GLP3R - retatrutide

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Triple GLP-1 / GIP / glucagon receptor agonist — the highest-recorded weight loss of any obesity peptide.

A 39-residue synthetic peptide reported in the literature to engage the GLP-1, GIP, and glucagon receptors simultaneously in in-vitro assays. For laboratory characterisation only.

GLP3-R (Retatrutide/LY3437943) is a first-in-class triple agonist targeting GIP, GLP-1, and glucagon receptors simultaneously. Phase 3 TRIUMPH-4 trial (2026) showed 28.7% weight loss at 12mg/68 weeks — the highest ever reported. Additional Phase 3 data shows A1C reductions of 1.7-2.0%, up to 100% liver fat reduction in MASLD, and 14 mmHg systolic BP reduction. FDA approval projected for 2027.

In-vitro cAMP assays report engagement of the GLP-1 receptor pathway; described in the primary literature as the canonical incretin arm of the molecule.

In-vitro receptor binding characterised at the GIP receptor. Discussed in the literature as a second incretin arm distinct from GLP-1R engagement.

In-vitro engagement at the glucagon receptor is the pharmacological feature distinguishing this compound from prior dual GLP-1/GIP analogs in the same literature.

In-vitro / preclinical characterisation only — no clinical or therapeutic claim is expressed or implied. Research use only.

GLP3-R is a synthetic 39-amino-acid triple incretin/glucagon receptor agonist. GLP3-R (Retatrutide/LY3437943) is a first-in-class triple agonist targeting GIP, GLP-1, and glucagon receptors simultaneously. Phase 3 TRIUMPH-4 trial (2026) showed 28.7% weight loss at 12mg/68 weeks — the highest ever reported. Additional Phase 3 data shows A1C reductions of 1.7-2.0%, up to 100% liver fat reduction in MASLD, and 14 mmHg systolic BP reduction. FDA approval projected for 2027. It has a mass 4624.2 Da. Common synonyms in the literature include Retatrutide, retatrutide, and LY3437943.

Investigation of GLP3-R to date is clinical-investigational, with the majority of citations concentrated in animal models and in-vitro assays rather than randomized controlled human trials. Published work referencing GLP3-R spans Phase 2 obesity trial (NEJM 2023): In 338 adults with BMI ≥30 (or ≥27 with comorbidities), glp3-r achieved dose-dependent weight loss: 8.7% (1 mg), 17.1% (4 mg), 22.8% (8 mg), and 24.2% (12 mg) at 48 weeks vs. 2.1% placebo. Weight loss trajectory showed no plateau, suggesting continued efficacy beyond 48 weeks, Phase 2 type 2 diabetes trial: In adults with T2D, glp3-r showed HbA1c reductions of 2.0% and significant weight loss while maintaining glycemic control despite glucagon component. Safety profile similar to GLP-1 agonists, and Ongoing Phase 3 TRIUMPH program: Multiple trials initiated in 2023-2024 including obesity (TRIUMPH-3), obesity with CKD, obesity with knee osteoarthritis (TRIUMPH-4), obesity with chronic low back pain, cardiovascular outcomes (5-year CVOT), and head-to-head comparison vs. glp2-t. Proposed mechanisms in the literature include GLP-1 receptor agonism: glucose-dependent insulin secretion, appetite suppression, delayed gastric emptying and GIP receptor agonism: enhanced insulin sensitivity, potentiation of GLP-1 effects, improved lipid handling. None of this material describes therapeutic outcomes in humans, and No vendor listed here provides dosing guidance for GLP3-R outside laboratory research.

For the full mechanistic profile, published references, and constraint notes on GLP3-R, see the GLP3-R research page. All references cited on that page are peer-reviewed primary literature.

Binding and functional-assay data for GLP3-R, from peer-reviewed in-vitro pharmacology publications. Values are receptor activity parameters — not clinical outcomes.

Study designs referencing this compound in the published literature. Descriptions cover framework only — phase, participant count, duration, and citation — not outcomes. Click a card to review the source directly.

Structural and in-vitro receptor-binding attributes of published incretin research compounds. Reference chemistry only — no comparative-effectiveness claim expressed or implied.