Description

Introduction to GLP-1 (Research Use Only)

GLP-1 is a synthetic peptide analog belonging to the glucagon-like peptide-1 (GLP-1) family. It is designed to mimic the effects of endogenous GLP-1, a naturally occurring incretin hormone that helps regulate insulin secretion, glucose metabolism, and appetite control.

As a research compound, GLP-1 provides scientists with a valuable model for studying GLP-1 receptor activation, metabolic signaling pathways, and peptide pharmacokinetics. Structural modifications to GLP-1 —including amino acid substitutions and a fatty acid side chain—extend its half-life and stability, making it a focus of ongoing investigation into long-acting peptide analogs.

Molecular Structure

Sequence: HXEGTFTSDVSSYLEGQAAK-OH.steric diacid-EFIAWLVRGRG
Molecular Formula: C₁₈₇H₂₉₁N₄₅O₅₉
Molecular Weight: 4113.58 g/mol
PubChem CID: 56843331
CAS Number: 910463-68-2
Synonyms: NN9535; OG217SC; NNC 0113-0217; GLP-1 receptor agonist (GLP-1RA); long-acting GLP-1 analog

Source: PubChem

Note: The molecular information above is provided for educational and comparative purposes. GLP-1 is a receptor agonist used in laboratory research to better understand receptor pharmacology and metabolic signaling. It is not intended for human use.

Research Highlights

1. GLP-1 Receptor Pharmacology

GLP-1 binds to and activates the GLP-1 receptor (GLP-1R), a G-protein–coupled receptor found in pancreatic β-cells, the gastrointestinal tract, and the central nervous system. Activation enhances glucose-dependent insulin release, inhibits glucagon secretion, and slows gastric emptying—mechanisms widely studied in metabolic research.

2. Metabolic Signaling and Energy Regulation

In experimental models, GLP-1 has been shown to influence pathways such as AMP-activated protein kinase (AMPK) and PI3K/Akt, promoting improved glucose uptake, lipid oxidation, and reduced inflammation. These effects have made it a cornerstone for exploring how GLP-1 analogs impact cellular energy balance and systemic metabolism.

3. Central Nervous System and Appetite Control

GLP-1 receptors are expressed in the hypothalamus and brainstem, key centers for appetite and satiety. Studies indicate that GLP-1 modulates neuronal signaling related to hunger and reward, contributing to a deeper understanding of gut-brain axis communication in metabolic homeostasis.

4. Structural Modifications and Stability

GLP-1’s enhanced stability results from strategic amino-acid substitutions and the attachment of a C18 fatty diacid chain, which promotes reversible binding to serum albumin and protects against degradation by dipeptidyl peptidase-4 (DPP-4). These modifications extend its half-life to approximately one week—critical for studying long-acting peptide pharmacology.

5. Safety and Research Context

While GLP-1 has been widely studied in clinical and preclinical contexts, it remains a research-use-only compound in laboratory environments. Reported findings from experimental models include gastrointestinal effects, altered feeding behavior, and dose-dependent metabolic responses. Laboratory results should not be interpreted as clinical outcomes.

Supporting References (Contextual GLP-1 Literature)

(GLP-1 -specific publications are included below to illustrate GLP-1 receptor biology and analog design.)

1. Lau J, Bloch P, Schäffer L, Pettersson I, Spetzler J, Kofoed J, et al. Discovery of the once-weekly glucagon-like peptide-1 (GLP-1) analogue Semaglutide. J Med Chem. 2015;58(18):7370-7380. doi:10.1021/acs.jmedchem.5b00726

2. Jensen L, Kupcova V, Arold G, et al. Pharmacokinetics of Semaglutide following once-weekly subcutaneous administration in healthy subjects and those with type 2 diabetes. Diabetes Obes Metab. 2018;20(4):821-831. doi:10.1111/dom.13148

3. Wilding JPH, Batterham RL, Davies M, et al. Once-weekly Semaglutide in adults with overweight or obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183

4. Drucker DJ. Mechanisms of action and therapeutic application of glucagon-like peptide-1. Cell Metab. 2018;27(4):740-756. doi:10.1016/j.cmet.2018.03.001