GLP-2 TRZ — also known as TRZ peptide, EP-2T, TRZ-2, G2-TRZ, AL-TRZ peptide, or GLP2-TRZ — is a synthetic dual agonist research compound that simultaneously activates both the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R). It shares its dual GIPR/GLP-1R mechanism with tirzepatide, making the clinical SURPASS and SURMOUNT trial literature directly relevant as research context.
Evo Peptides supplies GLP-2 TRZ (EP-2T) in 15mg and 30mg formats. Current lot-specific third-party HPLC purity values are 99.4% (15mg) and 99.8% (30mg). Batch-specific COAs are available for review before purchase. Orders placed before 3:00 PM CST ship same day from Wisconsin.
Research Use Only (RUO). GLP-2 TRZ is intended solely for in vitro laboratory research. Not for human or veterinary administration. Not evaluated by the FDA. Purchasers must be 21+ and acknowledge research-only intent.
GLP-2 TRZ is a synthetic 39-amino acid dual agonist research compound that simultaneously activates both the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R). Its dual mechanism distinguishes it from single GLP-1 agonists and positions it as a research tool for studying the additive and synergistic effects of co-activating both principal incretin receptor pathways in the same model system.
The compound shares its dual GIPR/GLP-1R mechanism with tirzepatide (Mounjaro/Zepbound), making the clinical literature from the SURPASS and SURMOUNT trial programs directly relevant as research context. As a research-grade compound, GLP-2 TRZ is supplied at 99.4–99.8% HPLC purity with per-batch COA verification for in-vitro laboratory research use only.
From a research design perspective, TRZ peptide is most useful when the study question requires dual incretin pathway engagement — distinguishing it from EP-3 RT (which adds glucagon receptor co-agonism) and from single GLP-1R agonists (which isolate GLP-1R signaling alone).
Incretins are gut-derived hormones secreted in response to nutrient ingestion that amplify glucose-stimulated insulin secretion beyond what glucose alone can produce — the incretin effect. Two incretins dominate the research landscape: GLP-1 (secreted by L-cells in the ileum and colon) and GIP (secreted by K-cells in the duodenum and jejunum). GLP-2 TRZ's research value lies in engaging both receptor arms simultaneously with a single compound.
GLP-1R signaling is among the best-characterized pathways in metabolic biology. Gs-coupled signaling elevates intracellular cAMP, potentiating glucose-dependent insulin exocytosis from pancreatic beta cells. GLP-1R is also expressed in the hypothalamus, brainstem, vagal afferents, stomach, liver, heart, kidney, and adipose tissue — producing pleiotropic effects including delayed gastric emptying, enhanced satiety signaling, reduced glucagon secretion, and in some preclinical models, cardioprotective and neuroprotective effects.
Single GLP-1R agonist benchmarks (semaglutide, liraglutide) established body weight reductions in the 15% range from baseline in human studies. GLP-2 TRZ research builds on this by adding GIPR co-agonism.
GIPR signaling has a more complex research narrative. Early literature positioned GIP as pro-adipogenic, suggesting GIPR agonism would worsen metabolic outcomes. This view has been substantially revised: in the context of obesity and insulin resistance, GIPR agonism combined with GLP-1R agonism produces additive reductions in body weight and glycemic parameters that exceed either agonist alone.
The mechanism involves complementary effects on energy homeostasis — GLP-1R agonism reduces intake while GIPR agonism modulates energy expenditure and adipose tissue metabolism. GIPR co-agonism also attenuates the nausea associated with high-dose pure GLP-1R agonism in preclinical models.
In cell-based assays, GLP-2 TRZ (TRZ peptide) demonstrates high-affinity binding at both GIPR (EC50 ~10 pM) and GLP-1R (EC50 ~6 pM) — potency comparable to or exceeding native incretin peptides. The approximately equimolar potency at both receptors simplifies dose-response study design compared to compounds with substantially mismatched receptor affinities.
GLP-2 TRZ (TRZ peptide) is a 39-amino acid synthetic peptide with a molecular weight of approximately 4,813.5 Da. Its sequence is engineered as a hybrid of GIP and GLP-1 analogues, incorporating modifications that enable simultaneous high-affinity binding to both GIPR and GLP-1R.
The preclinical and clinical research foundation for GLP-2 TRZ (TRZ peptide) is among the most robust of any dual incretin agonist studied to date, providing an unusually rich evidence base for researchers designing dual incretin mechanism studies.
In CHO cells expressing human GIPR or GLP-1R, GLP-2 TRZ produces full agonist cAMP responses at both receptors with efficacy ratios suggesting approximately equivalent GIP-to-GLP-1 activity at therapeutic concentrations. These in vitro parameters are essential for researchers designing receptor binding studies, competition assays, or intracellular signaling cascade investigations.
In diet-induced obesity (DIO) mouse and rat models, dual GIPR/GLP-1R agonism with TRZ peptide consistently produces greater reductions in body weight, adiposity, fasting glucose, and insulin resistance indices compared to equipotent GLP-1R single agonists. Representative DIO mouse studies show body weight reductions of 25–35% from peak versus 15–20% with single agonism — with additive effects attributable primarily to enhanced energy expenditure and differential adipose tissue remodeling in GIPR-expressing depots.
In db/db mice (leptin receptor-deficient T2D model), GLP-2 TRZ produces marked improvements in HbA1c, fasting insulin, and HOMA-IR relative to vehicle and single agonist controls, accompanied by preserved beta-cell mass in histological analyses.
The SURPASS (type 2 diabetes) and SURMOUNT (obesity) clinical trial programs provide essential context for GLP-2 TRZ research design. SURMOUNT-1 demonstrated mean body weight reductions of 20.9% at the highest dose over 72 weeks — exceeding the benchmark set by GLP-1R single agonists. SURPASS-2 provided direct comparative data against semaglutide showing superior HbA1c reduction and greater weight loss at all dose levels tested.
SURPASS/SURMOUNT data are from the FDA-approved pharmaceutical tirzepatide, not from GLP-2 TRZ research compound. This literature informs preclinical research design context only. GLP-2 TRZ (EP-2T) is for in-vitro research use only.
The figures below are lot-specific HPLC purity values from independent third-party COAs for material currently in stock. Full COAs are accessible on the product page and at evopeptidesus.com/coas prior to purchase.
The most relevant research comparison is against EP-3 RT (GLP-3 RT), Evo Peptides' triple agonist compound. EP-3 RT adds glucagon receptor (GCGR) co-agonism, introducing enhanced energy expenditure via thermogenic and hepatic glucose output effects. Running both compounds in parallel allows researchers to quantify the marginal contribution of GCGR agonism independently of the dual incretin effect.
| Factor | GLP-2 TRZ (EP-2T) | EP-3 RT (GLP-3 RT) |
|---|---|---|
| Also known as | TRZ peptide, TRZ-2, G2-TRZ, AL-TRZ peptide | Retatrutide analogue |
| Receptor targets | GIP + GLP-1 (dual) | GIP + GLP-1 + Glucagon (triple) |
| Half-life | ~5 days | ~6 days |
| Key research use | Dual incretin co-signaling, metabolic endpoints | Triple agonism, energy expenditure, hepatic effects |
| When to choose | GIP/GLP-1 co-signaling is the primary variable | Glucagon receptor contribution is the primary variable |
| Evo Peptides purity | 99.4% (15mg) / 99.8% (30mg) HPLC | 99.257–99.91% HPLC (lot-specific) |
| Source | GLP-2 TRZ product page | EP-3 RT product page |
For designs that compare dual versus triple receptor agonism, sourcing both GLP-2 TRZ and EP-3 RT from the same supplier under consistent COA methodology reduces analytical confounds across study arms.
Mechanistic investigation of dual incretin receptor signaling — how simultaneous GIPR and GLP-1R co-activation produces differential signaling outcomes versus either receptor alone. Key questions include biased receptor signaling profiles, downstream effector interactions (AMPK, mTOR, PI3K/Akt), and kinetic receptor internalization under dual agonist stimulation.
Given GIPR's expression in adipose tissue, GLP-2 TRZ provides a research tool for studying how GIPR co-agonism modulates adipocyte biology beyond GLP-1R agonism alone — including adipogenesis, lipolysis, adipokine secretion, and brown/beige adipose tissue thermogenesis. Differential effects on visceral versus subcutaneous depots are of particular interest in TRZ peptide studies.
Both GIP and GLP-1 receptors are expressed on pancreatic beta cells with established roles in proliferation, survival, and function. GLP-2 TRZ enables study of dual incretin pathway activation in MIN6 cells, primary islet preparations, and in vivo rodent models. Relevant endpoints: beta-cell mass quantification, proliferation markers (Ki67, BrdU), apoptosis indices, insulin granule dynamics.
Both GLP-1R and GIPR are expressed in the hypothalamus, brainstem, and mesolimbic regions. TRZ peptide's CNS effects — hypothalamic AMPK suppression, arcuate nucleus neuropeptide modulation, mesolimbic dopamine interactions — represent active research areas for dissecting how peripheral and central incretin signaling converge on appetite circuits.
In rodent models, dose-response studies with TRZ peptide typically span 0.1 to 10 nmol/kg body weight administered subcutaneously once or twice weekly. Given the extended albumin-bound half-life, accumulation occurs over 2–3 weeks of repeated dosing — allow a pharmacokinetic steady-state period before endpoint measurements in chronic studies. Titrate from lower doses upward to reduce nausea-related confounders in food intake measurements.
Robust GLP-2 TRZ study designs include: vehicle control (albumin or saline-based); body weight-matched pair-fed vehicle control (to separate weight-loss-dependent from direct drug effects); GLP-1R single agonist comparator arm (to isolate the GIPR co-agonism contribution); and in some designs, a GIPR single agonist arm.
Many metabolic benefits attributed to direct drug effects are partially explained by caloric restriction alone in rodent models. The pair-fed control is the key design element that allows separation of these effects. Do not omit it.
Relevant endpoints for metabolic TRZ peptide research: body weight and body composition (EchoMRI or DEXA), food intake, fasting and postprandial glucose/insulin/c-peptide, oGTT, ITT, HbA1c, plasma lipids, adipokines (leptin, adiponectin), inflammatory markers, and in terminal studies: pancreatic beta-cell mass, liver histology (steatosis scoring), and adipose tissue histology.
The C18 fatty-acid modification that extends half-life in research models also increases susceptibility to aggregation under suboptimal reconstitution conditions. Both the 15mg and 30mg vials follow the same protocol. For broader guidance see the peptide storage and reconstitution guide.
Each freeze-thaw cycle degrades the compound. Prepare single-use aliquots before freezing. Once thawed, do not refreeze.
Orders placed before 3:00 PM CST ship the same business day from Wisconsin to all 50 states. Free standard shipping on all orders over $200. All material is supplied under Research Use Only labeling.
TRZ peptide — also called GLP-2 TRZ, EP-2T, TRZ-2, or G2-TRZ — is a synthetic dual agonist research compound that simultaneously activates both GIPR and GLP-1R. It is used in preclinical research to study dual incretin co-signaling, metabolic regulation, adipose tissue biology, beta-cell function, and CNS appetite circuits. Sold strictly for in-vitro laboratory research use only.
GLP-2 TRZ (TRZ peptide / EP-2T) shares the same dual GIP/GLP-1 receptor agonist mechanism and sequence architecture as tirzepatide. As a research compound, GLP-2 TRZ is strictly for in-vitro laboratory research use only — it is not the pharmaceutical product Mounjaro or Zepbound, which are FDA-approved, manufactured under GMP, and dispensed by prescription for clinical use.
GLP-2 TRZ (EP-2T) is available at 99.4% HPLC purity (15mg) and 99.8% HPLC purity (30mg), verified by independent third-party laboratory. Per-batch COAs are published at evopeptidesus.com/coas and available before purchase.
AL-TRZ peptide, G2-TRZ, TRZ-2, GLP2-TRZ, and PP-2 TRZ are all informal or variant names used in researcher communities to refer to the same class of compound: a dual GIP/GLP-1 receptor agonist with the tirzepatide mechanism. Evo Peptides' GLP-2 TRZ (EP-2T) is a research compound in this class, sold for in-vitro laboratory use only.
GLP-2 TRZ / TRZ peptide (dual: GIP + GLP-1) and EP-3 RT (triple: GIP + GLP-1 + glucagon) differ by the addition of glucagon receptor co-agonism in EP-3 RT. Use GLP-2 TRZ for dual incretin mechanism studies; use EP-3 RT when glucagon receptor effects or enhanced energy expenditure are research-relevant.
Store lyophilized GLP-2 TRZ at −20°C, protected from light and moisture. Reconstitute with bacteriostatic water — add slowly down the vial wall, swirl gently, do not vortex. After reconstitution store at 2–8°C and use within 30 days. Do not freeze reconstituted solution. For long-term storage, aliquot into single-use volumes and store at −80°C.
Yes. For designs comparing dual versus triple receptor agonism, sourcing both compounds from the same supplier under consistent COA methodology reduces analytical confounds across study arms. Both GLP-2 TRZ and EP-3 RT are available from Evo Peptides for in-vitro research use only.