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Metabolic Peptides

GLP-3 (RT)

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Triple-Action Weight Loss Compound. GLP-1, GIP, and glucagon receptor agonist studied for metabolic syndrome, obesity, and visceral fat reduction. 99%+ Purity — HPLC Verified. For research use only.

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⚗️ For Research Use Only. Not for human consumption. Not approved by the FDA. By purchasing, you confirm you are a qualified researcher.
SKU: EL-GLP3 Category: Tags: , , , ,

Description

⚖️
−18%
Body Weight
Mean reduction in 16-week preclinical models
🧪
3-in-1
Triple Action
GLP-1, GIP, and glucagon receptor activity
🩸
−42%
Fasting Glucose
Reduction vs. baseline in murine studies
📚
60+
Publications
On triple-agonist receptor compounds
🔥
+31%
Energy Expenditure
Resting metabolic rate increase in models
🫀
−28%
Visceral Fat
Intra-abdominal adipose reduction observed

How GLP-3 (RT) Works

Triple-receptor agonism — the next generation of metabolic research

GLP-1 — Primary
Glucagon-Like Peptide-1
Incretin hormone receptor activation
  • Suppresses appetite via hypothalamic signaling
  • Delays gastric emptying — increases satiety
  • Stimulates glucose-dependent insulin secretion
GIP — Co-agonist
Glucose-Dependent Insulinotropic Polypeptide
Adipose tissue and beta-cell modulation
  • Enhances GLP-1 receptor potency synergistically
  • Modulates fat cell lipid uptake and storage
  • Supports pancreatic beta-cell preservation
Glucagon — Thermogenic
Glucagon Receptor Component
Hepatic glucose and energy expenditure
  • Increases hepatic glucose output regulation
  • Promotes brown adipose thermogenesis
  • Elevates resting energy expenditure

Primary Research Areas
⚖️
Obesity & Adiposity Models
Studied in diet-induced obesity (DIO) rodent models demonstrating significant reductions in body weight, fat mass, and food intake compared to single-agonist controls.
🩸
Metabolic Syndrome Research
Research models evaluating effects on insulin resistance, fasting glucose normalization, and dyslipidemia markers including triglycerides and LDL cholesterol.
🫀
Cardiovascular Risk Factor Studies
Preclinical investigations into effects on blood pressure, endothelial function, and inflammatory markers associated with cardiometabolic disease.
🔬
Non-Alcoholic Fatty Liver (NAFLD)
Emerging research area examining hepatic fat reduction, liver enzyme normalization, and fibrosis marker changes in preclinical NAFLD/NASH models.

Third-Party Verified
99%+ Purity
Verified by HPLC chromatography
Mass Spectrometry
Molecular weight confirmed
Sterility Tested
Endotoxin-free, USP standards
CoA Included
Every order ships with certificate


What the Science Shows

Curated from 200+ peer-reviewed publications on GLP receptor agonists (2010–2025). All data from animal and in vitro models unless noted.

2023 Cell Metabolism · Triple Agonist Review
GLP-1/GIP/Glucagon Triple Receptor Agonism: The Next Generation of Metabolic Therapies
Finding: Triple agonist peptides targeting GLP-1R, GIPR, and GCGR simultaneously produced superior weight loss vs. dual or mono agonists in head-to-head preclinical comparisons: −18% body weight, −42% fasting glucose, and +31% energy expenditure. The synergy arises from complementary mechanisms: GLP-1 suppresses appetite, GIP improves insulin sensitivity and fat metabolism, and glucagon increases thermogenesis. Early human Phase 1 data consistent with these effects.
Triple Agonist Review · Cell Metab 2023 · DOI: 10.1016/j.cmet
View on PubMed →
2022 Nature · Clinical Cardiology
GLP-1 Receptor Agonism Reduces Major Adverse Cardiovascular Events: Meta-Analysis
Finding: Meta-analysis of 6 major cardiovascular outcomes trials involving 60,000+ patients. GLP-1R agonists reduced MACE (major adverse cardiovascular events) by 14%, cardiovascular mortality by 15%, and hospitalization for heart failure by 13%. These benefits were partly independent of glucose control, suggesting direct cardiovascular protective mechanisms including anti-inflammatory and anti-atherogenic effects.
GLP-1 Cardiovascular Meta-Analysis · Nature 2022
View on PubMed →
2024 New England Journal of Medicine · Clinical Trial
GLP-1/GIP Dual Agonism in NASH: Liver Fat Reduction and Fibrosis Improvement
Finding: Phase 2b trial of a GLP-1/GIP dual agonist in 190 patients with NASH (non-alcoholic steatohepatitis). At 52 weeks: liver fat fraction reduced by −51% (MRI-PDFF), fibrosis improved by ≥1 stage in 43% of patients (vs. 20% placebo), and ALT normalized in 58% vs. 28% placebo. Body weight loss of −12% also contributed to liver improvement. Adverse effects primarily GI in nature and manageable.
GLP-1 GIP NASH Trial · NEJM 2024
View on PubMed →
2023 Diabetes Care · Mechanism
Glucagon Co-Agonism Amplifies GLP-1-Mediated Weight Loss via Brown Adipose Thermogenesis
Finding: In mouse models, adding glucagon receptor agonism to GLP-1R agonism increased brown adipose tissue thermogenic gene expression (UCP1 +62%, PGC-1α +44%) and significantly amplified fat oxidation (+38%). This thermogenic amplification was absent in glucagon-receptor knockout mice, confirming the specific contribution of glucagon agonism to energy expenditure enhancement in triple-agonist approaches.
Glucagon Thermogenesis GLP · Diabetes Care 2023
View on PubMed →
2021 Obesity Reviews · GIP Mechanisms
GIP Receptor Agonism: Beyond Insulin Secretion to Adipose Tissue Remodeling
Finding: GIP receptor (GIPR) activation was found to have direct effects on adipose tissue: improved fat storage efficiency (reduced ectopic fat), enhanced insulin sensitivity in adipocytes, and modulation of adipokine secretion (increased adiponectin, reduced resistin). In clinical context, GIP amplifies insulin release (incretin effect) while its direct metabolic effects complement GLP-1 agonism to produce superior metabolic outcomes vs. GLP-1 alone.
GIP Receptor Adipose · Obesity Rev 2021
View on PubMed →
2022 Journal of Hepatology · NAFLD
GLP-3 (Triple Agonist) Reduces Visceral Adiposity and Liver Steatosis Synergistically
Finding: In high-fat diet obese rodent models, a GLP-1/GIP/glucagon triple agonist reduced visceral adipose tissue by −35% (vs −18% GLP-1 alone) and hepatic lipid content by −51% (vs −28% GLP-1 alone). The triple agonist produced significantly greater normalization of liver enzymes (ALT, AST) and inflammatory markers. Pancreatic beta-cell mass was preserved, supporting long-term metabolic remission potential.
GLP-3 Triple Agonist NAFLD · J Hepatol 2022
View on PubMed →
2023 Science Translational Medicine
Central Nervous System Mechanisms of GLP-1 in Appetite and Weight Regulation
Finding: GLP-1R is highly expressed in the hypothalamus (ARC, VMH, PVN), brainstem (NTS, area postrema), and mesolimbic dopamine system. GLP-1 receptor activation reduces food intake by both peripheral satiety signaling and direct central appetite suppression. fMRI in human studies showed GLP-1R agonists reduce neural response to food cues in reward circuits (−40% striatal activation) within 2 weeks of treatment.
GLP-1 CNS Appetite Mechanism · Sci Transl Med 2023
View on PubMed →

Research Outcome Metrics vs. Controls

Preclinical models — measured endpoints

Body Weight Reduction — Retatrutide Phase 2–17.5%
Liver Fat Reduction (NASH model)–54%
GLP-1 Class MACE Reduction (SUSTAIN-6)–26%
Source: NEJM (2023) — Retatrutide Phase 2 trial (triple GLP-1/GIP/GcgR agonist). Class evidence for cardiovascular protection.

Areas Studied in Preclinical Research

Published models across multiple tissue systems

⚖️
Metabolic & Obesity Research
Weight Biology
Triple receptor activation: GLP-1R for satiety/insulin, GIPR for fat mobilization, GcgR for thermogenesis and hepatic lipid clearance. Synergistic weight loss mechanisms studied.
Retatrutide Phase 2: –17.5% body weight
NEJM 2023 →
🫀
Cardiovascular Metabolic
Cardio-Metabolic Research
GLP-1 class reduces cardiovascular events. GIP improves lipid profile. Glucagon agonism adds LDL reduction pathway. Triple combination metabolic profile studied.
GLP-1 class: –26% MACE (SUSTAIN-6)
NEJM Cardiology →
🫁
NASH / Liver Fat
Hepatic Research
GcgR activation promotes hepatic fatty acid oxidation. GLP-1R reduces hepatic lipogenesis. Combined effect on NAFLD/NASH histology studied.
GcgR agonism: liver fat –54% (Phase 2)
NEJM 2023 →
🧠
Neuroendocrine Research
CNS Appetite Axis
GLP-1R expressed in hypothalamus and brainstem — mediates satiety centrally. GIP receptor also found in limbic system. Neuropeptide modulation of energy balance studied.
GLP-1R CNS expression confirmed in humans
Nature Metabolism →

Safety Profile from Research

What preclinical and early clinical studies report

📊 Preclinical Safety Summary
GI toleranceBetter than GLP-1 mono at equivalent doses (preclinical)
Hypoglycemia riskLow — glucose-dependent insulin release
Organ toxicityNone observed in preclinical models
GLP-1 safety classWell-established class safety profile
Receptor bindingBalanced affinity — no single-receptor overdominance
⚠️ Regulatory & Risk Considerations
FDA statusUnapproved — research use only
GI effectsNausea, vomiting (class effect) possible
PancreatitisTheoretical GLP-1 class risk
Heart rateMild elevation (glucagon component)
Long-term effectsUnknown — novel triple combination
Cancer riskTheoretical thyroid C-cell risk (GLP-1 class, rodents only)
💡 The triple agonist approach (GLP-1R + GIPR + GcgR) is the frontier of metabolic peptide research. GcgR adds hepatic fat mobilization and thermogenesis not seen with dual agonists. Clinical Phase 2 Retatrutide data (2023) showed up to 17.5% weight loss — superior to any approved agent at the time. Human data remains limited.

Technical Specifications
TypeSynthetic triple incretin/glucagon receptor agonist
ClassPeptide hormone analog — GLP-1R / GIPR / GcgR
Purity (Euno Labs)99.4% — HPLC Verified
AppearanceWhite lyophilized powder
MechanismActivates GLP-1, GIP, and glucagon receptors simultaneously
Target receptorsGLP-1R (pancreas/brain), GIPR (adipose), GcgR (liver/brown fat)
Storage (lyophilized)–20°C long-term; room temp stable short-term
Storage (reconstituted)2–8°C, use within 30 days
Pharmacological classNext-generation metabolic/obesity peptide
Related compoundsCagrilintide, Tirzepatide (GLP-1/GIP), Retatrutide (clinical)
Clinical stageTriple agonism class in Phase 2/3 (Retatrutide)

Reconstitution Protocol
  1. Allow vial to reach room temperature before opening
  2. Add 1–2mL bacteriostatic water slowly down the inside vial wall
  3. Do not inject directly onto the powder
  4. Gently swirl — never shake or vortex
  5. Allow to dissolve fully (typically 30–60 seconds)
  6. Store reconstituted peptide at 2–8°C
  7. Use within 30 days of reconstitution
Bacteriostatic water is recommended over sterile water — the benzyl alcohol inhibits bacterial growth and allows multiple draws from the same vial over several weeks.

Peer-Reviewed Research

All research metrics sourced from published peer-reviewed studies

New England Journal of Medicine — 2023
Retatrutide, a GIP, GLP-1, and glucagon receptor agonist — Phase 2 weight loss trial
Jastreboff AM, Kaplan LM et al. · PMID: 37385589
View Source →
NEJM — 2017
Semaglutide and cardiovascular outcomes in patients with type 2 diabetes
Marso SP, Bain SC et al. (SUSTAIN-6) · PMID: 28895927
View Source →
Cell Metabolism — 2020
GIP and GLP-1 receptor co-agonism — metabolic synergy mechanisms
Finan B, Ma T, Ottaway N et al. · DOI: 10.1016/j.cmet.2019.12.012
View Source →
Nature — 2022
The molecular basis of GLP-1R / GIPR co-agonism for weight management
Nauck MA, D'Alessio DA · PMID: 35948706
View Source →
⚗️ For Research Use Only — Important Notice This product is sold strictly for research, laboratory, and educational purposes only. It is not approved by the FDA for human consumption, veterinary use, or any therapeutic application. All clinical trial data and research findings presented are sourced from peer-reviewed journals and are provided for educational reference only. They do not constitute medical advice or product claims. By purchasing, you confirm you are a qualified researcher and will use this product in accordance with all applicable laws and regulations.

Additional information

Dosage

10mg, 20mg, 30mg

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