Peptide Library synthesis Counter-Ion : TFA Salts (see option TFA removal)
Peptide library synthesis MAGE-A p248V9 (multi-MAGE-A) Delivery format : Freeze dried in propylene 2mL microtubes
peptide solubility guidelines Peptide Solubility Guideline
buy peptide price Bulk peptide quantities available


Product catalog Size Price € HT Price $ USD
SB178-1MG 1 mg 110 138
SB178-5MG 5 mg 385 481
SB178-25MG 25 mg 1540 1925



Endocrine-related Cancer. 2023 Jul 28;30(9):e230046. doi:
One century ago, in 1922, Frederick G Banting, Charles H Best, James B Collip and John J R Macleod first published their experiments resulting in the isolation of a hypoglycemic factor, named insulin, from a solution extract from a dog’s pancreas. One year later, in 1923, a hyperglycemic factor named glucagon was isolated by Charles P Kimball and John R Murlin. In the following years, it could be demonstrated that pancreatic islet alpha- and beta-cell neoplasms and hyperplasias could inappropriately secrete excessive amounts of these two hormones. This review is a sequel to the discovery of insulin and glucagon and introduces the history of this fascinating group of neuroendocrine neoplasms and hyperplasias of the pancreas.
The Journal of Endocrinology. 2023 Jul 01;:JOE-23-0081. doi:

Metabolic regulation of glucagon secretion.

Since the discovery of glucagon 100 years ago, the hormone, and the pancreatic islet alpha cells that produce it, have remained enigmatic relative to insulin producing beta cells. Canonically, alpha cells have been described in the context of glucagon’s role on glucose metabolism in liver, with glucose as the primary nutrient signal regulating alpha cell function. However, current data reveal a more holistic model of metabolic signalling, involving glucagon-regulated metabolism of multiple nutrients by the liver and other tissues, with circulating nutrient availability, including amino acids and lipids, providing reciprocal feedback to regulate glucagon secretion and even alpha cell mass. Here we describe how various nutrients are sensed, transported, and metabolised in alpha cells, providing an integrative model for the metabolic regulation of glucagon secretion and action. Importantly, we discuss where these nutrient sensing pathways intersect to regulate alpha cell function and highlight key areas for future research.
Journal of Diabetes Investigation. 2023 Apr 13;14(7):829-837. doi:

Newly discovered knowledge pertaining to glucagon and its clinical applications.

Glucagon has been defined as an ‘insulin counteracting hormone’, which raises blood glucose levels. Recent progress in basic research has shown that glucagon is closely involved in glucose and amino acid metabolism. Additionally, its secretion is intricately, but precisely, regulated by various mechanisms involving molecules in addition to glucose, thus showing its critical role in systemic nutrient metabolism. An innovative dual-antibody-linked immunosorbent assay for glucagon that improves measurement accuracy has been developed, and substantial clinical findings have been obtained using this new system. This discovery expanded the pathophysiological significance of glucagon and accelerated the development of its clinical applications in diabetes.
Front. Endocrinol. Sec. Diabetes: Molecular Mechanisms. 2022 Jun 16;Volume 13. doi:

Role of Glucagon and Its Receptor in the Pathogenesis of Diabetes

Various theories for the hormonal basis of diabetes have been proposed and debated over the past few decades. Insulin insufficiency was previously regarded as the only hormone deficiency directly leading to metabolic disorders associated with diabetes. Although glucagon and its receptor are ignored in this framework, an increasing number of studies have shown that they play essential roles in the development and progression of diabetes. However, the molecular mechanisms underlying the effects of glucagon are still not clear. In this review, recent research on the mechanisms by which glucagon and its receptor contribute to the pathogenesis of diabetes as well as correlations between GCGR mutation rates in populations and the occurrence of diabetes are summarized. Furthermore, we summarize how recent research clearly establishes glucagon as a potential therapeutic target for diabetes.

Diabetes Care. 2012 Apr 19;35(6):1364-1379. doi:

Management of hyperglycemia in type 2 diabetes: a patient-centered approach: position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD).

Glycemic management in type 2 diabetes mellitus has become increasingly complex and, to some extent, controversial, with a widening array of pharmacological agents now available (15), mounting concerns about their potential adverse effects and new uncertainties regarding the benefits of intensive glycemic control on macrovascular complications (69). Many clinicians are therefore perplexed as to the optimal strategies for their patients. As a consequence, the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) convened a joint task force to examine the evidence and develop recommendations for antihyperglycemic therapy in nonpregnant adults with type 2 diabetes. Several guideline documents have been developed by members of these two organizations (10) and by other societies and federations (2,1115). However, an update was deemed necessary because of contemporary information on the benefits/risks of glycemic control, recent evidence concerning efficacy and safety of several new drug classes (16,17), the withdrawal/restriction of others, and increasing calls for a move toward more patient-centered care (18,19)…