Peptide · Research Monograph · DPP-IV-resistant 33-amino-acid GLP-2 receptor agonist peptide ([Gly2]GLP-2 / teduglutide-type analog)

GLP-2 TZ

Intestinal Adaptation Studies

GLP-2 TZ is a 33 amino acid analog of glucagon-like peptide-2, the teduglutide-type sequence. A substitution at the second position resists DPP-4, the enzyme that clears the natural hormone within minutes. Studies have measured intestinal villus height, crypt depth, and mucosal barrier function in resection and injury models.

Formula
Available on request
Mol. weight
3752 Da
Length
33 residues
Size
10mg, 30mg, 60mg, 100mg

For laboratory research use only - not for human or animal use

GLP-2 TZ vial from the Eon Peptides research catalog
GLP-2 TZ · 10mg / 30mg / 60mg / 100mg · catalog photograph

Molecular data

Molecular formulaAvailable on request
Molecular weight3752 Da
SequenceHADGSFSDEMNTILDNLAARDFINWLIQTKITD
Sequence length33 residues
Physical formLyophilized powder (5mg)
Available sizes10mg, 30mg, 60mg, 100mg

How it works

  1. GLP-2R Agonism

    Glucagon-Like Peptide-2 Receptor Activation

    GLP-2-TZ is a synthetic analog of glucagon-like peptide-2 (GLP-2), a 33-amino acid hormone secreted by enteroendocrine L-cells in the distal intestine. It binds and activates the GLP-2 receptor (GLP-2R), a G-protein coupled receptor expressed primarily on intestinal subepithelial myofibroblasts, enteric neurons, and intestinal epithelial cells. GLP-2R activation initiates trophic signaling cascades relevant to intestinal adaptation research.

    • Selective GLP-2R agonist (Gs-coupled GPCR)
    • Activates cAMP/PKA signaling in intestinal subepithelial cells
    • Downstream IGF-1 and EGF receptor cross-talk measured
  2. Mucosal Trophism

    Intestinal Villus Growth & Crypt Expansion

    GLP-2 signalling is studied against intestinal mucosal growth, with crypt cell proliferation and apoptosis in villus epithelial cells as the measured endpoints. In short bowel syndrome research models, villus height, crypt depth and total mucosal surface area were recorded - the parameter that determines absorptive capacity.

    • Intestinal villus height and crypt depth measured
    • Enterocyte apoptosis measured in mucosal injury models
    • Intestinal mucosal surface area measured
  3. DPP-IV Resistance

    Extended Biological Half-Life

    Native GLP-2 is rapidly degraded by dipeptidyl peptidase-IV (DPP-IV) cleaving at position 2, limiting its half-life to ~7 minutes. GLP-2-TZ incorporates structural modifications (analogous to teduglutide's Gly2→Ala2 substitution) that confer resistance to DPP-IV cleavage, extending the plasma half-life and enabling more sustained GLP-2R activation in preclinical and clinical contexts.

    • Resistant to DPP-IV cleavage at N-terminus
    • Extended plasma half-life vs. native GLP-2
    • More sustained GLP-2R activation in research models

What the research shows

  1. GI Research

    Short Bowel Models

    GLP-2 analogs structurally related to GLP-2-TZ are a primary research model for intestinal adaptation. Teduglutide is an approved pharmaceutical in this class; this research material is not.

  2. Mucosal Biology

    Intestinal Adaptation

    GLP-2R activation is studied against intestinal adaptation endpoints including villus hyperplasia, nutrient transporter expression and mucosal blood flow - measured in resection and injury models.

  3. Barrier Function

    Intestinal Permeability

    GLP-2 signalling has been studied in intestinal barrier function research, with paracellular permeability and tight junction integrity measured in injury models - endpoints also used in inflammatory bowel disease research.

  4. IBD Research

    Crohn's Disease Models

    In rodent models of colitis and Crohn's disease, mucosal inflammation, barrier integrity and mucosal repair endpoints were measured following GLP-2 analog administration.

Specification

Also Known AsGLP-2 Analog, [Gly2]GLP-2, Teduglutide-type GLP-2
TypeSynthetic GLP-2 receptor agonist peptide
Length33 amino acids
Molecular Weight~3752 Da
Target ReceptorGLP-2 Receptor (GLP-2R, GPCR)
MechanismDPP-IV-resistant GLP-2R agonist; intestinal trophic signaling
FormLyophilized powder (5mg)
Purity≥99% (HPLC verified)
TestingThird-party HPLC, Mass Spec, Endotoxin
Storage-20°C for long-term stability
SolubilityWater-soluble
COAIncluded with every order
Molecular FormulaAvailable on request
AppearanceWhite to off-white powder
Quantity5mg
Stability24 months from manufacture date when stored properly

How it's tested

Every lot of GLP-2 TZ released to the catalog carries a third-party certificate of analysis. 7 documented lots are on file for this compound, with reported HPLC purity from 99.84% to 99.99% (mean 99.94%), issued by Accurate Test Labs and Freedom Diagnostics. 7 of 7 certificates record identity as confirmed.

Documented lots
7
Reported purity
99.84% to 99.99%
Mean purity
99.94%
Issuing labs
Accurate Test Labs, Freedom Diagnostics

All certificates in the COA library →

Frequently asked questions

What is GLP-2-TZ and how does it relate to clinically developed GLP-2 analogs?

GLP-2-TZ is a synthetic analog of glucagon-like peptide-2 (GLP-2), designed with structural modifications that confer resistance to DPP-IV degradation - the same design principle used in clinically developed GLP-2 analogs. Native GLP-2 has a ~7-minute plasma half-life due to rapid DPP-IV cleavage at position 2; DPP-IV-resistant analogs including GLP-2-TZ incorporate an Ala2 substitution (replacing Gly2 in native GLP-2) to resist this degradation. GLP-2-TZ is used as a research tool to study GLP-2R-mediated intestinal physiology.

What is the GLP-2 receptor and where is it expressed?

The GLP-2 receptor (GLP-2R) is a G-protein coupled receptor (GPCR) whose expression is highly restricted to the gastrointestinal tract. Primary expression sites include intestinal subepithelial myofibroblasts (ISEMFs), enteric neurons of the submucosal and myenteric plexus, and scattered enteroendocrine cells. This tissue specificity distinguishes GLP-2R from GLP-1R, which is expressed broadly (pancreas, heart, brain, kidney). The restricted expression pattern means GLP-2 analogs primarily affect intestinal physiology, which is central to their research relevance for intestinal adaptation and short bowel syndrome.

What is short bowel syndrome (SBS) and why is GLP-2 relevant?

Short bowel syndrome (SBS) results from surgical resection of large portions of the small intestine, leaving insufficient absorptive surface area to maintain nutrition without parenteral support. The intestine undergoes adaptation after resection - villus hyperplasia and crypt expansion - which GLP-2 signalling modulates. GLP-2 rises after intestinal resection, indicating a physiological role in that adaptation. Teduglutide, the approved GLP-2 analog, acts on this mechanism; that approval covers the licensed medicine only, not this research material.

What research models is GLP-2-TZ used in?

GLP-2-TZ is used in intestinal biology research models including: small bowel resection/intestinal adaptation models (rodents); intestinal organoid/enteroid culture systems for mucosal growth studies; intestinal permeability and barrier function assays; inflammatory bowel disease models (colitis, Crohn's); and in vitro GLP-2R binding and signaling studies. The compound is also used to investigate paracrine signaling between enteric neurons, ISEMFs, and epithelial cells in the intestinal niche.

How does GLP-2-TZ differ from an approved GLP-2 pharmaceutical?

An approved GLP-2 analog pharmaceutical exists for one clinical indication. GLP-2-TZ is not that compound and has not undergone independent clinical development. The research-grade GLP-2-TZ sold on eonpeptides.com is a research tool for studying GLP-2 receptor biology: it is for in vitro research purposes only and is not the approved pharmaceutical product.

How should GLP-2-TZ be stored?

Store lyophilized GLP-2-TZ at -20°C, protected from light, and minimize freeze-thaw cycles.

For laboratory research use only. Not a drug, supplement, or medical product; not for human or animal use. All findings referenced are from published preclinical/laboratory research.