Liraglutide is a palmitoylated 31-residue GLP-1 receptor agonist analog and the molecule that established the acylation strategy the entire incretin field now uses. It differs from native GLP-1 at a single amino acid position and carries a C16 palmitic acid chain, giving it a circulating persistence measured in hours rather than minutes — long enough to be useful, short enough to make it a genuinely different experimental tool from the multi-day analogs that followed. We supply research-grade liraglutide as lyophilized powder in sealed vials, for laboratory use only.
Human clinical data exist for the approved pharmaceutical products built on this molecule. They describe a regulated medicine, not the reference material on this page.
What is liraglutide, precisely
Liraglutide is the first-generation solution to the problem that makes native GLP-1 useless as a research tool: a plasma half-life of one to two minutes, driven by dipeptidyl peptidase-4 cleavage and rapid renal clearance. Its design keeps the GLP-1(7-37) sequence almost intact — only Lys34 is changed to arginine — and attaches a C16 palmitic acid to Lys26 through a glutamic acid spacer. The palmitate drives two effects at once: reversible albumin binding, which shields the peptide from clearance, and self-association into heptamers at the injection site and in solution, which slows release further.
Its near-identity to native GLP-1 is the reason liraglutide remains valuable. Where an experiment needs a GLP-1 receptor agonist whose sequence is as close to endogenous as practical stability allows, liraglutide is a closer match than semaglutide, which carries an additional non-proteinogenic Aib substitution and a longer diacid.
Origin and structure
- Backbone. GLP-1(7-37), 31 residues, with a single Lys34 to Arg substitution.
- Acylation. C16 palmitic acid on Lys26 via a gamma-glutamyl spacer — a shorter, non-diacid lipid compared with the C18 and C20 fatty diacids used by later analogs.
- No Aib8 substitution. Liraglutide retains the native alanine at position 8, so it remains a DPP-4 substrate. Albumin binding and self-association, not protease resistance, are what extend its duration. This is the single most important structural fact about the molecule.
- Identifiers. CAS 204656-20-2, molecular formula C172H265N43O51, molecular weight 3751.20 Da — the lightest of the acylated GLP-1 analogs in our range.
How liraglutide is thought to work
Receptor pharmacology is conventional for the class. Liraglutide binds the GLP-1 receptor, a class B G-protein-coupled receptor, stabilises the active conformation, and drives Gs-coupled cAMP accumulation with downstream PKA and Epac2 signalling. In islet preparations this amplifies insulin secretion in a glucose-dependent manner. Receptor populations in the area postrema, nucleus tractus solitarius, arcuate nucleus and on vagal afferents are implicated in the reduced food intake and slowed gastric emptying reported in rodent studies.
Where liraglutide diverges from later analogs is not the receptor but the exposure profile. A duration measured in hours produces peak-and-trough kinetics, whereas a multi-day analog produces near-steady-state exposure. Those are different pharmacological experiments even when the receptor engaged is identical, and several published observations about receptor desensitisation and tachyphylaxis in the GLP-1 field depend on which exposure pattern was used. If your research question concerns the consequences of intermittent versus continuous receptor occupancy, that difference is the whole experiment rather than a nuisance variable.
What research has examined
- Receptor and cell studies. cAMP accumulation, binding, beta-arrestin recruitment and receptor internalisation assays in cells expressing the human GLP-1 receptor. Liraglutide is one of the standard reference agonists in this literature, so most newer molecules are characterised against it.
- Biophysical work. Self-association and heptamer formation studies, albumin-binding measurements, and formulation stability work. This strand is unusually well developed for liraglutide because its self-association behaviour is central to its kinetics.
- Rodent studies. Feeding behaviour, gastric transit, islet morphology and beta-cell mass, neuronal activation mapping, and models of hepatic steatosis and neuroinflammation.
- Human clinical trials of the approved products. Randomised programmes in type 2 diabetes and in weight management, plus a published cardiovascular outcome trial. These studied prescription medicines under medical supervision and confer nothing on research-grade powder.
For the wider map see the GLP-1 and incretin pathway hub.
Liraglutide also occupies a specific historical position that shapes how the literature reads. It was the first acylated GLP-1 analog to be characterised in depth, so a large share of foundational GLP-1 receptor pharmacology — internalisation kinetics, recycling behaviour, the relationship between cAMP output and insulin secretion in isolated islets — was established using it. Newer molecules are routinely benchmarked against liraglutide rather than against native GLP-1, which means that if you are reproducing or extending a published comparison, having the same reference agonist on the bench removes an entire class of cross-study discrepancy.
Forms and sizes we supply
| Attribute | Specification |
|---|---|
| Form | Lyophilized powder, sealed glass vial |
| Sizes | 5 mg, 10 mg |
| Purity | Greater than or equal to 99% by HPLC, lot-matched COA |
| CAS | 204656-20-2 |
| Molecular weight | 3751.20 Da |
| Formula | C172H265N43O51 |
| Class | Palmitoylated GLP-1 receptor agonist (mono-agonist) |
| Intended use | Laboratory research only |
Sizes and pricing are on the liraglutide product page, within the GLP-1 and incretin peptides collection.
Reconstitution and storage in a lab context
The arithmetic is standard: a 5 mg vial reconstituted with 2 mL of bacteriostatic water gives 2.5 mg/mL, equal to 2,500 mcg/mL, so 0.1 mL of that solution contains 250 mcg of peptide. One handling detail is specific to liraglutide. Its self-association behaviour is pH-sensitive — the molecule is most soluble in mildly alkaline conditions and least soluble near its isoelectric point, where it can come out of solution. If a preparation looks hazy, the usual cause is buffer pH rather than degradation, and forcing it back into solution by vigorous shaking will do more harm than adjusting the buffer.
Store sealed lyophilized powder at minus 20 degrees Celsius protected from light and moisture; hold reconstituted solution at 2 to 8 degrees Celsius and use within the study window. Aliquot at reconstitution rather than repeatedly freezing and thawing a shared stock. See our reconstitution guide, pH and solubility note.
One further practical point about self-association. The heptamer equilibrium is concentration-dependent, so a concentrated stock and a dilute working solution do not contain the same distribution of species. At assay concentrations the peptide is largely monomeric; in a concentrated stock a substantial fraction is associated. This matters when a protocol calls for preparing a stock well above the working range and holding it, because the association state at storage is not the state at use, and re-equilibration is not instantaneous. Preparing dilutions with adequate equilibration time, rather than immediately before reading a plate, removes a real source of variability.
Purity, COA and how to read it
A liraglutide certificate should show an HPLC chromatogram with main-peak area percentage, a mass spectrometry identity result checked against the theoretical 3751.20 Da, net peptide content, lot number and analysis date. Two impurity classes are worth understanding for an acylated peptide made this way: incompletely acylated peptide, which lacks the palmitate and therefore has a shorter duration and different kinetics without looking obviously wrong in a purity figure, and des-amino or deletion sequences from incomplete coupling. A chromatogram with resolved shoulders tells you more than a headline percentage. Read how to read a COA, and match the lot to your vial.
Finally, a word on why the shorter half-life is sometimes an advantage at the bench rather than a limitation. A compound that clears within hours allows a washout to be performed and a baseline to be re-established inside a single experiment, which a multi-day analog does not permit without extending the study by a week. For crossover designs, repeated-measure protocols and any question involving recovery of receptor responsiveness after agonist exposure, that property is the reason to select liraglutide deliberately rather than defaulting to the most potent long-acting molecule available.
Regulatory status
Liraglutide as a pharmaceutical is an approved prescription medicine in the United States and many other jurisdictions, and generic versions have entered several markets since the originator patents lapsed. Research-grade liraglutide is a different category entirely: a chemical reference material sold research use only, not approved, formulated or permitted for administration to humans or animals. Patent expiry has no bearing on that distinction — see research use only, explained.
Related peptides and comparisons
The obvious comparison is with its longer-acting successor on the same backbone, covered in liraglutide vs semaglutide; the product page for semaglutide lists the alternative. For multi-receptor molecules see retatrutide, and for the older exendin-based agonist, exenatide.