GLP-1 (7-37)
Also known as: Glucagon-Like Peptide-1, Native GLP-1, GLP-1 (7-36) amide, Incretin
GLP-1 (7-37) is the biologically active form of the endogenous incretin hormone glucagon-like peptide-1. It is the natural peptide that semaglutide, tirzepatide, and other GLP-1 receptor agonists are designed to mimic, playing a central role in glucose homeostasis, appetite regulation, and metabolic function.
GLP-1 (7-37) is a 3,297.7 Da (GLP-1 7-36 amide) research peptide. GLP-1 (7-37) is the biologically active form of the endogenous incretin hormone glucagon-like peptide-1. It is the natural peptide that semaglutide, tirzepatide, and other GLP-1 receptor agonists are designed to mimic, playing a central role in glucose homeostasis, appetite regulation, and metabolic function.
Also called: Glucagon-Like Peptide-1, Native GLP-1, GLP-1 (7-36) amide
3,297.7 (GLP-1 7-36 amide)
Molecular Weight
Daltons
5
Strong Evidence
benefits
5
Studies Cited
peer-reviewed
0-0
Typical Dose
0.5-1.5 pmol/kg/min
Overview
GLP-1 (7-37) is the bioactive form of glucagon-like peptide-1, an incretin hormone produced primarily by intestinal L-cells in response to nutrient ingestion. The full proglucagon precursor generates multiple peptides including GLP-1, GLP-2, and glucagon. The biologically active forms of GLP-1 are GLP-1 (7-37) and GLP-1 (7-36) amide, with the amidated form being the predominant circulating species in humans (accounting for approximately 80% of active GLP-1). Both forms have equivalent biological activity at the GLP-1 receptor. Native GLP-1 has a very short plasma half-life of approximately 2 minutes due to rapid degradation by the enzyme dipeptidyl peptidase-4 (DPP-4) and renal clearance. This rapid degradation is the primary reason synthetic GLP-1 receptor agonists (semaglutide, liraglutide, tirzepatide, etc.) were developed with structural modifications to resist DPP-4 cleavage and extend duration of action. The discovery and characterization of GLP-1 and its receptor was a landmark in metabolic physiology, leading to an entire class of blockbuster pharmaceuticals and contributing to the 2024 Nobel Prize in Physiology or Medicine for Joel Habener, Lotte Bjerre Knudsen, and Svetlana Mojsov.
Key Takeaways: GLP-1 (7-37)
- Strongest evidence supports GLP-1 (7-37) for glucose-dependent insulin secretion and appetite suppression
- Research doses typically range from 0 to 0 0.5-1.5 pmol/kg/min via intravenous infusion
- 5 benefits with strong evidence, 0 moderate, 1 preliminary
- Half-life: ~2 minutes (rapidly degraded by DPP-4)
- 5 cited research studies in this guide
Mechanism of Action
GLP-1 (7-37) binds to the GLP-1 receptor (GLP-1R), a class B G-protein coupled receptor expressed on pancreatic beta cells, hypothalamic neurons, cardiac tissue, GI tract, and other organs. On pancreatic beta cells, GLP-1R activation triggers the cAMP/PKA and Epac2 signaling cascades, potentiating glucose-dependent insulin secretion; meaning insulin is released only when blood glucose is elevated, providing an inherent safety mechanism against hypoglycemia. GLP-1 simultaneously suppresses glucagon secretion from alpha cells (also glucose-dependent), reducing hepatic glucose output. In the GI tract, GLP-1 slows gastric emptying by inhibiting antral motility and promoting pyloric contraction, prolonging nutrient absorption and contributing to postprandial satiety. In the hypothalamus, GLP-1R activation in the arcuate nucleus and paraventricular nucleus suppresses appetite through modulation of POMC/CART (anorexigenic) and NPY/AgRP (orexigenic) neuron activity. GLP-1 also has trophic effects on beta cells, promoting proliferation, inhibiting apoptosis, and enhancing beta-cell mass through PDX-1 and Irs-2 signaling. Cardiovascular GLP-1R activation provides cardioprotective effects including improved endothelial function, reduced inflammation, and cardioprotection in ischemic models. The rapid degradation by DPP-4 (which cleaves the N-terminal His-Ala dipeptide to produce inactive GLP-1 9-37) limits native GLP-1's therapeutic utility and is the reason DPP-4 inhibitors and DPP-4-resistant analogs were developed.
Research Benefits
GLP-1 (7-37) at a Glance
GLP-1 (7-37) binds to the GLP-1 receptor (GLP-1R), a class B G-protein coupled receptor expressed on pancreatic beta cells, hypothalamic neurons, cardiac tissue, GI tract, and other organs.
Glucose-Dependent Insulin Secretion
Strong EvidenceThe defining incretin effect — GLP-1 enhances insulin secretion only when blood glucose is elevated, providing effective glycemic control with minimal hypoglycemia risk. This mechanism underlies all GLP-1-based diabetes drugs.
Appetite Suppression
Strong EvidenceCentral GLP-1R activation in the hypothalamus produces potent appetite suppression and increased satiety. This effect is the basis for all GLP-1 receptor agonist weight-loss medications.
Beta Cell Preservation
Strong EvidenceGLP-1 promotes pancreatic beta cell proliferation, inhibits apoptosis, and enhances beta cell mass. This trophic effect may help preserve insulin-producing capacity in type 2 diabetes.
Cardiovascular Protection
Strong EvidenceGLP-1R activation provides direct cardiovascular benefits including improved endothelial function, reduced myocardial ischemic injury, and anti-inflammatory effects. Clinical outcome trials of GLP-1 analogs confirm reduced cardiovascular events.
Delayed Gastric Emptying
Strong EvidenceGLP-1 slows gastric emptying, prolonging nutrient absorption, contributing to postprandial satiety, and reducing glycemic excursions after meals.
Neuroprotective Potential
PreliminaryEmerging research shows GLP-1R activation in the brain has neuroprotective and anti-inflammatory effects, with clinical trials exploring GLP-1 agonists for Alzheimer's disease, Parkinson's disease, and other neurodegenerative conditions.
Research Dosing Protocols
Research Purposes Only: All content is for informational and research purposes only. This site does not provide medical advice, diagnosis, or treatment. Consult a qualified healthcare professional before using any peptide or supplement.
| Research Protocol | Dose Range | Route |
|---|---|---|
| Continuous IV infusion (research/diagnostic) | 0–0 0.5-1.5 pmol/kg/min | Intravenous infusion |
| Subcutaneous research dose | 25–100 nmol | Subcutaneous injection |
Frequency
Continuous infusion (research) or multiple daily injections (impractical due to short half-life)
Timing
Pre-prandial or continuous infusion in research settings
Cycle Length
Not practical as a standalone therapeutic due to 2-minute half-life
Research Notes
- 1Native GLP-1 has a ~2 minute half-life and is not practical as a standalone medication.
- 2Therapeutic applications use DPP-4-resistant analogs: semaglutide, liraglutide, tirzepatide, etc.
- 3DPP-4 inhibitors (sitagliptin, saxagliptin, etc.) extend native GLP-1 activity by blocking its degradation.
- 4GLP-1 (7-37) and GLP-1 (7-36) amide have equivalent biological activity.
- 5IV GLP-1 infusion is used primarily in metabolic research and diagnostic testing.
- 6The incretin effect accounts for approximately 50-70% of postprandial insulin secretion.
Reconstitution Guide
Standard Reconstitution
Vial Size
1 mg
Bacteriostatic Water
1 mL
Concentration
10 mcg
per 0.1 mL (10 units)
Step-by-Step Guide
Gather Materials
GLP-1 (7-37) vial, bacteriostatic water, alcohol swabs, insulin syringes.
Equilibrate Temperature
Remove the vial from storage and allow it to reach room temperature (5-10 minutes).
Sanitize
Swab the rubber stopper of both the peptide vial and bacteriostatic water vial with alcohol.
Draw Water
Draw 1 mL of bacteriostatic water into a syringe.
Add Water to Vial
Insert the needle into the peptide vial and direct the water stream against the glass wall — not directly onto the powder.
Mix Gently
Swirl the vial gently until the powder is fully dissolved. Never shake. The solution should be clear and colorless.
Store Properly
Refrigerate at Frozen (-20°C) for long-term; refrigerated (2-8°C) for short-term after reconstitution. Use immediately after reconstitution (extremely labile peptide).
Storage Temperature
Frozen (-20°C) for long-term; refrigerated (2-8°C) for short-term after reconstitution
Shelf Life
Use immediately after reconstitution (extremely labile peptide)
Important Notes
- •Native GLP-1 is highly susceptible to DPP-4 degradation, handle rapidly.
- •For research use, reconstitute with sterile saline or buffer immediately before use.
- •Add DPP-4 inhibitor to collection tubes when measuring endogenous GLP-1 in blood samples.
- •Not available as a pharmaceutical product; only synthetic analogs are marketed.
- •Store lyophilized powder at -20°C or -80°C.
GLP-1 (7-37) Dosing Calculator
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GLP-1 (7-37) Reconstitution Calculator
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Safety & Side Effects
Reported Side Effects
- !Nausea (common with supra-physiological doses or analogs)
- !Vomiting (dose-dependent)
- !Delayed gastric emptying (pharmacological effect, can cause discomfort)
- !Hypoglycemia (very rare with native GLP-1 due to glucose-dependent mechanism, but possible with concomitant sulfonylureas/insulin)
- !Native GLP-1 is generally very well tolerated at physiological levels
- !Side effect profiles of synthetic analogs (semaglutide, tirzepatide) are related but not identical to native GLP-1
Potential Interactions
- ⚡DPP-4 inhibitors (sitagliptin, saxagliptin, etc.) enhance native GLP-1 activity by preventing degradation.
- ⚡Sulfonylureas and insulin: GLP-1 may increase hypoglycemia risk when combined with these agents.
- ⚡Slowed gastric emptying may affect absorption of co-administered oral medications.
- ⚡Metformin may increase endogenous GLP-1 secretion (one proposed mechanism for metformin's incretin effect).
- ⚡Dietary fiber and certain nutrients stimulate endogenous GLP-1 release.
Important: Side effects and interactions listed here are compiled from published research and community reports. This is not a complete list. No formal drug interaction studies have been conducted for most research peptides. Always consult a qualified healthcare provider.
Research Studies
The following studies are referenced in this profile. PubMed IDs are provided where available for independent verification.
Insulinotropic glucagon-like peptide I agonists and their therapeutic potential
thorough review by a pioneer in GLP-1 research, covering the biology of GLP-1, its receptor signaling, and the rationale for developing GLP-1-based therapeutics for diabetes and obesity.
The incretin system: glucagon-like peptide-1 receptor agonists and DPP-4 inhibitors
Authoritative Lancet review of the incretin system, covering GLP-1 physiology, the development of GLP-1 receptor agonists and DPP-4 inhibitors, and clinical evidence for cardiovascular and metabolic benefits.
GLP-1 receptor activation and the beta cell: mechanisms of protection
Detailed analysis of GLP-1's trophic effects on pancreatic beta cells, including anti-apoptotic signaling, proliferation induction, and potential for beta cell mass preservation in type 2 diabetes.
Cardiovascular biology of the incretin system
Review of GLP-1R signaling in the cardiovascular system, documenting direct cardioprotective effects including improved endothelial function, reduced atherosclerosis, and cardioprotection in ischemic models.
GLP-1 agonists in neurodegenerative disease: mechanistic and clinical evidence
Review of emerging evidence that GLP-1 receptor agonists have neuroprotective properties relevant to Alzheimer's and Parkinson's disease, including ongoing clinical trials of semaglutide and liraglutide for neurodegeneration.
Note: This is not an exhaustive list of all published research. Studies are selected for relevance and quality. Click PubMed IDs to verify sources independently. Inclusion does not imply endorsement of the peptide for any clinical use.
Frequently Asked Questions
GLP-1 (7-37) is the biologically active form of the incretin hormone glucagon-like peptide-1, produced naturally by intestinal L-cells after eating. It stimulates insulin secretion, suppresses appetite, and slows gastric emptying. It is the natural hormone that semaglutide, tirzepatide, and other GLP-1 drugs are designed to mimic.
Native GLP-1 has a half-life of only ~2 minutes because it is rapidly degraded by the enzyme DPP-4. This makes it impractical as a medication — it would require continuous intravenous infusion. Synthetic analogs (semaglutide, liraglutide, tirzepatide) are structurally modified to resist DPP-4 and last days to weeks.
The incretin effect refers to the observation that oral glucose produces a larger insulin response than the same amount of glucose given intravenously. This is because oral nutrients stimulate GLP-1 and GIP release from the gut, which amplify insulin secretion. The incretin effect accounts for 50-70% of postprandial insulin.
DPP-4 inhibitors (sitagliptin, saxagliptin, etc.) block the enzyme that degrades native GLP-1, extending its activity from 2 minutes to roughly 10-15 minutes. This doubles circulating active GLP-1 levels. They provide a more modest effect than GLP-1 receptor agonists which achieve pharmacological (supra-physiological) receptor activation.
Both are biologically active forms with equivalent potency at the GLP-1 receptor. GLP-1 (7-36) amide has an amidated C-terminus and is the predominant circulating form (~80% of active GLP-1). GLP-1 (7-37) has a free glycine at position 37. In practice, the terms are often used interchangeably.
Yes. Dietary factors that stimulate GLP-1 release include protein, healthy fats, fiber, and certain nutrients like berberine and curcumin. Exercise also increases GLP-1 secretion. However, the magnitude of natural stimulation is much less than pharmacological GLP-1 receptor agonists.
Research & Educational Use Only
All content is for informational and research purposes only. This site does not provide medical advice, diagnosis, or treatment. Consult a qualified healthcare professional before using any peptide or supplement.
The information presented here is compiled from published research studies and is intended for informational purposes only. Individual results may vary. Always consult with a licensed healthcare provider.