Metabolic & Body Composition
Retatrutide
Triple GIP, GLP-1 and glucagon receptor agonist in clinical-stage research. Studied for caloric intake pathways and hepatic glucose output.
Also known asLY3437943
Identity
Residue chain
One bead per amino acid residue, N-terminus to C-terminus. Long chains are shown truncated.
- Molecular weight
- 4769.5 Da
- Amino acid residues
- 39
- Half-life
- ~6 days
- CAS number
- 2381272-90-6
Monograph
Specifications
- Research area
- Metabolic & Body Composition
- Half-life
- ~6 days
- Molecular weight
- 4769.5 Da
- Amino acid residues
- 39
- CAS number
- 2381272-90-6
- Formula
- 39 AA + C₁₈ fatty diacid conjugate
- Sequence
- 39 aa lipidated peptide (C₁₈ fatty diacid at Lys²⁰), abbreviated
- Designation
- LY3437943, triple GLP-1R / GIPR / GCGR co-agonist
Pharmacokinetics
- Half-life
- ~6 days
- T-max
- 24–72 h
- Bioavailability
- ~50–60% (SC)
- Route
- Subcutaneous (research use)
Receptor targets
- GLP-1RIncretin / appetite suppression
- GIPRGlucose-dependent insulinotropic
- GCGR (glucagon)Energy expenditure ↑
Signalling cascade
- 1Triple receptor binding
- 2Central appetite ↓
- 3Insulin sensitization
- 4Glucagon-driven thermogenesis
- 5Visceral adiposity ↓
- Mechanism of action
- Triple agonist of GIP, GLP-1, and glucagon receptors. Simultaneously reduces caloric intake via central GLP-1 and GIP pathways, increases energy expenditure through glucagon receptor activation, and modulates hepatic glucose output. Represents the first triple incretin approach in clinical-stage research.
- Storage and handling
- Store at 2–8 °C.
Research focus
- 01Triple incretin receptor agonism (GIP / GLP-1 / glucagon)
- 02Caloric intake regulation via central appetite pathways
- 03Energy expenditure augmentation through glucagon receptor
- 04Adipose tissue metabolism and visceral fat reduction models
- 05Glucose homeostasis and hepatic insulin sensitivity
Overview
Retatrutide is a triple agonist of the GIP, GLP-1 and glucagon receptors. It is studied for caloric intake pathways through central GLP-1 and GIP signalling, energy expenditure through glucagon receptor activation, and hepatic glucose output.