GLP3-R
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These products are for laboratory research only and not intended for medical use. They are not FDA-approved to diagnose, treat, cure, or prevent any disease. By purchasing, you certify they will be used solely for research and not for human or animal consumption.
Research Summary
17 PubMed CitationsResearch Overview Retatrutide (LY3437943) is a first-in-class incretin-based triple hormone receptor agonist developed by Eli Lilly and Company to address the limitations of current obesity and type 2 diabetes therapeutics by simultaneously engaging three distinct metabolic pathways. The molecule was first described by Coskun et al. in a 2022 publication in Cell Metabolism, detailing its discovery, mechanism, and proof of concept from preclinical models through Phase 1 human data.[4] Structurally, retatrutide is a 39-amino acid synthetic peptide engineered from a GIP peptide backbone. It incorporates three non-coded amino acid residues — two α-aminoisobutyric acid (Aib) residues at positions 2 and 20, and one α-methyl-L-leucine residue at position 13 — to enhance metabolic stability and receptor binding. A C20 fatty diacid moiety is conjugated at lysine-17 via an AEEA-γGlu linker, promoting albumin binding and extending the plasma half-life to approximately 6 days, enabling convenient once-weekly subcutaneous administration.[4][8] The foundational therapeutic rationale...
GLP3-R — Research Data at a Glance
| Property | Value |
|---|---|
| PubMed Citations Referenced | 17 |
| Contributing Researchers | 3 |
| Storage Conditions | Lyophilized: -20°C to -80°C (stable 1–2 years); Reconstituted: aliquot and store at -20°C; avoid repeated freeze-thaw cycles; protect from moisture and light. |
| Purity Standard | ≥99% (HPLC verified, 3rd-party COA) |
| Research Use Only | Not for human consumption. RUO only. |
Overview
Research Overview
Retatrutide (LY3437943) is a first-in-class incretin-based triple hormone receptor agonist developed by Eli Lilly and Company to address the limitations of current obesity and type 2 diabetes therapeutics by simultaneously engaging three distinct metabolic pathways. The molecule was first described by Coskun et al. in a 2022 publication in Cell Metabolism, detailing its discovery, mechanism, and proof of concept from preclinical models through Phase 1 human data.[4]
Structurally, retatrutide is a 39-amino acid synthetic peptide engineered from a GIP peptide backbone. It incorporates three non-coded amino acid residues — two α-aminoisobutyric acid (Aib) residues at positions 2 and 20, and one α-methyl-L-leucine residue at position 13 — to enhance metabolic stability and receptor binding. A C20 fatty diacid moiety is conjugated at lysine-17 via an AEEA-γGlu linker, promoting albumin binding and extending the plasma half-life to approximately 6 days, enabling convenient once-weekly subcutaneous administration.[4][8]
The foundational therapeutic rationale for retatrutide rests on the hypothesis that simultaneously activating receptors for GLP-1, GIP, and glucagon can produce superior metabolic outcomes compared to mono- or dual-receptor agonists. GLP-1 receptor agonism suppresses appetite and stimulates insulin secretion; GIP receptor agonism enhances the insulinotropic response and supports lipid metabolism; and critically, glucagon receptor agonism increases energy expenditure and drives lipolysis and hepatic fatty acid oxidation — a mechanism absent from existing dual agonists like tirzepatide.[1][10][11]
Clinical trials have demonstrated remarkable efficacy. The pivotal Phase 2 trial by Jastreboff et al. (2023) in the New England Journal of Medicine reported dose-dependent weight loss in adults with obesity, reaching up to 24.2% mean body weight reduction at 48 weeks with the 12 mg dose — and weight loss had not plateaued at study conclusion.[1] A parallel Phase 2 trial by Rosenstock et al. (2023) in The Lancet demonstrated HbA1c reductions of up to -2.02% in participants with type 2 diabetes.[2] Phase 3 results from the TRIUMPH program have since confirmed these findings, with data showing up to 28.7% mean weight loss at 68 weeks and significant relief from obesity-related comorbidities including knee osteoarthritis.[5]
Beyond obesity and diabetes, retatrutide is under investigation for metabolic dysfunction-associated steatotic liver disease (MASLD), where a Phase 2a substudy by Sanyal et al. (2024) published in Nature Medicine demonstrated that the 8 mg and 12 mg doses normalized liver fat (<5%) in over 85% of participants, with relative reductions of up to 86% from baseline.[3] Additional ongoing Phase 3 trials are evaluating the drug for cardiovascular outcomes (TRIUMPH-OUTCOMES), chronic kidney disease (TRANSCEND-CKD), obstructive sleep apnea, and knee osteoarthritis.[5][7][9] Preclinical research has also revealed intriguing potential in obesity-associated cancer progression, with Marathe et al. (2025) demonstrating that retatrutide reduced tumor engraftment and delayed tumor onset, outperforming semaglutide in tumor suppression.[14]
Mechanism of Action
Mechanism of Action
Retatrutide functions as a simultaneous triple G protein-coupled receptor agonist, activating the GIP receptor, the GLP-1 receptor, and the glucagon receptor from a single peptide molecule. This "Triple G" mechanism integrates appetite suppression, insulinotropic effects, and enhanced energy expenditure into one pharmacological agent.[4][10]
Receptor Binding Properties
| Property | GIP Receptor (GIPR) | GLP-1 Receptor (GLP-1R) | Glucagon Receptor (GCGR) |
|---|---|---|---|
| Relative Potency (vs. endogenous ligand) | 8.9× that of native GIP | 0.4× that of native GLP-1 | 0.3× that of native glucagon |
| EC50 (Human, In Vitro) | 0.0643 nM | 0.775 nM | 5.79 nM |
| EC50 (Mouse) | 0.191 nM | 0.794 nM | 2.32 nM |
| Design Profile | Highest potency — primary backbone origin | Attenuated — improves GI tolerability | Attenuated — balanced by insulinotropic effects |
| Evidence | Coskun et al. (2022)[4] | Coskun et al. (2022)[4] | Coskun et al. (2022)[4] |
Downstream Signaling Cascade
| Step | Signaling Event | Molecular Detail |
|---|---|---|
| 1. Receptor Binding | Retatrutide binds to GIPR, GLP-1R, and/or GCGR on target cell membranes | All three are Gs-coupled GPCRs[4] |
| 2. G-Protein Coupling | Conformational change activates Gs proteins | Stimulates adenylate cyclase[4] |
| 3. cAMP Elevation | Adenylate cyclase converts ATP to cyclic AMP (cAMP) | cAMP acts as second messenger[11] |
| 4. PKA Activation | Elevated cAMP activates Protein Kinase A (PKA) and RAPGEF4 (Epac2) | Downstream effector activation[11] |
| 5. Ion Channel Modulation | In β-cells: closure of KATP channels, opening of voltage-gated Ca2+ channels | Ca2+ influx triggers insulin granule exocytosis[11] |
| 6. Gene Expression | Nuclear signaling promotes insulin biosynthesis and β-cell proliferation | Long-term metabolic adaptation[11] |
Tissue-Level Effects by Organ System
| Tissue / Organ | Effect | Primary Receptor(s) | Evidence |
|---|---|---|---|
| Pancreas (β-cells) | Glucose-dependent insulin secretion potentiated | GLP-1R, GIPR | Coskun et al. (2022)[4] |
| Pancreas (α-cells) | Suppressed glucagon secretion during hyperglycemia (net glycemic improvement despite GCGR activation) | GLP-1R (suppressive), GCGR (counterbalanced) | Rosenstock et al. (2023)[2] |
| Liver | Increased mitochondrial fatty acid oxidation; reduced hepatic lipogenesis; up to 86% relative liver fat reduction | GCGR (primary), GLP-1R | Sanyal et al. (2024)[3] |
| Adipose Tissue | Increased energy expenditure; promoted lipolysis in white adipose tissue; improved lipid-buffering capacity | GCGR (lipolysis/EE), GIPR (lipid buffering) | Katsi et al. (2025)[10] |
| Central Nervous System | Hypothalamic appetite suppression and enhanced satiety signaling | GLP-1R, GIPR | Abdul-Rahman et al. (2024)[11] |
| GI Tract | Delayed gastric emptying (attenuates with chronic dosing) | GLP-1R | Urva et al. (2023)[17] |
| Kidney | Potential renoprotective effects: reduced albuminuria, improved renal hemodynamics over time | GLP-1R, indirect (visceral fat reduction) | Heerspink et al. (2025)[7] |
Comparison with Related Compounds
| Feature | Retatrutide (Triple Agonist) | Tirzepatide (Dual Agonist) | Semaglutide (Mono Agonist) |
|---|---|---|---|
| Receptor Targets | GLP-1, GIP, Glucagon | GLP-1, GIP | GLP-1 only |
| Glucagon Activity | Yes — increases energy expenditure & lipid oxidation | No | No |
| Primary Weight-Loss Mechanism | Appetite suppression + increased energy expenditure | Appetite suppression + metabolic regulation | Appetite suppression |
| Weight Loss (Phase 2, 48 wks) | Up to 24.2%[1] | ~11–12% | ~15–17% (Phase 3, 68 wks) |
| Weight Loss (Phase 3) | Up to 28.7% at 68 wks[5] | ~20–22% (Phase 3) | ~15–17% (Phase 3) |
| Liver Fat Reduction (MASLD) | >85% resolution of steatosis[3] | Significant reduction | Significant reduction |
The addition of glucagon receptor agonism is the critical pharmacological differentiator. While glucagon would normally raise blood glucose via hepatic glycogenolysis, the strong insulinotropic effects of GIP and GLP-1 receptor activation "buffer" this effect, allowing the metabolic benefits of glucagon signaling — increased energy expenditure, enhanced lipolysis, and hepatic fat oxidation — to be safely harnessed without worsening hyperglycemia.[4][10]
Research Applications
Research Applications
Retatrutide is under active preclinical and clinical investigation across 7+ major research domains, leveraging its unique triple-receptor agonist mechanism:
- Obesity and Weight Management — The primary investigational focus. Phase 2 trials (Jastreboff et al., 2023) demonstrated dose-dependent weight loss up to 24.2% at 48 weeks with the 12 mg dose, and weight loss had not plateaued at study conclusion.[1] Phase 3 TRIUMPH program data confirmed up to 28.7% mean weight loss at 68 weeks (approximately 71.2 lbs average), with the 12 mg dose group showing the greatest reductions.[5] Preclinical studies in diet-induced obese mice demonstrated 36.9% body weight loss (vs. 21.2% for tirzepatide) with 86.8% fat mass reduction.[4]
- Type 2 Diabetes Mellitus (T2D) — Rosenstock et al. (2023) demonstrated significant glycemic improvements in Phase 2, with HbA1c reductions of up to -2.02% at the 12 mg dose over 36 weeks, along with improvements in fasting glucose, insulin sensitivity, and beta-cell function.[2] Body composition substudies confirmed that weight loss was primarily driven by fat mass reduction.[6]
- Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD/NAFLD) — A Phase 2a substudy by Sanyal et al. (2024) published in Nature Medicine demonstrated that the 8 mg and 12 mg doses normalized liver fat (<5%) in over 85% of participants, with relative liver fat reductions of up to 86% from baseline. This effect is linked to glucagon receptor-mediated increases in hepatic fatty acid oxidation and elevated beta-hydroxybutyrate biomarkers.[3]
- Cardiovascular Disease (CVD) — The TRIUMPH-OUTCOMES Phase 3 trial is assessing whether retatrutide reduces the incidence of major adverse cardiovascular events (MACE) in adults with obesity and established atherosclerotic cardiovascular disease. Pre-trial data show dose-dependent heart rate increases that peak at 24 weeks before declining.[5][10]
- Chronic Kidney Disease (CKD) — The TRANSCEND-CKD trial is investigating retatrutide's effects on kidney structure and function, including measured glomerular filtration rate (mGFR). Post-hoc analyses from Phase 2 data suggested potential renoprotective effects, including reduced albuminuria and improved renal hemodynamics over time.[7][9]
- Knee Osteoarthritis (OA) — The TRIUMPH-4 Phase 3 trial evaluates retatrutide in patients with obesity and knee osteoarthritis. Results showed a significant reduction in WOMAC pain scores (up to 75.8% improvement) and improved physical function, alongside substantial weight loss.[5]
- Obstructive Sleep Apnea (OSA) — Included within the TRIUMPH-1 and TRIUMPH-2 basket trials, research aims to determine retatrutide's efficacy in reducing the apnea-hypopnea index in patients with obesity.[5]
- Obesity-Associated Cancer — Preclinical research by Marathe et al. (2025) demonstrated that retatrutide-induced weight loss reduced tumor engraftment, delayed tumor onset, and significantly attenuated tumor growth in pancreatic and lung cancer models, outperforming semaglutide. Antitumor effects persisted despite partial weight regain, suggesting durable systemic and tumor immune reprogramming.[14]
- Diabetic Kidney Disease (DKD) — In preclinical studies, Ma et al. (2025) showed retatrutide demonstrated superior efficacy over liraglutide and tirzepatide in controlling risk factors associated with diabetic kidney disease in db/db mice, effectively mitigating inflammatory and fibrotic processes.[15]
Clinical Efficacy Summary by Dose (Phase 2)
| Dose | Weight Loss (48 wks, Obesity) | HbA1c Reduction (36 wks, T2D) | Evidence |
|---|---|---|---|
| 1 mg | -8.7% | — | Jastreboff et al. (2023)[1] |
| 0.5 mg | — | -0.43% | Rosenstock et al. (2023)[2] |
| 4 mg | -17.1% | ~-1.3% | [1][2] |
| 8 mg | -22.8% | ~-1.9% | [1][2] |
| 12 mg | -24.2% | -2.02% | [1][2] |
Biochemical Characteristics
| Property | Value |
|---|---|
| Molecular Formula | C₂₂₁H₃₄₂N₄₆O₆₈ |
| Molecular Weight | 4731.33 Da |
| CAS Number | 2381089-83-2 |
| PubChem CID | 171390338 |
| Sequence (1-Letter) | Y-Aib-QGTFTSDYSI-αMeL-LDK-K*-AQ-Aib-AFIEYLLEGGPSSGAPPPS-NH₂ (* = Lys modified with AEEA-γGlu-C20 diacid) |
| Sequence (3-Letter) | Tyr-Aib-Gln-Gly-Thr-Phe-Thr-Ser-Asp-Tyr-Ser-Ile-αMeLeu-Leu-Asp-Lys-Lys(AEEA-γGlu-C20 diacid)-Ala-Gln-Aib-Ala-Phe-Ile-Glu-Tyr-Leu-Leu-Glu-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Pro-Ser-NH₂ |
| Structure | 39-amino acid linear peptide; GIP backbone; non-coded residues: Aib at positions 2 & 20, α-methyl-L-leucine at position 13; C20 fatty diacid conjugated at Lys-17 via AEEA-γGlu linker; C-terminus amidated |
| Origin | Synthetic peptide engineered from GIP (glucose-dependent insulinotropic polypeptide) backbone; developed by Eli Lilly and Company |
| Classification | Triple Incretin/Hormone Receptor Agonist (GLP-1/GIP/Glucagon) / Acylated Peptide / Investigational Drug |
| Half-Life | Approximately 6 days in humans, supporting once-weekly dosing |
| Bioavailability | Subcutaneous injection; Tmax 12–72 hours; albumin binding via C20 fatty diacid extends duration of action |
Identifiers
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|---|---|
| Synonyms | |
| InChI Key | |
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Preclinical Research Summary
Preclinical & Clinical Research Summary
Key Preclinical (Animal) Studies
| Study | Model | Key Findings | Ref |
|---|---|---|---|
| Coskun et al. (2022) Cell Metabolism | DIO C57/Bl6 mice; 10 nmol/kg daily SC | 36.9% body weight loss (vs. 21.2% tirzepatide); 86.8% fat mass reduction; improved blood glucose, insulin, ALT, liver triglycerides; engages all three receptors in vivo | [4] |
| Urva et al. (2023) Diabetes Obes. Metab. | C57/Bl6 obese mice; 10 nmol/kg SC | Dose-dependent gastric emptying delay; chronic treatment attenuated GI slowing (tachyphylaxis); superior weight/food intake reduction vs. semaglutide alone | [17] |
| Ma et al. (2025) Endocrine | Diabetic db/db mice; 10 nmol/kg daily SC, 10 weeks | Superior efficacy over liraglutide and tirzepatide in reducing ALT, AST, cholesterol, triglycerides, LDL; mitigated inflammatory and fibrotic processes in diabetic kidney | [15] |
| Marathe et al. (2025) NPJ Metab. Health Dis. | Pancreatic and lung cancer models in obese mice | Reduced tumor engraftment; delayed tumor onset; greater tumor suppression than semaglutide; durable antitumor effects despite partial weight regain | [14] |
Key Clinical (Human) Studies
| Study | Population / Design | Key Results | Ref |
|---|---|---|---|
| Urva et al. (2022) Lancet (Phase 1b) | T2D patients; MAD, 0.5–12 mg SC weekly; RCT | Dose-dependent HbA1c and weight reductions; t1/2 ~6 days confirmed; GI AEs dose-related; well-tolerated overall | [8] |
| Jastreboff et al. (2023) NEJM (Phase 2) | Adults with obesity (no T2D); 1, 4, 8, 12 mg SC weekly; 48 wks; RCT | -24.2% mean weight loss (12 mg); dose-dependent; not plateaued at 48 wks; GI AEs most common | [1] |
| Rosenstock et al. (2023) Lancet (Phase 2) | Adults with T2D; 0.5–12 mg SC weekly; 36 wks; RCT | HbA1c -2.02% (12 mg); significant weight loss; improved insulin sensitivity; well-tolerated | [2] |
| Sanyal et al. (2024) Nature Med. (Phase 2a) | MASLD substudy; MRI-PDFF assessed liver fat; 48 wks | >85% achieved liver fat normalization (<5%) at 8–12 mg doses; up to 86% relative liver fat reduction | [3] |
| TRIUMPH-4 (Phase 3, 2025) Eli Lilly Press Release | Obesity + knee OA; 9 & 12 mg SC weekly; 68 wks | Up to 28.7% mean weight loss; WOMAC pain scores improved by up to 75.8%; first successful Phase 3 trial | [5] |
Safety Profile Summary
| Category | Detail | Incidence / Notes |
|---|---|---|
| Common GI AEs | Nausea, diarrhea, vomiting, constipation, decreased appetite | Nausea up to 63% at highest doses; dose-dependent; most common during titration[12][13] |
| Skin Hyperesthesia | Increased skin sensitivity, dysesthesia, "skin pain" | Up to 7% (vs. 1% placebo) in Phase 2[10] |
| Heart Rate | Dose-dependent increase, peaking at 24 weeks before declining | Mild to moderate arrhythmias reported[10] |
| Serious AEs | Acute pancreatitis (single cases); gallbladder disease; hypotension | SAE rate similar to placebo (~4–5%)[12] |
| Hepatic Safety | No hepatotoxicity signals; transient ALT/AST elevations resolved | Monitored in all trials[12] |
Dosage Summary
| Setting | Dose | Route / Schedule | Notes |
|---|---|---|---|
| In Vitro (EC50) | 0.0643 nM (GIPR), 0.775 nM (GLP-1R), 5.79 nM (GCGR) | Cell culture | Biased toward GIP potency[4] |
| Animal (Mice) | 10 nmol/kg daily | SC injection | Standard efficacy dosing; t1/2 21 h in mice[4] |
| Phase 1 (SAD) | 0.1–6 mg (single dose) | SC injection | Safety/PK assessment[8] |
| Phase 2 (Maintenance) | 1, 4, 8, 12 mg | SC once weekly; titrated from 2 or 4 mg | Titration by 2–4 mg every 4 weeks[1][2] |
| Phase 3 (TRIUMPH) | Target doses: 9 mg and 12 mg | SC once weekly; initiated at 2 mg | Ongoing registrational trials[5] |
Pharmacokinetic Profile
| Parameter | Value | Notes |
|---|---|---|
| Half-life (Human) | ~6 days | Supports once-weekly dosing[8] |
| Half-life (Mouse) | ~21 hours | Single 47 μg/kg dose[4] |
| Tmax | 12–72 hours | Post-SC dose in humans |
| Metabolism | Hepatic proteolysis; fatty acid β-oxidation | No CYP450 interaction |
| Clearance (Mouse) | 11.22 mL/h/kg | CD-1 mice |
&x26A0;️ Important Disclaimer
This product is sold strictly for in-vitro research and laboratory use only. It is not approved by the FDA for human consumption, medical use, diagnostic use, or veterinary use. Bodily introduction of any kind into humans or animals is strictly forbidden by law. All products are supplied as research chemicals only. The information provided here is compiled from peer-reviewed scientific literature and is intended solely for educational and informational purposes.
About This Research Profile
This research profile was compiled from peer-reviewed sources including publications in the New England Journal of Medicine, The Lancet, Nature Medicine, Cell Metabolism, and other high-impact journals. All citations reference publicly available scientific literature. The profile is regularly reviewed and updated to reflect the latest research findings. Last reviewed: February 2026.
Authors & Attribution
✍️ Article Author
Tamer Coskun, MD, PhD
Tamer Coskun, MD, PhD, is a senior researcher at Eli Lilly and Company (Indianapolis, IN, USA) and a key figure in the discovery and early development of retatrutide (LY3437943). He served as the lead author on the foundational 2022 publication in Cell Metabolism detailing the molecule's discovery, mechanism of action, and proof of concept from preclinical models through Phase 1 human data. Dr. Coskun has been a senior or co-author on subsequent Phase 2 clinical trials, including substudies focusing on body composition, eating behavior, and kidney parameters. His research contributions span the entire translational pipeline of retatrutide, from molecular design through clinical validation. His key publications include "LY3437943, a novel triple glucagon, GIP, and GLP-1 receptor agonist for glycemic control and weight loss: From discovery to clinical proof of concept" (2022, Cell Metabolism) and "Effects of retatrutide on body composition in people with type 2 diabetes" (2025, The Lancet Diabetes & Endocrinology). Tamer Coskun is being referenced as one of the leading scientists involved in retatrutide research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →🎓 Scientific Journal Author
Ania M. Jastreboff, MD, PhD
Ania M. Jastreboff, MD, PhD, is an Associate Professor at Yale University School of Medicine (New Haven, CT, USA) and Director of the Yale Obesity Research Center. She served as the lead investigator for the pivotal Phase 2 clinical trial evaluating retatrutide for the treatment of obesity, published in the New England Journal of Medicine in 2023. Her work demonstrated that the drug could achieve up to 24.2% mean body weight reduction over 48 weeks, establishing retatrutide as one of the most potent investigational anti-obesity agents. Dr. Jastreboff is recognized as a leading clinical researcher in the incretin-based obesity therapeutics field, having also led pivotal trials for tirzepatide and other novel agents. Her key publications include "Triple-Hormone-Receptor Agonist Retatrutide for Obesity — A Phase 2 Trial" (2023, New England Journal of Medicine). Ania M. Jastreboff is being referenced as one of the leading scientists involved in retatrutide research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Ania M. Jastreboff, MD, PhD is being referenced as one of the leading scientists involved in the research and development of GLP3-R. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
🔬 Contributing Researcher
Julio Rosenstock, MD
Julio Rosenstock, MD, is a clinical researcher affiliated with Velocity Clinical Research at Medical City (Dallas, TX, USA) and a world-renowned expert in diabetes clinical trials and incretin-based therapies. He led the Phase 2 clinical trial assessing the safety and efficacy of retatrutide in people with type 2 diabetes, published in The Lancet in 2023. His research highlighted the drug's ability to provide robust, dose-dependent reductions in both HbA1c (up to -2.02%) and body weight compared to placebo and the active comparator dulaglutide. Dr. Rosenstock has been a principal investigator on numerous landmark diabetes drug trials and has authored hundreds of peer-reviewed publications. His key publications include "Retatrutide, a GIP, GLP-1 and glucagon receptor agonist, for people with type 2 diabetes: a randomised, double-blind, placebo and active-controlled, parallel-group, phase 2 trial conducted in the USA" (2023, The Lancet). Julio Rosenstock is being referenced as one of the leading scientists involved in retatrutide research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
View Full Researcher Profile →Julio Rosenstock, MD is being referenced as one of the leading scientists involved in the research and development of GLP3-R. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide.
Referenced Citations
Jastreboff AM, Kaplan LM, Frias JP, Wu Q, Du Y, Gurbuz S, Coskun T, Haupt A, Milicevic Z, Hartman ML. Triple-Hormone-Receptor Agonist Retatrutide for Obesity - A Phase 2 Trial. New England Journal of Medicine, 389(6), 514-526, 2023.
PubMedRosenstock J, Frias J, Jastreboff AM, Du Y, Lou J, Gurbuz S, Thomas MK, Hartman ML, Haupt A, Milicevic Z, Coskun T. Retatrutide, a GIP, GLP-1 and glucagon receptor agonist, for people with type 2 diabetes: a randomised, double-blind, placebo and active-controlled, parallel-group, phase 2 trial conducted in the USA. Lancet, 402(10401), 529-544, 2023.
DOISanyal AJ, Kaplan LM, Frias JP, Brouwers B, Wu Q, Thomas MK, Harris C, Schloot NC, Du Y, Mather KJ, Haupt A, Hartman ML. Triple hormone receptor agonist retatrutide for metabolic dysfunction-associated steatotic liver disease: a randomized phase 2a trial. Nature Medicine, 30(7), 2037-2048, 2024.
DOICoskun T, Urva S, Roell WC, Qu H, Loghin C, Moyers JS, O'Farrell LS, Briere DA, Sloop KW, Thomas MK, Pirro V, Wainscott DB, Willard FS, Abernathy M, Morford L, Du Y, Benson C, Gimeno RE, Haupt A, Milicevic Z. LY3437943, a novel triple glucagon, GIP, and GLP-1 receptor agonist for glycemic control and weight loss: From discovery to clinical proof of concept. Cell Metabolism, 34(9), 1234-1247.e9, 2022.
DOIGiblin K, Kaplan LM, Somers VK, Le Roux CW, Hunter DJ, Wu Q, Lalonde A, Ahmad N, Bethel MA. Retatrutide for the treatment of obesity, obstructive sleep apnea and knee osteoarthritis: Rationale and design of the TRIUMPH registrational clinical trials. Diabetes, Obesity and Metabolism, 28(1), 83-93, 2026.
DOICoskun T, Wu Q, Schloot NC, Haupt A, Milicevic Z, Khouli C, Harris C. Effects of retatrutide on body composition in people with type 2 diabetes: a substudy of a phase 2, double-blind, parallel-group, placebo-controlled, randomised trial. The Lancet Diabetes & Endocrinology, 13(8), 674-684, 2025.
DOIHeerspink HJL, Lu Z, Du Y, Duffin KL, Coskun T, Haupt A, Hartman ML. The Effect of Retatrutide on Kidney Parameters in Participants With Type 2 Diabetes Mellitus and/or Obesity. Kidney International Reports, 10(6), 1980-1992, 2025.
DOIUrva S, Coskun T, Loh MT, Du Y, Thomas MK, Gurbuz S, Haupt A, Benson CT, Hernandez-Illas M, D'Alessio DA, Milicevic Z. LY3437943, a novel triple GIP, GLP-1, and glucagon receptor agonist in people with type 2 diabetes: a phase 1b, multicentre, double-blind, placebo-controlled, randomised, multiple-ascending dose trial. Lancet, 400(10366), 1869-1881, 2022.
DOIHeerspink HJL, van Raalte DH, Bjornstad P, Bunck MC, Wu P, Tunali I, Milicevic Z, Koeneman L. Rationale, design and baseline characteristics of the TRANSCEND-CKD trial of retatrutide in patients with chronic kidney disease. Nephrology Dialysis Transplantation, gfaf230, 2025.
DOIKatsi V, Koutsopoulos G, Fragoulis C, Dimitriadis K, Tsioufis K. Retatrutide - A Game Changer in Obesity Pharmacotherapy. Biomolecules, 15(6), 796, 2025.
DOIAbdul-Rahman T, Roy P, Ahmed FK, Mueller-Gomez JL, Sarkar S, Garg N, Femi-Lawal VO, Wireko AA, Thaalibi HI, Hashmi MU, Dzebu AS, Banimusa SB, Sood A. The power of three: Retatrutide's role in modern obesity and diabetes therapy. European Journal of Pharmacology, 985, 177095, 2024.
DOIMaharshi V, Singh S, Manjhi PK, Singh SK, Kumar A, Kumar R. Navigating retatrutide safety: comprehensive insights from systematic review and meta-analysis. Journal of Public Health and Development, 24(1), 318-338, 2026.
DOIAbouelmagd AA, Abdelrehim AM, Bashir MN, Abdelsalam F, Marey A, Tanas Y, Abuklish DM, Belal MM. Efficacy and safety of retatrutide, a novel GLP-1, GIP, and glucagon receptor agonist for obesity treatment: a systematic review and meta-analysis of randomized controlled trials. Proceedings (Baylor University Medical Center), 38(3), 291-303, 2025.
DOIMarathe SJ, Grey EW, Bohm MS, Joseph SC, Ramesh AV, Cottam MA, et al. Incretin triple agonist retatrutide (LY3437943) alleviates obesity-associated cancer progression. NPJ Metabolic Health and Disease, 3(1), 10, 2025.
DOIMa J, Hu X, Zhang W, Tao M, Wang M, Lu W. Comparison of the effects of Liraglutide, Tirzepatide, and Retatrutide on diabetic kidney disease in db/db mice. Endocrine, 87(1), 159-169, 2025.
DOITewari J, Qidwai KA, Tewari A, Kaur S, Tewari V, Maheshwari A. Efficacy and safety of triple hormone receptor agonist retatrutide for the management of obesity: a systematic review and meta-analysis. Expert Review of Clinical Pharmacology, 18(1-2), 51-66, 2025.
DOIUrva S, O'Farrell L, Du Y, Loh MT, Hemmingway A, Qu H, Alsina-Fernandez J, Haupt A, Milicevic Z, Coskun T. The novel GIP, GLP-1 and glucagon receptor agonist retatrutide delays gastric emptying. Diabetes, Obesity and Metabolism, 25(11), 2784-2788, 2023.
DOIRUO Disclaimer
For Research Use Only (RUO). This product is intended solely for in-vitro research and laboratory experimentation. It is not a drug, food, cosmetic, or medical device and has not been approved by the FDA for any human or veterinary use. It must not be used for therapeutic, diagnostic, or any other non-research purpose. Pure US Peptide does not condone or encourage the use of this product for anything other than strictly defined research applications. Users assume full responsibility for compliance with all applicable regulations and guidelines.
Certificate of Analysis (COA)
Every batch is strictly tested by accredited third-party laboratories (ISO 17025) to ensure 99%+ purity.
Latest Lab Report
Storage & Handling
Summary
Lyophilized: -20°C to -80°C (stable 1–2 years); Reconstituted: aliquot and store at -20°C; avoid repeated freeze-thaw cycles; protect from moisture and light.
Lyophilized Powder
Store at -80°C for optimal long-term stability (approximately 2 years) or at -20°C for up to 1 year. Keep in sealed containers, protected from moisture and light, ideally under nitrogen atmosphere. The lyophilized form appears as a white to off-white solid powder.
Reconstituted Solution
Dissolve in sterile water (soluble at 20 mg/mL with pH adjustment) or DMSO. Prepare working aliquots immediately upon reconstitution to prevent repeated freeze-thaw cycles, which can inactivate the peptide. Store aliquots at -20°C and use within 1 month for best results.
Quality Control
Purity is assessed by RP-HPLC (targeting ≥99% for research grade). Molecular identity is confirmed by Mass Spectrometry (expected MW ~4731.33 Da). Additional characterization may include NMR spectroscopy (H-NMR) for structural verification. The C20 fatty diacid conjugation at Lys-17 enhances metabolic stability in biological systems.
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